جستجوی مقالات مرتبط با کلیدواژه « mouse » در نشریات گروه « پزشکی »

The toxicity of silver nanoparticles (AgNPs) has been proven in the female reproductive system. Thymoquinone (TQ) is a natural antioxidant and bioactive component of Nigella sativa.

We evaluated the efficacy of TQ on ovarian tissue following toxicity induced by AgNPs in female mice.

24 female NMRI mice (5-6 wk, an average weight of 33 gr) were randomly divided into 4 groups (n = 6/each): control, AgNPs (500 mg/kg, gavage), TQ (2.5 mg/kg, intraperitoneal injection), and TQ+AgNPs. Mice were treated every day for 35 days. Serum levels of malondialdehyde (MDA), total antioxidant capacity (TAC), luteinizing hormone, and follicle-stimulating hormone were measured. The optical disector and stereological techniques were utilized to estimate the follicular count, their volume at different developmental stages, and the structure of ovarian tissue.

In the AgNPs group, the serum concentrations of TAC (p = 0.01), luteinizing hormone (p < 0.001), follicle-stimulating hormone, the volume of corpus luteum (p < 0.001), and the number of follicles decreased significantly compared to the control group. Nevertheless, AgNPs significantly increased the MDA level. In the TQ+AgNPs group compared to the AgNPs group, a significant decrease in MDA level (p < 0.001) and a significant improvement in TAC (p = 0.03), and hormonal levels, the number of primary, preantral, and antral follicles (p = 0.04), and the volume of corpus luteum (p = 0.01) were observed.

TQ improved the number of follicles by reducing oxidative stress and lipid peroxidation in AgNPs-damaged ovarian tissue.

Vascular endothelial growth factor (VEGF) signaling pathway plays an important role in the pathogenesis of seizure. The oxidant/antioxidant factors and miRNA expression in the brain are differentially regulated in seizure.

We aim to investigate the potential mechanism of action for the recombinant human VEGF (rhVEGF) in mice with maximal electroshock (MES)-induced seizure.

A total of 40 male mice (weight: 20-25 g) were treated intraperitoneally with normal saline, or rhVEGF (50, 100, and 150 µg/kg, daily for 4 consecutive days). One hour after the last injection, seizures were induced in each animal by MES. The latency for the onset of the first clonus and the duration of hind limb extension (HLE) were recorded. The levels of nitric oxide (NO), total antioxidant capacity (TAC), and micoRNA-142-5p expression were determined in the hippocampus of mice. Blood-brain barrier (BBB) permeability was also estimated by Evans blue dye extravasation method.

The administration of rhVEGF at all doses significantly reduced the HLE duration. However, latency for the seizure onset increased after administration of 50 and 150 μg/kg rhVEGF and decreased after administration of 100 μg/kg rhVEGF. In the brain, the NO level decreased, while TAC level and microRNA-142-5p expression increased by rhVEGF treatment in mice with MES-induced seizure. Pretreatment with rhVEGF at doses of 100 and 150 μg/kg reversed the increase in BBB leakage induced by MES-induced seizures.

The rhVEGF administration can prevent MES-induced seizures by regulating NO, TAC, and miR-142-5 expression levels in the hippocampus and reducing BBB leakage in mice.

This study is done to investigate the hypolipidemic and hepatoprotective effects of corn silk extract in nicotine-administered male mice.

Nicotine can induce pathophysiological effects in the liver tissue through oxidative stress and damage cells. Corn silk can improve liver function with its antioxidant effects.

In this experimental study, 30 male NMRI mice (25-30 gr) were divided into 5 groups: controls, sham, nicotine 2.5 mg/kg, nicotine+aqueous extract of corn silk 400 mg/kg, and nicotine+methanolic extract of corn silk 400 mg/kg for 1 month. One day after the last nicotine and extracts consumption, the serum samples were performed for biochemical measurement, and the supernatant of the homogenized liver was administered for antioxidant variables assessment.

