tourandokht baluchnejadmojarad

Alzheimer’s disease (AD) as the most common neurodegenerative disorder. Klotho is an anti-aging protein with important roles in neurodegenerative disorders. This study was done to evaluate the expression of klotho gene and protein in the plasma of AD patients treated with blood pressure control drugs (inhibitors of angiotensin-converting enzyme (ACE)) or blood lipids control drug (simvastatin).

Target population was selected from people with AD who visited the neurology clinic of Firouzgar hospital. The tested groups included the control group, Alzheimer's group, Alzheimer's group treated with blood pressure control drugs, and Alzheimer's patients group treated with blood lipid control drug. Expression of klotho gene and protein in the plasma of studied groups was determined using real-time PCR and ELISA techniques and the individual's cognitive disorders were also evaluated using Mini-Mental State Exam (MMSE) and Clinical Dementia Rating (CDR) tests.

The results obtained in this study showed that in addition to the significant difference in cognitive indices between the control groups and three groups of Alzheimer's patients, the level of klotho gene and protein expression was also lower in three groups of Alzheimer's patients compared to healthy group. However, there was no significant difference (p>0.05) between the Alzheimer's group and the two Alzheimer's groups treated with blood pressure or blood lipid control drugs.

Drugs controlling blood pressure or blood lipids in Alzheimer's patients possibly have no significant effect on the level of klotho protein. Obviously, more studies are needed in this field.

Alzheimer's disease (AD) is the most prevalent cause of dementia globally, with its incidence continuing to increase. Cis phosphorylated tau (Cis p-tau) is postulated as the earliest detectable pathogenic marker in AD and as a novel diagnostic and therapeutic factor. This study was conducted to evaluate stage of AD patients based on plasma level of Cis p-tau.
Target population (65-80 years) was chosen from people with AD who visited the neurology clinic of Firouzgar hospital. Selection of cases was according to their medical history and they were divided into control and AD groups at two early and late stages. Individual's cognitive performance was evaluated using Mini-Mental State Exam (MMSE) and Clinical Dementia Rating (CDR) tests besides measurement of plasma level of Cis p-tau.
The results obtained for this study showed that besides significant difference in cognitive indices between control group and two groups of AD patients at early and late stages of the disease, plasma level of Cis p-tau is significantly higher in AD groups (especially in late stage AD group) as compared to the control and healthy group (p<0.05).
It seems that routine measurement of plasma Cis p-tau in AD patients may be of clinical diagnostic value to differentiate AD stages and to evaluate efficacy of used therapies. However, further large-scale research studies are still required to affirm this issue.

Kidney diseases are endangering conditions to public health. Carbon tetrachloride (CCL4)-induced model of acute kidney injury (AKI) is a reliable model for studying renal damage under different conditions. S-allyl cysteine (SAC) is a natural organosulfur compound in aged garlic extract with multiple protective effects. In this study, possible preventive effect of SAC in CCl4 model of AKI was investigated.
For induction of AKI, CCl4 (10 ml/kg body weight; 0.175% in olive oil) was intraperitoneally injected and SAC was given orally at doses of 25 or 100 mg/kg. Functional markers of kidney were determined besides renal analysis of oxidative stress and inflammatory indices.
SAC pretreatment at a dose of 100 mg/kg for 1 week before CCL4 challenge significantly and markedly reduced level of blood urea nitrogen (BUN), malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and significantly enhanced superoxide dismutase (SOD) activity and with no significant effect on creatinine and catalase activity. In addition, such valuable effects were not observed for SAC at a dose of 25 mg/kg in CCL4-exposed group.
Findings of this study indicated beneficial effect of SAC subsequent to CCL4-induced kidney injury that is partly mediated through its regulation of oxidative and inflammatory events and upregulating some of the antioxidants.

Liver disorders are associated with high rate of morbidity and mortality. Carbon tetrachloride (CCL4)-instigated model of ALI is a valid model for exploring liver damage. Licochalcone A is a bioflavonoid which is primarily isolated from roots of Glycyrrhiza species. In this study, the effect of this flavonoid in CCl4 mouse model of acute liver injury (ALI) was assessed.
For induction of ALI, CCl4 (10 ml/kg body weight, 0.175% in olive oil) was intraperitoneally injected and licochalcone A was orally administered at doses of 10 or 50 mg/kg. Functional markers of liver dysfunction were determined in addition to hepatic analysis of oxidative stress and inflammatory factors.
Licochalcone A pretreatment at a dose of 50 mg/kg significantly and notably decreased level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and myeloperoxidase (MPO) and significantly improved total antioxidant capacity (TAC) and superoxide dismutase (SOD) activity and with no significant effect on interleukin-1β (IL-1β). In addition, these beneficial effects were not obtained for licochalcone A at a dose of 10 mg/kg in CCL4-injured group.
These findings show beneficial property of licochalcone A following CCL4-induced liver injury that is exerted via its regulation of oxidative and inflammatory processes and upregulating antioxidant power.

