محمدامین عدالت منش

Pre-eclampsia (PE) can cause brain damage before birth. However, its mechanism is not clear. The present study evaluated the effect of cinnamic acid (CIN) on the expression of inflammatory cytokines of the forebrain and neuronal damage in the hippocampus of PE model fetuses induced with l-NAME.

25 pregnant female rats were randomly divided into 5 groups: control group (no treatment), PE+NS group (daily injection of 250 mg l-NAME from embryonic day (ED) 15 to 20 to induce PE and then one hour later normal saline gavage), PE+CIN25, PE+CIN50 and PE+CIN100 groups (CIN gavage with doses of 25, 50 and 100 mg, respectively, one hour after l-NAME injection). On the ED21, after cesarean section, the fetal brain was dissected. The content of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin-1 beta (IL-1β) in the forebrain and cell density in the CA1 and CA3 regions of the fetal hippocampus were measured.

A significant increase in TNF-α, IL-6 and IL-1β in the forebrain along with a decrease in neuronal density in the CA1/CA3 regions was seen in the PE+NS group compared to the control group (p<0.05). While in the groups receiving CIN, they showed a significant decrease in TNF-α, IL-6 and IL-1β in the forebrain and an increase in CA1/CA3 neuronal density compared to the PE+NS group (p<0.05).

CIN improved the inflammation and reduced cell damage in the hippocampus of PE model fetuses through modulating the level of anti-inflammatory cytokines in the fetal forebrain.

Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive damage of dopaminergic neurons in the substantia nigra and reduction of dopamine in the striatum. Several studies have shown that oxidative stress plays an important role in the pathophysiology of PD, and antioxidant agents can be useful in reducing the rate of neurodegeneration. This study aimed to evaluate the antioxidant and neuroprotective effect of p-Cymene in the reserpine-induced (RES) PD rat model.

40 male Wistar rats were divided into 5 groups, including control, receiving vehicle of p-Cymene + receiving vehicle of reserpine (VP+VR), receiving reserpine (1 mg/5 days/intraperitoneal) + vehicle of p-Cymene (RES+VP), receiving p-Cymene (50 mg/14 days/oral) + vehicle of reserpine (p-Cymene+VR) and receiving reserpine+p-Cymene (RES+p-Cymene) were divided. After the treatment, the animals were subjected to behavioral evaluation (catalepsy test and shuttle box test). At the end, the level of hippocampal catalase (CAT), superoxide dismutase (SOD) by ELISA and malondialdehyde (MDA) by thiobarbituric acid method and the density of apoptotic neurons in different areas of the hippocampus were measured.

The results showed a significant reduction in catalepsy behavior, amelioration of avoidance memory, a significant increase in CAT and SOD, and a decrease in MDA in the RES+p-Cymene group compared to the p-Cymene+VR group. On the other hand, p-Cymene prevented the increase in the density of apoptotic neurons caused by RES in the CA1 and CA3 regions of the hippocampus.

In general, the results showed that p-cymene had a protective effect in the PD model and prevented motor-cognitive disorders and neuronal damage caused by RES.

Parkinson's disease is characterized by an increase in alpha-synuclein (α-Syn) and a decrease in cAMP-responsive element-binding protein (CREB) levels in the brain. This study aimed at investigating the effects of a period of high-intensity interval training in swimming on α-Syn and CREB gene expression in rats with Parkinson's disease.

In this experimental study, 21 male Wistar rats aged 8 to 10 weeks were selected. Fourteen rats were induced with Parkinson's disease through intraperitoneal injection of reserpine and randomly divided into patient and training groups. Additionally, seven healthy rats served as the control group. Rats in the training group underwent 20 sets of 30-second swims with 30-second rest intervals over a period of 6 weeks. α-Syn and CREB gene expression levels were measured using Real-Time PCR in blood samples collected 48 hours after the final training session in all groups.

The patient group exhibited significantly higher α-Syn gene expression compared to both the control group and the training group (P=0.001 and P=0.002, respectively). However, no significant difference was observed between the training and control groups (P=0.2). Additionally, CREB gene expression was significantly lower in the patient group compared to both the control group and the training group (P=0.006 and P=0.003, respectively), with no significant difference between the training and control groups (P=0.6).