There was no significant difference in the body weight of different groups. Liver weight and GSH decreased in the nicotine group compared to the control group (P<0.05). Triglycerides, total cholesterol, HDL-C, LDL-C, liver enzymes, and MDA increased in the nicotine group compared to the control group (P<0.05). Also, the expansion of sinusoids, the presence of inflammatory cells, and necrosis of liver cells were observed in the nicotine group compared to the control group. Using aqueous and methanolic extracts of corn silk in mice receiving nicotine led to the improvement of the mentioned variables (P<0.05).

The results of this study showed that the use of nicotine can lead to the induction of hepatotoxicity. The use of aqueous and methanolic extracts of corn silk improved them through its antioxidant activity.

Bevacizumab is a commonly used anticancer drug in clinical practice, but it often leads to adverse reactions such as vascular endothelial damage, hypertension, arterial and venous thrombosis, and bleeding. This study investigated the protective effects of metformin against bevacizumab-induced vascular injury in a mouse model and examined the possible involvement of GDF15/PI3K/AKT/FOXO/PPARγ signaling in the effects. C57 male mice were purchased. To investigate metformin, the mice were assigned to the saline, bevacizumab (15 mg every 3 days), metformin (1200 mg/day), and bevacizumab+metformin groups. To investigate GDF15, the mice were assigned to the siNC+bevacizumab, siNC+bevacizumab+metformin, siGDF15+bevacizumab, and siGDF15+bevacizumab+metformin groups. Histological staining was used to evaluate vascular injury. Flow cytometry was used to evaluate apoptosis. ELISA was used to measure plasma endothelial injury markers and proinflammatory cytokines. qRT-PCR and western blot were used to determine the expression of GDF15 and PI3K/AKT/FOXO/PPARγ in aortic tissues. Metformin alleviated bevacizumab-induced abdominal aortic injury, endothelial cell apoptosis, and systemic inflammation in mice (all P<0.05). Metformin up-regulated GDF15 expression and PI3K/AKT/FOXO/PPARγ signaling in the abdominal aorta of mice treated with bevacizumab (all P<0.05). siGDF15 abolished the vascular protective and anti-inflammatory effects of metformin (all P<0.05). siGDF15 suppressed PI3K/AKT/FOXO/PPARγ signaling in the abdominal aorta of mice treated with bevacizumab (all P<0.05). Metformin attenuates bevacizumab-induced vascular endothelial injury, apoptosis, and systemic inflammation by activating GDF15/PI3K/AKT/FOXO/PPARγ signaling.

Knowing the detrimental role of oxidative stress in wound healing and the anti-oxidant properties of Dexpanthenol (Dex), we aimed to produce Dex-loaded electrospun core/shell nanofibers for wound healing study. The novelty was measuring oxidative stress in wounds to know how oxidative stress was affected by Dex-loaded fibers.

TPVA solution containing Dex 6% (w/v) (core) and PVA/chitosan solution (shell) were coaxially electrospun with variable injection rates of the shell solution. Fibers were then tested for physicochemical properties, drug release profile, and effects on wound healing. Levels of tissue lipid peroxidation and superoxide dismutase activity were measured.

Fibers produced at shell injection rate of 0.3 ml/hr (F3 fibers) showed core/shell structure with an average diameter of 252 nm, high hydrophilicity (swelling: 157% at equilibrium), and low weight loss (13.6%). Dex release from F3 fibers seemed to be ruled by the Fickian mechanism based on the Korsmeyer-Peppas model (R2 = 0.94, n = 0.37). Dex-loaded F3 fibers promoted fibroblast viability (128.4%) significantly on day 5 and also accelerated wound healing compared to the neat F3 fibers at macroscopic and microscopic levels on day 14 post-wounding. The important finding was a significant decrease in malondialdehyde (0.39 nmol/ mg protein) level and an increase in superoxide dismutase (5.29 unit/mg protein) activity in Dex-loaded F3 fiber-treated wound tissues. 

Dex-loaded core/shell fibers provided nano-scale scaffolds with sustained release profile that significantly lowered tissue oxidative stress. This finding pointed to the importance of lowering oxidative stress to achieve proper wound healing.