Cognitive deficits are associated with neurodegenerative disorders including Alzheimer’s disease (AD). Trimethyltin chloride (TMT) with potent neurotoxicity is used to induce cognitive dysfunction in rodents. Crocin is the main effective component of saffron with anti-oxidant and anti-inflammatory potential. In the present study, we investigated the effect of crocin on TMT-induced cognitive dysfunction.
TMT was i.p. administered (8 mg/kg, once) and crocin was daily given p.o. 1 h after TMT for 3 weeks at doses of 10 or 50 mg/kg. Cognitive performance was assessed in different behavioral tasks. In addition, hippocampal oxidative stress and apoptosis were measured.
Treatment of TMT-challenged rats with crocin (at a dose of 50 mg/kg) prevented deficits of recognition memory in Y maze, discrimination ability in novel object discrimination (NOD) test and conditional learning and memory index in passive avoidance task. Besides, crocin significantly lowered hippocampal level of ROS and improved activity of superoxide dismutase (SOD) besides ablation of apoptotic factors including caspase 3 activity and DNA fragmentation.
In conclusion, crocin administration could ameliorate TMT-induced cognitive dysfunction, in part through targeting hippocampal apoptosis and oxidative stress.

Expenditure credits are allocated to universities and institutes of higher education every semester based on the number of students and the number of courses, but identifying the actual completed cost of the various courses can help to better allocate scarce resources. The purpose of this study was to determine the cost of educational activities of postgraduate students of medical school in independent hospitals of Iran University of Medical Sciences.

The purpose of this study was to calculate the direct costs of educational services for postgraduate students (MSc and Ph.D.) in the independent medical education centers of Iran University of Medical Sciences in the academic year 2018-2019. After identifying the cost headings, interviews were conducted with vice chancellors for education, department chairs, heads of clinical and financial departments, professors, and students in the medical school (about 20). Then, to determine the students' use of cost headings, work, and time Measurement were done. Firoozgar, Rasoul Akram, Akbarabadi, Shahid Rajaee and Ali Asghar hospitals were the study sites. The calculation and analysis were performed in Excel 2013 software.

The costs of educational activities of postgraduate students were reported to be 49000000 Rials for Ph.D. students and 400,000 Rials for postgraduate students.

Postgraduate and Ph.D. students do not impose significant costs for their internships. These learners rotate their practice units in the teaching hospitals of the University of Iran under the supervision of their respective instructors and more in an observational approach.

Alzheimerchr('39')s disease registry system is of great help in generating big data through collecting data over time. Visual analysis tools such as dashboards can be used to convert this data into knowledge. Based on the needs of stakeholders, we in the present study determined the key indicators of Alzheimerchr('39')s disease; then, based on the Alzheimerchr('39')s disease registry system, we designed and evaluated the dashboard.

In the first stage, we determined the key performance indicators through a questionnaire completed by 31 members of the Alzheimerchr('39')s disease research core at Iran University of Medical Sciences. In the second stage, we designed the dashboard based on previous studies and using QlickView software. Finally, we designed the dashboard by the System Usability Scale which was conducted by four members of the Alzheimerchr('39')s disease research core and three medical and health information technology graduates.

Among the 15 key performance indicators approved by members of the Alzheimerchr('39')s disease registry, three indicators have got the highest score; these indicators are as follows: the ratio of patients with a history of mental disorders compared to the total number of patients, the ratio of patients with a history of depression compared to the total number patients, and comparing the prevalence and incidence of the total population. Then, we evaluated the usability of the dashboard by the system usability scale whose average score was 71.7.

Implementing the Alzheimerchr('39')s disease dashboard will play an important role in meeting the needs of each stakeholder and increasing the ability to analyze information in order to make better decisions.

Alzheimer’s disease is one of the neurodegenerative disorders typified by the aggregate of amyloid-β (Aβ) and phosphorylated tau protein. Oxidative stress and neuroinflammation, because of Aβ peptides, are strongly involved in the pathophysiology of Alzheimer’s disease (AD). Linagliptin shows neuroprotective properties against AD pathological processes through alleviation of neural inflammation and AMPK activation.