High-intensity interval training in swimming may reduce α-Syn expression and increase CREB levels, potentially contributing to the survival of dopamine neurons and improvement in Parkinson's disease symptoms. Further research in this area is warranted to validate these findings.

Parkinson’s disease characterized by loss of the dopaminergic neurons, accompanied by neuroinflammation. The effect of high intensity interval training on dopaminergic neurons survival is not well known. The aim of present study was to examine the effect of high intensity interval swimming on DJ-1 and mir-874 gene expression of hippocampal cells in rats with Parkinson’s disease. In this experimental study, twenty-one 8 to 10-week-old male Wistar rats (weight 200 ± 10.2 grams) were divided into three groups (7 rats in each group), including: healthy control, PD and training. PD induced by injection of 1 mg/kg reserpine during 5 days. The rats in the training group performed high intensity interval swimming, including 20 times of 30 seconds of swimming with 30 seconds of rest between each time for 6 weeks. Data were analyzed using one-way ANOVA and LSD post hoc test were run using SPSS-22 at the P <0.05. The study results indicated that DJ-1 gene expression were lower in the PD group compare to the healthy group and training group (p=0.02 and p=0.04 respectively); while, mir-874 gene expression was higher in the PD group compare to the healthy group and training group (p=0.001 and p=0.02 respectively). No significant difference was observed between training group and healthy group for these proteins' gene expression (p=0.6 and p=0.08 respectively). In general, it seems that high intensity swimming interval training is effective for improving PD by enhancing the mechanisms of dopaminergic neurons survival.

Dysregulation of miRNAs will result in development and progression of numerous diseases, such as in Parkinson’s disease (PD). The effect of exercise training on mechanisms of development and progression of PD are not well known. The aim of present study was to examine the effect of high intensity interval swimming on LRRK2 and mir-205 gene expression in rats with PD.

PD induced in fourteen 8 to 10-week-old male Wistar rats by injection of 1 mg/kg reserpine during 5 days. Then, these rats were divided into PD group or training group. Seven rats were considered as the healthy control group without any reserpine injection. The rats in the training group performed high intensity interval swimming, including 20 times of 30 seconds of swimming with 30 seconds of rest between each time for 6 weeks. 48h after last session of training, sacrificed animals and hypocampic LRKK2 and mir-205 gene expression was measured. To analyze data, the statistical method of one-way analysis of variance was used with significance P<0.05.

The results indicated that LRRK2 gene expression were higher in the PD group compare to the healthy group and training group (P=0.001 and P=0.001 respectively) and no significant difference was observed between training group and healthy group (P=0.1). mir-205 gene expression was lower in the PD group compare to the healthy group and training group (P=0.001 and P=0.01 respectively). There was negative correlation between hypocampic LRKK2 and mir-205 gene expression (r=-0.71 and P=0.01).

It seems that high intensity interval swimming improves PD by reducing LRRK2 and increasing mir-205 gene expression.

Parkinson’s disease is a progressive neurological disorder where loss of dopamine neurons in the substantia nigra and dopamine depletion in the striatum cause characteristic motor and nonmotor symptoms. Glial cell line-derived neurotrophic factor (GDNF) is one of the most important neurotrophins that regenerates dopaminergic neurons by receptor tyrosine kinase Ret in Parkinson's disease. The effect of exercise on these proteins are not well known. The present study was conducted to examine the effect of high intensity swimming training on GDNF and Ret gene expression in hippocampal tissue in rats with Parkinson's disease.

In this experimental study, twenty-one male Wistar rats (age 8 to 10 weeks and weight 200-250 gr) were obtained from the Animal Breeding Center of Islamic Azad University, Shiraz branch and transferred to the animal laboratory of this university. Parkinson's disease induced in fourteen rats by injection of 1 mg/kg reserpine during 5 days and then these rats were divided into Parkinson's disease group or training group randomly. The rats in the training group swam 20 times of 30 seconds with 30 seconds of rest between each time for 6 weeks. Additionally, seven remaining rats were included in the healthy control group without any intervention. GDNF and Ret gene expressions were measured in hippocampus 48h after the last session of training using Real Time-PCR. Data were analyzed using one-way ANOVA test and Bonferoni post hoc using SPSS-22 at the P < 0.05.