Lung cancer is an important burden, causing a massive rate of deaths every year. Using a specialized treatment regimen can improve treatment outcomes and reduce treatmentrelated adverse events. This study aimed to evaluate the protective effects of the Opuntia dillenii fruit hydroalcoholic extract (ODHAE) in a mouse model of lung cancer.

Eight groups of lung cancer-induced BALB/c mice (each containing twelve animals) were included in this study. They were the control group, groups receiving the ODHAE extract at doses of 50, 100, and 200 mg/kg by oral gavage, the cisplatin group receiving cisplatin intraperitoneal injection, and groups receiving cisplatin and different doses of ODHAE (50, 100, and 200 mg/kg). Weight and tumor changes were evaluated in the short and long phases of the study, including 30 and 90 days, respectively. Liver transaminase and survival time were evaluated in different groups. Malondialdehyde (MDA) was evaluated in different groups as an indicator of lipid peroxidation. Statistical tests were performed using GraphPad Prism 8. Graphs were designed using GraphPad Prism 8 as well.

The observed weight changes were not statistically significant across all groups, except for group 8. However, in groups that did not receive cisplatin treatment, there was a significant increase in tumor volume. Conversely, tumor volume change did not reach statistical significance in all groups receiving cisplatin. The administration of ODHAE, along with cisplatin, demonstrated a dose-dependent increase in the survival time among the relevant groups. Furthermore, oral administration of ODHAE exhibited a significant reduction in transaminase levels, serving as a reliable biomarker for assessing the hepatoprotective effect of the ODHAE extract. Additionally, ODHAE displayed a dose-dependent reduction in MDA levels, indicating its potential as a therapeutic agent for mitigating oxidative stress.

The administration of ODHAE was not effective in reducing tumor growth but significantly increased survival time and healed the liver injury induced by cisplatin.

The aim of this study was to investigate the effect of saffron extract on the embryo development of mice.

Pregnant NMRI mice were randomized into control and treatment groups at 25, 50, and 100 mg/kg saffron doses. Saffron extract was administered to mice by gavage on days 7-12 of pregnancy. On the 17th day of pregnancy, the embryos were removed from the uterus and their weight and height measured. Moreover, their brain tissue has been evaluated histologically. Subsequently, the expression of the Foxp2 and Ascl1 genes in the brain tissue was assessed using the real-time PCR method.

All embryos were aborted in mothers that received 100 mg/kg of saffron. At dose 50 mg/kg, only embryos of a mother reached the end of pregnancy. Embryos treated with 25 mg/kg saffron were significantly heavier than controls (P<0.05). Furthermore, the tail length was significantly shorter (P<0.05). Histological findings showed that there was no difference between the control and treated groups, and the brain tissue was well developed. Foxp2 and Ascl1 genes were significantly overexpressed in both the 25 and 50 mg/kg treatment groups compared to the control group (P<0.05).

The results of this study showed that saffron extract can have significant effects in low concentrations (25 mg/kg) on the development of the mouse embryos as well as the expression of Foxp2 and Ascl1 genes.

Human diet is branded with higher caloric and protein content and cooking processes in comparison with the diet of the primate species. The aim of this study was to explore the differences between human diet and chimpanzee diet which consists of fruits and vegetables, to find benefits and harmful aspects of human nutritional behavior.

Differentially expressed genes (DEGs) of mouse liver in response to consume “human cafeteria diet” and “chimpanzee diet” were acquired form Gene Expression Omnibus (GEO) database. The DEGs were assessed based on p-adj and fold change criteria. The significant DEGs were included in a protein-protein interaction (PPI) network to form an interactome unit. Central nodes of the studied network were determined based on degree value and betweenness centrality. The identified central genes were evaluated via gene ontology.

Numbers of 150 significant DEGs that discriminated the two nutrition diet regimes were introduced. Fatty acid synthase (FASN), stearoylCoA desaturase (SCD), and farnesyl-diphosphate farnesyltransferase 1 (FDFT1) were pointed out as the central DEGs. “Activation of gene expression by SREBF (SREBP)” and “NR1H2 & NR1H3 regulate gene expression linked to lipogenesis” were highlighted as two classes of the biological terms that were related to the central DEGs.