We assessed the benefits of linagliptin pretreatment (at 10, 20, and 50 nM concentrations), against Aβ1-42 toxicity (20 μM) in SH-SY5Y cells. The concentrations of secreted cytokines, such as TNF-α, IL-6, and IL-1β, and signaling proteins, including pCREB, Wnt1, and PKCε, were quantified by ELISA.

We observed that Aβ led to cellular inflammation, which was assessed by measuring inflammatory cytokines (TNF-α, IL-1β, and IL-6). Moreover, Aβ1-42 treatment impaired pCREB, PKCε, and Wnt1 signaling in human SH-SY5Y neuroblastoma cells. Addition of Linagliptin significantly reduced IL-6 levels in the lysates of cells, treated with Aβ1-42. Furthermore, linagliptin prevented the downregulation of Wnt1 in Aβ1-42-treated cells exposed.

The current findings reveal that linagliptin alleviates Aβ1-42-induced inflammation in SH-SY5Y cells, probably through the suppression of IL-6 release, and some of its benefits are mediated through the activation of the Wnt1 signaling pathway.

Acute liver failure (ALF) is a fatal clinical situation that rapidly leads to the loss of normal liver function. Esculetin is a natural herbal compound used for the management of various diseases such as cardiovascular and renal disorders. In this study, we evaluated the protective effects of esculetin in a mouse model of ALF.

This article is a report on an experimental study that was conducted at Iran University of Medical Sciences in 2019. Forty-eight male C57BL/6 mice were randomly divided into control, LPS/D-Gal, and LPS/D-Gal+Esculetin (40 mg/kg) groups (n=16 per group). ALF was induced with an intraperitoneal injection of lipopolysaccharide (LPS)/D-galactosamine (D-Gal).The LPS/D-Gal group received a mixture of LPS (50 μg/kg) and D-Gal (400 mg/kg). The LPS/D-Gal+Esculetin group received esculetin by gavage 24 hours and one hour before receiving LPS/D-Gal. Six hours after LPS/D-Gal injection, the mice were sacrificed. Liver injury markers, including alanine aminotransferase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP), were measured in the serum. Oxidative stress indices and inflammatory markers such as interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) were measured in hepatic tissue. The histopathology of liver tissue was also assessed. The data were analyzed using one-way ANOVA, followed by the post hoc Tukey test.

Esculetin lowered oxidative stress and myeloperoxidase activity (P<0.001); reduced the serum levels of ALT (P=0.037), AST (P=0.032), and ALP (P=0.004); and decreased the hepatic levels of IL-1β (P=0.002), IL-6 (P=0.004), toll-like receptor 4 (P<0.001), TNF-α (P=0.003), and nuclear factor-kappa B (P<0.001) as compared with LPS/D-Gal. Additionally, esculetin ameliorated hepatic tissue injury following LPS/D-Gal challenge.

Esculetin can reduce liver injury through the mitigation of oxidative burden, inflammation, and neutrophil infiltration and also exerts hepatoprotective effects against ALF.

Parkinsonchr('39')s disease (PD) presentations comprise frequent movement disorders in the elderly with various symptoms consisting of motor and non-motor complications. Paeonol is a phenolic chemical agent that has shown antioxidant and anti-inflammatory effects in different disorders and promising effects on metabotropic glutamate receptors (mGluR)- and GABAA-mediated neurotransmission. In this research, we tried to show the neuroprotective potential of paeonol in rat PD model induced by intrastriatal 6-hydroxydopamine (6-OHDA).

Rats with intrastriatal 6-OHDA lesioning received with paeonol at a dosage of 100 mg/kg/d for one week. In the end, some biomarkers of oxidative stress, apoptosis, and astrogliosis in nigral and striatal tissues were evaluated in addition to behavioral and Tyrosine Hydroxylase (TH) immunohistochemical analysis.

The obtained data showed that paeonol alleviates apomorphine-induced rotations and reduces the delay time to initiate and the total time in the narrow beam test. However, its beneficial behavioral effect vanished after intracerebroventricular administration of mGluR III or GABAA receptor antagonists. Moreover, paeonol significantly restored striatal malondialdehyde, tissue levels of reactive oxygen species, the activity of the protective and vital enzymes consisting of superoxide dismutase and catalase, Glial Fibrillary Acidic Protein (GFAP), DNA fragmentation, phosphor apoptosis signal-regulating kinase 1, and nigral aquaporin 4 with no significant and proper change of nitrite, interleukin-1β, inducible nitric oxide synthase, and angiotensin II. Additionally, paeonol prevented injury and reduced tyrosine hydroxylase-containing neurons in the midbrain nigral tissue.