Data indicated that GDNF gene expression was reduced after induction of Parkinson's disease and this gene was lower in Parkinson's disease group compare to the healthy control group (p=0.001). For Ret gene expression also our results indicated that this gene was reduced after induction of Parkinson's disease and this gene was lower in Parkinson's disease group compare to the healthy control group (p=0.03). After 6-week of training, GDNF gene expression increases compare to the Parkinson's disease group (p=0.009). For Ret gene expression also our results indicated that this gene expression increases compare to the Parkinson's disease group (p=0.007 respectively); while on significant differences were observed between training group and healthy group (p=0.6 and p=0.9 respectively).

In summary it seems that high-intensity interval swimming training that used in this study improves dopaminergic neuron survival in Parkinson's disease by increasing GDNF as a neurotrophine factor and subsequent signaling, receptor tyrosine kinase Ret. According to limit of information, future studies are needed specially in human cases.

Parkinson disease (PD) is a progressive neurodegenerative disease that affects peripheral organs as well as the central nervous system (CNS). The present study was done to examine the effect of high intensity swimming interval training on gene expression of some hippocampal inflammatory markers in rats with PD. In this experimental study, 21 male Wistar rats (aged 8-10 weeks; weight 200 ± 10.2 grams) were divided into three groups including: healthy control, PD and training. PD was induced by injection of 1 mg/kg of reserpine during 5 days. The rats in the training group performed 6 weeks of HIIT including 20 times of 30 seconds of swimming with 30 seconds of rest between each time. Data were analyzed using one-way ANOVA and LSD post hoc test were run using SPSS-22 at the P <0.05. Data revealed that TNF-α gene expression was reduced after 6 weeks of swimming interval training (p=0.01) compared to the PD group. We observed non-significant decrease in IL-1β after the intervention as compared to the PD group (p=0.6). According the results of this study, high intensity swimming interval training is effective in reducing the gene expression of some hippocampal inflammatory markers in rats with PD and it is suggested as the effective strategy to improve PD.

Polycystic ovary syndrome (PCOS) is associated with hormonal-metabolic disorders, oxidative stress and ovulation disorders. The present study evaluated the effect of selenium nanoparticles (SeNPs) on the activity of antioxidant enzymes and ovarian tissue structure and oxidative DNA damage in the polycystic ovary syndrome (PCOS) model. 32 female Wistar rats were divided into 4 control groups, PCOS, PCOS+SeNPs0.1 and PCOS+SeNPs0.1. Polycystic ovary syndrome was induced by a single intramuscular injection of estradiol valerate (4 mg/kg) and SeNPs with doses of 0.1 and 0.2 mg/kg were administered orally for 14 days. At the end, the tissue level of superoxide dismutase (SOD), catalase (CAT) enzymes, content of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) in the ovarian tissue was measured by ELISA technique and the ovarian tissue structure was examined histopathologically. A significant decrease in the number of follicular cysts, 8-OHdG and MDA levels along with a significant increase in tissue levels of SOD and CAT enzymes were seen in the SeNPs treatment groups compared to the PCOS group. In fact, SeNPs with antioxidant function improved ovarian tissue structure in polycystic ovary syndrome model.

Uteroplacental insufficiency (UPI) by inducing oxidative stress in the fetal brain leads to disruption of its development. The present study evaluated the effects of Naringin on the antioxidant defense system in the fetal forebrain and prevention of the hippocampal damage following UPI.

20 pregnant Wistar rats were randomly divided into 4 groups: control, UPI+Saline, UPI+Nar50 (UPI+naringin with a dose of 50 mg/kg) and UPI+Nar100 (UPI+ naringin with a dose of 100 mg/kg). In order to induce UPI, permanent occlusion of the anterior uterine vessels was performed on the embryonic day (ED) 18. Naringin and saline were gavagd from ED12-18. On the ED21, measuring the level of catalase (CAT), superoxide dismutase (SOD) and antioxidant capacity (TAC) by ELISA technique and malondialdehyde (MDA) by thiobarbituric acid method in the fetal forebrain and evaluating neuronal density in the CA1 and CA3 areas of the hippocampus were done.

A significant decrease in the brain activity of CAT, SOD, TAC and neuronal density in the CA1/CA3 areas of the hippocampus along with a significant increase in MDA was seen in the UPI+Saline group compared to the control group (p<0.05). While, a significant increase in CAT, SOD, TAC and CA1/CA3 neuronal density and a significant decrease in MDA was seen in the groups receiving Naringin compared to the UPI+Saline group (p<0.05).