The findings indicated that human cafeteria diet is a lipogenic regime compared to the chimpanzee diet which is enriched with vegetables. The studied human nutrition behavior was accompanied with increased level of fatty acid synthesis enzymes beside cholesterol accumulation in body.

Asthma is a chronic respiratory ailment characterized by bronchospasm, airway inflammation and hyperresponsiveness, and recurrent episodes of breathing complications. Due to the high incidence of this disease, there has been a surge in the use of complementary branches of medicine such as Iranian traditional medicine (ITM) in recent times.

In this study, the efficacy of an ITM polyherbal formulation (Compound Honey Syrup) in the management of allergic asthma was explored.

60 Balb/c mice were divided into five groups (n = 12) as follows: G1, ovalbumin (OVA)-sensitized; G2, PBS-treated; G3, OVA + oral Compound Honey Syrup; G4, OVA + inhalational compound honey; G5, OVA + inhalational Budesonide. Subsequently, airway hyperresponsiveness (AHR) was assessed using methacholine test, cytokines levels were determined in bronchoalveolar lavage fluid (BALF) and eosinophilia was assayed in blood and BALF. Also, histological transformation of the lungs was analyzed.

Oral Compound Honey Syrup prevented the development of AHR. Both oral and inhalational Compound Honey Syrup significantly diminished eosinophil counts in blood and BALF specimens. Moreover, both types of Compound Honey Syrup treatments remarkably reduced the levels of IL-5 and IL-13 in BALF and blood samples in comparison to the OVA-received animals (P < 0.05).

The present data show that Compound Honey Syrup is an effective herbal formulation to alleviate asthma-induced inflammatory response and therefore can be a promising remedy for the management of this disease.

Liver fibrosis is a common liver disease caused by chronic liver damage. However, there are currently no approved drugs available to treat it. Therefore, the therapeutic effect of indirubin on liver fibrosis was evaluated. This study investigated the protective effect and related molecular mechanism of indirubin against CCl4-induced liver fibrosis in mice. We first detected the effect of indirubin on liver fibrosis in mice (n=8 per group, 32 mice total) by ELISA, HE, and Masson staining. Subsequently, the proliferation of activated HSCs was detected by MTT and EdU. Finally, the changes of related proteins and signaling pathways in mice treated with indirubin were investigated by qRT-PCR and Western blot. One-way ANOVA or two-tailed student’s t-test was used for comparison between groups. Firstly, we found that indirubin (25 mg/kg) therapy could attenuate liver injury and significantly down-regulate α-SMA (P=0.0038) and collagen 1 (P=0.0057) in the liver using CCl4-induced liver fibrosis in mice. Secondly, we showed that indirubin (25 μM) could significantly inhibit hepatic stellate cell (HSC) trans-differentiation into myofibroblasts and proliferation (P=0.0063) in HSC-T6 cells treated by TGF-β. Finally, we showed that indirubin could greatly reduce the protein levels of p-Smad2/3, p38, p-ERK, and p-JNK in vivo and in vitro. Our results suggested that indirubin alleviated liver fibrosis and HSC activation mainly through TGF-β-mediated signaling pathways in vivo and in vitro. In conclusion, our data showed that indirubin could be a promising clinical therapeutic drug for the prevention and treatment of liver fibrosis.

One of the environmental factors leading to Alzheimer's disease (AD) is traumatic brain injury (TBI). Meanwhile, tau protein hyperphosphorylation is known as one of the mechanisms of AD development. In the present study, the effect of Rosa damascena and Ginkgo biloba aqueous extracts on tau hyperphosphorylation was studied on SH-SY5Y cell lines and mouse TBI models.

Tau protein hyperphosphorylation was induced in SH-SY5Y cells using 10 μM retinoic acid (RA). Then, cells were treated with 500 and 1000 μg/ml aqueous extracts of Rosa damascena and Ginkgo biloba. Cell viability was studied by MTT test and tau protein hyperphosphorylation was studied by western blot and immunostaining techniques. Also, after the induction of TBI by pneumatic cylinder, mice were treated with 500 and 1000 μg/ml aqueous extracts of Rosa damascena and Ginkgo biloba, and the animals were tested for beam balance and walk tests to measure balance and muscle stiffness. Finally, tau protein hyperphosphorylation in the brain was investigated using an immunostaining technique.