Administering Naringin before induction of UPI by strengthening the antioxidant system in the fetal forebrain caused the prevention of neurological complications caused by UPI in the fetal brain.

Trimethyltin (TMT) intoxication is associated with damage to the cholinergic system in the hippocampus. The aim of this study was to evaluate the effect of trans-cinnamic acid on cognitive deficit and cell damage in CA1/CA3 regions of the hippocampus, as well as measure the activity of acetyl choline esterase (AChE) in the hippocampus of a rat model of Alzheimer’s disease (AD).

In this experimental study, 40 adult male Wistar rats were randomly divided into four groups: control, TMT+Saline, TMT+CIN20, and TMT+CIN40. The AD model was induced by intraperitoneal injection of 8 mg/kg TMT body weight, and 72 h after TMT administration, doses of 20 and 40 mg of trans-cinnamic acid were gavaged daily for four weeks. Subsequently, working memory, passive avoidance learning, neuronal density in hippocampal CA1 and CA3 regions, and AChE enzyme activity were measured in this study.

There was a significant increase in CA1/CA3 neuronal density, percentage of motor frequency, and improved passive avoidance memory in the groups receiving trans-cinnamic acid, compared to the group receiving normal saline. Moreover, AChE enzyme activity in the hippocampus, especially in the TMT+CIN40 group, increased significantly, compared to the TMT+Saline group.

It seems that trans-cinnamic acid with AChE inhibitory effects improves cognitive decline and hippocampal cell damage in the TMT model of AD.

As the world's population increases, the incidence of infertility is increasing, and infertility is now considered to affect 8–12% of couples worldwide. Assisted reproductive technology (ART) such as in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) is revolutionizing the field of reproductive medicine and strives continuously to provide infertile patients with access to appropriate and efficient treatments. However, some causes leading to total/low fertilization rate in ART have been addressed. Phospholipase C zeta (PLCζ) is the main sperm-specific factor responsible for triggering oocyte activation (OA). Therefore, PLCζ abnormalities, including low and absent expression as well as its mutation has been described as one of the fertility rate inducers resulted from the oocyte activation deficiency and sperm parameters abnormalities and failed IVF and ICSI cycles. In this review article we have aimed to focus on the latest information of the PLCζ published data in the Web of Science, Scopus, Science Direct and PubMed databases and resulted in the failed IVF and ICSI and recurrent ICSI and IVF failure. In addition the investigations on PLCζ gene and its coded protein in the animals have been also reported.

Studies have shown that the change in PLCζ expression and its mutations can cause a decrease in the fertilization rate due to egg activation defects and abnormalities in sperm parameters and failure in ART.

Although acute renal injury (AKI) is a consequence of renal ischemia-reperfusion (RIR), RIR-induced oxidative damage also affects distant organs. The aim of this study was to evaluate the effect of gallic acid (GA) on oxidative stress parameters and neuronal density in the brain hippocampus following RIR.

48 male Wistar rats were randomly divided into 4 groups, including control, ischemia/reperfusion+normal saline (RIR+Saline), and ischemia/reperfusion+GA groups at doses of 100 mg/kg (RIR+GA100) and 200 mg/kg (RIR+GA200). Animals in all groups except control underwent unilateral nephrectomy (right). The treatments were performed for 14 days and then, the left kidney was ischemized for 45 minutes. After 72 hours, hippocampal activity levels of catalase (CAT), glutathione peroxidase (GPx), total antioxidant capacity (TAC) and malondialdehyde (MDA) were evaluated. Finally, neuronal density was measured in CA1 and CA3 regions of the hippocampus.

A significant decrease in CAT, GPx and TAC and an increase in MDA was observed in RIR + Saline group compared to the control group, which was associated with a significant decrease in neuronal density in CA1/CA3 (p<0.05). While in the GA-treated groups, along with a significant increase in CAT, GPx and TAC and a decrease in MDA in the hippocampus, showed a significant increase in neuronal density of CA1/CA3 regions compared to the RIR+Saline group (p˂0.05).

GA pretreatment can ameliorate oxidative damage and neuronal death in the brain hippocampus of rats with RIR-induced acute renal damage.

Polycystic Ovary Syndrome (PCOS) is the leading cause of infertility due to lack of ovulation and the result of oxidative stress of ovarian tissue, which is associated with disability in ovarian functions. This study aims at evaluating the effect of 4 weeks of Gallic Acid (GA) prescription and swimming (EX) training on ovarian tissue parameters in PCOS model. Forty adult Wistar female rats weighing 180 ± 10 g were randomly divided into 5 groups: PCOS, PCOS + GA, PCOS + EX and PCOS + GA + EX. To induce the PCOS model, letrozole (1 mg / kg) was NG tubed for 28 days. Then, GA was prescribed orally for 4 weeks and swimming was performed for 4 weeks and 3 sessions per week. Finally, after dissection of the ovary and staining with hematoxylin-eosin, histological evaluations were performed. The results showed a significant decrease in corpus luteum diameter, number of monolayer, multilayer, secondary and Graafian follicles and corpus luteum in PCOS group and also a significant increase in the number of atretic and cystic follicles compared with control group. While the interaction of GA prescription and swimming improved ovarian parameters. However, no significant change in the diameter of oocytes and primary and multilayered follicles was observed in the groups. GA and swimming appear to be effective on restoring the folliculogenesis of PCOS rat model and the ovulation process.

Prenatal intoxication with trimethyletin (TMT) induces widespread neuronal death in the central nervous system by inducing oxidative stress. The aim of this study was to evaluate the antioxidant effect of gallic acid (GA) on the neuronal density of the entorhinal cortex, hippocampal pyramidal cells and oxidative stress parameters in the fetal forebrain following TMT intoxication.

25 pregnant Wistar female rats were randomly divided into 5 groups, including control, TMT+Saline, TMT+GA100, TMT+GA200 and TMT+GA400. To induce TMT intoxication, TMT (9 mg/kg body weight) was injected intraperitoneally into pregnant rats on embryonic day (ED) 14. From the ED12 to ED18, the treatment groups received orally GA at different doses. After fetal cesarean section on the ED21, neuronal density assessment of the entorhinal cortex, CA1 and CA3 regions of the hippocampus and forebrain level of catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) was performed by ELISA.

The results showed a significant increase in the activity of CAT and SOD enzymes and a significant decrease in MDA in the forebrain of GA-receiving groups compared to the TMT + Saline group. In addition, increased neuronal density was observed in the entorhinal cortex and CA1/CA3 regions of the hippocampus in the GA treated rats compared to the TMT + Saline group.

Prenatal TMT intoxication induced oxidative stress in the fetal forebrain, causing damage to the entorhinal cortex and hippocampus of rat fetal brain. On the other hand, GA prevented and improved neuronal damage in these areas of the fetal brain.

Pre-sex selection is the process by which Y or X-bearing spermatozoa are used to produce the desired sex in the offspring. X-bearing spermatozoa are believed to have a longer lifespan, and are more resistant to acidic conditions, temperature changes, and even oxidative stress compared to Y-bearing.

The present study was aimed to investigate the effect of heat stress on sperm parameters and sex ratio of sperm containing X or Y chromosome after freezing-thawing of goat semen. The diluted semen of the heat stress group was first placed at 43 ° C for 30 minutes and then frozen-thawed as in the control group.

The results showed that heat stress led to a significant reduction in the overall sperm motility, viability and sperm cell membrane integrity compared to the control group. Also, in the heat stress group, the mean Y to X ratio was 94.4%, which showed a significant difference (p <001) compared to the expected Y to X ratio of 1.

Applying heat stress to sperm in vitro can lead to a significant reduction in sperm parameters. In addition, the decrease in the number of Y-bearing spermatozoa in the survived population post thawing, may indicate that the Y-bearing spermatozoa are more sensitive and fragile compared to X-bearing spermatozoa in goat species. Keywords: Sex determination, Cryopreservation, Heat stress, Goat sperm