Both aqueous extracts of Rosa damascena and Ginkgo biloba were able to improve SH-SY5Y viability. Also, a decrease in phosphorylated tau protein was observed in cells treated with aqueous extracts of Rosa damascena and Ginkgo biloba. Performance improvements in beam balance and walk tests in TBI mice treated with 1000 μg/ml Rosa damascena and Ginkgo biloba aqueous extracts were seen. Also, tau protein phosphorylation was significantly decreased in the brain of TBI rats treated with those aqueous extracts.

aqueous extracts of Rosa damascena and Ginkgo biloba have neuroprotective effects and are beneficial in reducing TBI-induced tau protein hyperphosphorylation, and they can prevent tau pathology.

Ovarian tissue extract (OTE) and sodium selenite (SS) enhance the growth and maturation of preantral follicles in a dose-dependent manner.

The present study was designed to bring more information regarding the mechanism of OTE and SS on the mRNA expression of follicle-stimulating hormone receptors (FSHR) and the proliferation cell nuclear antigens (PCNA) of in vitro matured isolated follicles.

The tissue extract was prepared from adult ovaries. The preantral follicles (n = 266) were isolated from 12-16-day-old mice and cultured in the control, experimental I (10 ng/ml SS), and experimental II (OTE) groups for 12 days. The follicular diameter, survival, and maturation rates, also, the production of 17-β-estradiol and progesterone, and the follicular expression of PCNA and FSH receptor genes were analyzed.

The survival rate of follicles in the SS-treated group (84.58%) was significantly higher than that OTE (75.63%; p = 0.023) and control (69.38%; p = 0.032) groups. The mean diameter of culture follicles in experimental group I (403.8 μm) and experimental group II (383.97 μm) increased significantly in comparison with the control group (342.05 μm; p = 0.032). The developmental rate of follicles, percentages of antrum formation, released metaphase II oocytes (p = 0.027; p = 0.019 respectively), production of hormones and the expression of 2 studied genes were significantly increased in both experimental groups in compare with control group (p = 0.021; p = 0.023 respectively).

The OTE and SS have a positive effect on development of mouse preantral follicles via over-expression of FSHR and PCNA genes.

Researchers have mentioned many beneficial effects for the compounds present in the toothbrush tree (Miswak) (Salvadora persica: SP); such as anti-inflammatory, antioxidant and antimicrobial activities. The current study aimed to evaluate the effect of aqueous-alcoholic extract of toothbrush tree on the wound healing of second-degree skin burns in BALB/c mice.

In this study, 60 mature mice (8 weeks) were used. The mice were divided into 5 groups of twelve. Groups 1 and 2 were respectively treated with concentrations of 5% and 10% of aqueous-alcoholic extract of the toothbrush plant, group3 was treated with silver sulfadiazine ointment (positive control), group4 was treated with Vaseline (negative control), and group 5 (sham) received no treatment. A second-degree circular burn wound with a diameter of 1 cm was made on the back of the animal. The first to fourth groups were dressed twice a day. On days 4, 7, 10 and 14, sampling was performed from the wounded site and wound healing was evaluated histopathologically.

Inflammation and infiltration of neutrophils and lymphocytes, being compared to the negative and sham control groups, were significantly reduced in the group treated with 10% SP extract (P<0.01); besides, on days 10 and 14 in the group treated with 10% and 5% SP extracts, the number of fibroblasts, followed by collagen production, epithelialization and formation of new hair follicles in the wound margins significantly increased compared to the negative control and sham group (P<0.05). The number of fibroblasts and collagen fiber density in the group treated with 10% SP extract, compared to the 5% extract group and silver sulfadiazine, showed a significant increase (P<0.05).

The findings showed that using extract of toothbrush plant accelerates the healing process of burn wounds.