Trimethyltin (TMT) intoxication with hippocampal degeneration induces the production of dark neurons in different areas of the hippocampus. The present study assessed the effect of Gallic acid (GA) on working memory, avoidance memory, and the density of dark neurons in the CA1/CA3 regions of the rat hippocampus following TMT intoxication. In this study, 32 adult male Wistar rats were randomly assigned to four groups including control, TMT+NS, TMT+GA100, and TMT+GA200. GA at doses of 100 and 200 mg/kg per body weight was administered orally 24 hours after TMT injection (8 mg/kg). The Y-maze was used to assess the working memory and the shuttle box was used to measure avoidance memory. The density of dark neurons in CA1 and CA3 regions of the hippocampus was then assessed by dissector method. Moreover, in order to determine the existence of significant differences between the groups, one-way ANOVA and Tukey’s post hoc test were used and p <0.05 was considered statistically significant. There was a significant decrease in the percentage of alteration behavior, delay in entering the dark room of shuttle box, along with an increased density of dark neurons in the TMT+NS group compared to the control group (p<0.001). While, administration of GA ameliorated the working and avoidance memory and reduced the density of CA1/CA3 dark neurons in the hippocampus compared to TMT+NS group (p˂0.001). GA administration appears to improve cognitive symptoms following TMT intoxication by reducing neuronal damage to CA1/CA3 areas of the hippocampus..

Monosodium glutamate (MSG) induced excitotoxicity leads to oxidative stress in different areas of the brain. The aim of this study was to evaluate the neuroprotective effect of coenzyme Q10 (Co-Q10) on amelioration of short-term and long-term memory and oxidative stress parameters in MSG-treated rats.

In this experimental study, 40 adult male Wistar rats were randomly divided into 4 groups including control, MSG, MSG + Q10-10 and MSG + Q10-20. MSG gavage (4 mg / kg) and coenzyme Q10 injection at doses of 10 and 20 mg / kg (intraperitoneally; i.p.) were performed for 4 weeks. Then, short-term working memory was assessed using the Y maze and long-term avoidance memory was performed with the shuttle box. Hippocampal level of catalase (CAT) and total antioxidant capacity (TAC) were determined by ELISA method and malondialdehyde (MDA) content was determined by thiobarbituric acid method.

In MSG group, there was a significant decrease in alteration behavior, increased latency time to the dark room of the shuttle box, decreased CAT, TAC expression and increased MDA compared to the control group (p <0.05). While in the Q10 treated groups, there was an increase in working and avoidance memory, an increase in CAT and TAC expression and a decrease in MDA in the hippocampus compared to the MSG group (p˂0.05).

It seems that Co-Q10 ameliorates MSG induced neurotoxicity and cognitive symptoms through preventing oxidative stress in the hippocampus.

Diseases caused by high-fat diets and obesity are now recognized as a health problem. The aim of this study was to evaluate effect of aloe Vera hydroalcoholic extract on spermatogenesis parameters and tissue structure of testis of rats fed with a high-fat diet.

40 adult male Wistar rats were randomly divided into 5 groups (control group (Con), control group fed with a high-fat diet (HFD), and experimental groups 1 to 3 (HFD +150 mg aloe Vera, HFD +300 mg aloe Vera, and HFD + 600 mg aloe Vera(. High-fat emulsion and three doses of aloe Vera were administered orally for 60 days. Finally, after dissection and preparation, testicular tissue was examined histopathologically. The number of spermatogonia, spermatocytes, spermatids, Sertoli, and Leydig cells was counted. Data were analyzed by SPSS software and the means were compared using ANOVA and Post hoc Tukey's test at 0.05%.

The results showed a significant decrease in mean of spermatogonia, spermatocytes, spermatids, and Leydig cells in the group receiving a high-fat diet (HFD) compared to the control group. Aloe Vera extract significantly increased the number of sex cells in the testis. Increasing the dose of aloe Vera to 600 mg/kg further improved histopathological tissue damage.

The results of study showed that the hydroalcoholic extract of aloe Vera in mice fed with a high-fat diet significantly reduces the risk of pathological tissue damage in testes and increases fertility by increasing the number of sex cells.

Varicocele is one of the most common causes of infertility in men. Various studies have been performed on the treatment of varicocele and hormonal changes in the testicles. One of the non-invasive treatments for varicocele is treatment with Tilia platyphyllos L. as a medicine used to treat stomach ulcers, spasms and sedatives. Chemical compounds such as terpenoids and flavonoids have been identified in the linden. The aim of this study was to evaluate the effect of linden extract on testicular pathology of healthy and varicocele rats.

In this study, 48 rats were randomly divided into 8 groups: healthy control, healthy groups receiving linden extract (50, 100 and 200 mg / kg intragastrically, daily) alone, infertile control (varicocele surgery), varicocele groups together with linden extract (50, 100 and 200 mg / kg intragastrically, daily). After 60 days, serum was obtained and hormonal assays and histopathological examinations were performed and the data were analyzed using one-way analysis of variance.

The results showed that the level of testosterone decreased and levels of LH and FSH increased significantly in varicocele control animals compared with healthy controls. Also, administration of linden extract has prevented hormonal changes and has significantly improved the sex hormones level and histological index in varicocele rats.

The linden extract acts as a potent antioxidant against varicocele-induced damage in rats.

 Stem cell-based therapies create new hope for the treatment of Alzheimer's disease (AD). Since the mesenchymal stem cells have neuroprotective and regeneration effects, this study aimed to investigate the memory, learning, and antioxidant capacity of the hippocampus following human adipose-derived mesenchymal stem cell (Ad-MSC) transplantation in Trimethyltin (TMT) rat's model of AD.

In total, 24 male Wistar rats were randomly divided into three groups (8 animals per group) of control (without any treatment), TMT+PBS (Trimethyltin+Phosphate buffer saline), and TMT+Ad-MSC (Trimethyltin+Stem cells). For the induction of the AD, TMT was peritoneally injected (8 mg/Kg). After 48 h, the TMT+Ad-MSC group received 1 million stem cells intravenously. One month after transplantation, avoidance and working memories were evaluated. Afterward, hippocampal levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and malondialdehyde (MDA) were measured using ELISA.

The results showed a significant increase in the percentage of correct motor frequency in the Y maze, a decrease in the spent time in the dark room (P<0.05), and an increase in the latency time to the dark room in the TMT+Ad-MSC group, compared to the TMT+PBS group (P<0.01). Moreover, a significant increase in the CAT, SOD, and GPX enzymes activity, as well as a decrease in the MDA level in the hippocampus were observed in the TMT+Ad-MSC group, compared to the TMT+PBS group (P<0.05).

Xenotransplantation of human adipose tissue stem cell improved learning and memory, reduced tissue oxidative stress, and increased hippocampal antioxidant capacity in an animal model of AD.

Monosodium glutamate (MSG) induces excitotoxicity and cell damage in different areas of the brain, especially the hippocampus. The present study evaluated the anti-inflammatory and neuroprotective effects of coenzyme Q10 (Co-Q10) on hippocampal cell damage in MSG-treated rats.

Forty adult male Wistar rats were randomly divided into 4 groups: control, MSG, MSG+Q10-10 and MSG+Q10-20. MSG (3 gr/kg, orally) and Co-Q10 (20 mg/kg and 10 mg/kg, intraperitoneally) were administered day after day for 4 weeks. After 4 weeks, the animals were sacrificed and the brain hippocampus was isolated quickly on ice. Hippocampal levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) were estimated by ELISA technique. Finally, the density of dark neurons in different areas of the hippocampus was measured by stereology method.

In comparison with MSG group, Co-Q10 treatment significantly reduced inflammatory factors (TNF-α, IL-1β and IL-6) in the hippocampus of Co-Q10-treated rats (p <0.05). The density of dark neurons in CA1, CA2, CA3 and dentate gyrus regions of the hippocampus was significantly reduced in the Co-Q10 group compared with the MSG group (p˂0.05).

The anti-inflammatory properties of coenzyme Q10 may be responsible for its neuroprotective function in the hippocampus and ameliorates MSG-induced neurotoxicity in rats.

Acrylamide (ACR) is a chemical with toxic effects on various body tissues. The present study was conducted to investigate the antioxidant effect of N-acetylcysteine (NAC) on the level of testicular apoptosis in acrylamide-treated adult rats.

Thirty-six adult male Wistar rats were randomly divided into 6 equal groups. The intact control group was without treatment, the positive control group (PC) received 50 mg/kg ACR by oral gavage, the negative control group (NC) received 40 mg/kg NAC intraperitoneally, the animals in experimental groups of 1 (EXP1), 2 (EXP2) and 3 (EXP3) received 10, 20 and 40 mg/kg NAC intraperitoneally, respectively, and then all groups received 50 mg/kg acrylamide by oral gavage. The treatment period in all groups was 28 days. At the end of the study, FAS mRNA expression level was measured by real-time PCR and testicular tissue was evaluated histopathologically.