Maslinic acid (MA) is an olive-derived extract with the structure of pentacyclic triterpenes, which potents anti-inflammatory effects. It has been reported that the combination of MA and resistance exercise increases skeletal muscle mass, but there are many unknowns regarding its detailed molecular mechanism. The present study aimed to clarify the effect of MA supplementation on muscle hypertrophic response to acute muscle contraction-induced resistance exercise using animal model. Seven-week-old ICR (Institute of Cancer Research) male mice fed a diet containing 0.27% MA during an acclimatization of 1 week. After an overnight fast, the right gastrocnemius muscle was subjected to acute resistance exercise using percutaneous electrical stimulationinduced muscle contractions, while the left gastrocnemius muscle was saved as control. The muscle was excised at 1, 3, and 6 hours after exercise and protein synthesis-related signaling expressions were examined. MA was demonstrated to significantly activate the downstream targets of mammalian/mechanistic target of rapamycin (mTOR), phosphorylated ribosomal protein S6 (rpS6) at Ser240/244 site particularly, while Akt/glycogen synthase kinase-3β (GSK-3β) pathway and mitogenactivated protein kinase (MAPK) signaling were unaffected. Our results suggested that acute resistance exercise-induced muscle protein synthesis-promoting effect of MA is supported by the activation of downstream signaling of mTOR.

Vitamins A, D, and microRNAs contribute to T cell differentiation into TH2 phenotypes. We investigated the molecular mechanisms and effects of vitamin A and D on the expression of GATA3 and miR-27-3p isoforms in experimental autoimmune encephalomyelitis (EAE) animal model of multiple sclerosis. EAE was induced in C57BL/6 mice by immunization with myelin oligodendrocyte glycoprotein, mixed with Complete Freund's Adjuvant, together with injection of pertussis toxin. Treatments began one day before immunization with (200 μg and 100 ng of vitamin A and vitamin D per mouse, respectively, and vitamin A+D (100 μg+50 ng) per mouse. Expression levels of GATA3 and miR‑27‑3p isoforms were measured in the CNS and splenocytes by real-time RT-PCR. The expression level of GATA3 in the mice spinal cords and splenocytes was increased in the vitamin A and A+D-treated EAE mice at 24 h and 48 h after restimulation by 10 µg and 40 µg of myelin oligodendrocyte glycoprotein. Vitamins A and D and their combination upregulated the miR-27-3p isoforms compared with EAE mice with no treatments. We also demonstrated that miR-273p isoform expression was altered in splenocytes of vitamin-treated EAE mice. The results showed a positive correlation between splenocyte GATA3 levels and miR-27-3p isoform expression. The protective impacts of vitamins A and D in EAE mice may be mediated by the upregulation of GATA3. However, it is not specified whether suppression of GATA3-targeting miRNAs of the miR-27-3p family is involved in this effect. These results do not rule out the possibility that miR-27-3p isoforms might have beneficial effects by targeting other transcripts, such as GluA2 and NR2B.

Epilepsy is a neurological disorder causing brain dysfunctions. Treatment and control of epilepsy have long been a challenge in medical sciences. Despite the variety of current anticonvulsant drugs, research continues to discover new drugs with the highest efficacy and the lowest side effects. In the present study, the anticonvulsant effects of anethole in the seizure induction with pentylenetetrazole (PTZ) were evaluated in a mice model with respect to its possible antioxidant effects. PTZ is known to cause generalized epilepsy in animal models. Accordingly, in this experimental study, 40 mice were divided into 5 groups; the first group received normal saline, the second group received 10 mg/kg diazepam, and the third to fifth groups were given anethole at 31.25, 62.5 and 125 mg/kg, respectively. Injections were conducted intraperitoneally for one week; then seizures were induced by the intravenous injection of 90 mg/kg PTZ. After determination of the duration of seizures in different groups, the mice were finally placed under deep anesthesia and their prefrontal cortex tissue was isolated to measure nitric oxide (NO), antioxidant capacity and malondialdehyde (MDA) concentrations. The results showed that anethole increased the delay in the onset of seizures, decreased the amount of nitrite in the brain, enhanced antioxidant capacity, and reduced MDA content in a dose-dependent manner. Overall, our results indicated the anticonvulsant effects of anethole that could be mediated by inhibiting oxidative stress.