The PC group showed a significant increase in FAS gene expression level (p<0.05) and spermatogenic degradation compared to the intact control and NC groups. The EXP1 and EXP2 groups showed decrease in FAS gene expression level (p˃0.05) and spermatogenesis improvement in a dose-dependent manner while the EXP3 group exhibited a significant decrease in FAS gene expression level (p˂0.05) and complete spermatogenesis recovery compared to the PC group.

The findings indicate that ACR increases apoptosis and destroys spermatogenesis by increasing FAS gene expression levels. In contrast, at the maximum dose (40 mg/kg), NAC could inhibit ACR-induced apoptosis by reducing FAS gene expression and improves spermatogenesis in rats.

Intruduction: 

Perinatal seizure cause hippocampal neuronal apoptosis by inducing oxidative stress in the fetal central nervous system. This study evaluates the effect of swim training (ST) and trans-cinnamic acid (CIN) administration during pregnancy on anxiety, cell damage and density of apoptic neurons in the neonatal hippocampus following penthylentetrazol (PTZ)-induced perinatal seizures.

In this experimental study neonates from 25 Wistar pregnant rats were randomly divided into 5 healthy control, PTZ+NS, PTZ+CIN, PTZ+ST and PTZ+CIN+ST groups were used. From embryonic day (ED) 14, the animals were treated with repeated PTZ administration (50 mg / kg, intraperitoneally) for 5 consecutive days. During pregnancy, moderate intensity swimming (20 min, 3 sessions per week) and CIN gavage (100 mg/kg) were performed daily until term delivery. Anxiety-like behaviors and working memory were assessed with elevated plus maze and Y maze, respectively and dark neurons density was measured in the hippocampus of male neonate at postnatal day (PND) 30.

Significant decrease in alteration behavior, increase in anxiety with high density of dark neuron in different areas of hippocampus were observed in the PTZ+NS group compared to the control group (p ˂ 0.05). On the other hand, in PTZ+CIN+ST group, in comparison with PTZ+NS group, a decrease in anxiety, amelioration of working memory deficit and a decrease in hippocampal dark neuron density were observed (p ˂ 0.05).

Interaction of swimming training with trans-cinnamic acid administration ameliorates cognitive-behavioral deficits and cell damage in the hippocampus of rats exposed to maternal seizures.

Trimethyltin (TMT) is an organotin with selectively damage in the cerebral cortex and hippocampus which leads hyperactivity in prenatal exposure. The aim of this study was the evaluation of Ferulic acid (FER) effect on amelioration of motor and cognitive deficits in prenatal TMT-intoxication rat model.

In this experimental study, 30 Wistar pregnant rats were randomly divided into 5 groups, including control group, TMT+Saline group and TMT+FER25, TMT+FER50 and TMT+FER100 groups. TMT (9 mg/kg) were intraperitoneally injected to the pregnant rats on embryonic day (ED) 14. Ferulic acid groups were treated by 25, 50 and 100 mg/kg doses of Ferulic acid during ED12 to ED18. Open field test for evaluation of anxiety and locomotor activity, beam walking and grid walking test for assessment of motor learning and Y-maze for evaluation of working memory were used on postnatal day (PND) 30. The data were analyzed by ANOVA and Tukey post hoc.

Increased rates of anxiety- like behaviors, decrease of motor learning and working memory were shown in TMT+Saline group compared to the control. Although, Ferulic acid treated groups were shown a significant amelioration in correct alteration behavior and motor learning with reduction of anxiety- like behaviors (p˂0.05).

TMT prenatal exposure impairs learning and attention in rats and Ferulic acid may reduce cognitive-behavioral deficits.

In recent years, the discovery of stem cells in breast milk, the fate of these cells in infants, and their potential role in regenerative medicine are taken into consideration. Due to the high plasticity and differentiation capacity of these cells as well as the possibility of their differentiation into neural-like cells, the role of these cells during infancy and the possibility of their migration along the intestinal-brain axis are extensively investigated.

Considering the attractive properties of breast milk, the possible role of milk stem cells in the amelioration of pediatric neurological disorders in newborns, and the possibility of increasing neonatal intelligence quotient by migration to the neonatal brain, and their therapeutic potentials in regenerative medicine were reviewed.