These obtained findings evidently designate neuroprotective property of paeonol in 6-OHDA murine model of PD that is exerted via easing of oxidative stress, apoptosis, astrogliosis, and its advantageous effect is to some extent mediated via mGluR III/GABAA pathway.

Autoimmune inflammation of the central nervous system followed by myelin destruction, oxidative stress, and reduced neuroprotective factors play key roles in the pathogenesis of multiple sclerosis (MS). S-allyl cysteine (SAC), an active ingredient in the aged garlic extract, has known anti-inflammatory and neuroprotective effects. Therefore, this study aimed to investigate the anti-inflammatory and neuroprotective effects of S-allyl cysteine and related mechanisms in experimental autoimmune encephalomyelitis (EAE, a validated animal model of MS).

C57BL/6 mice were divided into the following three groups, with each group comprising of ten animals: Group 1: Control, Group 2: EAE induction, and Group 3: EAE induction and daily administration of SAC (EAE+SAC). The EAE induction was performed using the Hooke kit. It should be noted that daily gavage of SAC was carried out and clinical score (severity of tail and limbs paralysis) was assessed daily. The inflammation of the lumbar spinal cord was measured through hematoxylin and eosin staining. Moreover, tumor necrosis factor α (TNF-α) level in spinal cord and serum; Interleukin17(IL-17, Inflammatory factors) level in spinal cord; Activity-dependent neuroprotector homeobox (ADNP), and Microtubule-associated Proteins 1A/1B Light Chain 3A (MAP1LC3A, neuroprotective factors) were measured using ELISA. The data were analyzed using a one-way analysis of variance.

The daily administration of SAC significantly reduced the score of clinical paralysis on days 13 to 18 following EAE induction (from P>0.05 to P<0.01). It also significantly reduced spinal cord inflammation (P<0.01), elevated levels of TNFα in serum and spinal cord, and IL-17 in the spinal cord (P<0.05). On the other hand, daily administration of SAC elevated the reduced spinal cord levels of ADNP and MAP1LC3A (P<0.05).

Daily oral administration of SAC improved MS symptoms through the reduction of spinal inflammation and inflammatory factors, and elevation of neuroprotective factors. In addition, SAC can be utilized in the prevention and treatment of MS due to its herbal origin.

Hepcidin is the main modulator of systemic iron metabolism, and its role in the brain has been clarified recently. Studies have shown that hepcidin plays an important role in neuronal iron load and inflammation. This issue is of significance because neuronal iron load and inflammation are pathophysiological processes that are highly linked to neurodegeneration. Moreover, the activity of hepcidin has recently been manipulated to recover the neuronal impairment caused by brain inflammation in animal models.

Streptozotocin (STZ) was used to induce type 1 diabetes. Male Wistar rats (n = 40) with a weight range of 200–250 g were divided into control, diabetic, diabetic + insulin, and diabetic + dalteparin groups. Dalteparin (100 mg/kg IP) and insulin (100 mg/kg SC) were administered for 8 weeks. At the end of the experiment, Y-maze and passive avoidance tasks were carried out. The animals were perfused randomly and their hippocampal tissue was isolated for the analysis of markers such as lipid peroxidation like Malondialdehyde (MDA), hepcidin expression, iron, and ferritin. Blood samples were taken for the measurement of serum inflammatory cytokine Interleukin (IL)-6.

The findings indicated that treatment with dalteparin reduced IL-6, MDA, ferritin, and hepcidin expression in diabetic rats compared to treatment with insulin (P<0.05). Moreover, treatment with dalteparin did not decrease the iron level or prevented its decline.

Treatment with dalteparin improved the cognitive dysfunctions and symptoms of Alzheimer disease in STZ-induced diabetic rats by appropriately modulating and reducing oxidative stress and neuroinflammation. This may enhance the existing knowledge of therapeutics to reduce cognitive impairment in diabetes and is suggested to be a potential therapeutic agent in diabetes.

Synaptic plasticity is inappropriately affected by neurodegenerative diseases, including Alzheimer Disease (AD). In this study, we examined the effect of intrahippocampal amyloid-beta (Aβ1-40) on dentate gyrus Long-term Potentiation (LTP) and presynaptic short-term plasticity in a rat model of AD. 

The experimental groups in this research included the control with no treatment, sham-operated receiving the vehicle (normal saline), and Aβ-lesioned groups. For modeling AD, aggregated Aβ1-40 (10 μg/2 μl on each side) was injected into the hippocampal CA1. Three weeks later, Population Spike (PS) amplitude and slope ratios were determined at different Inter-pulse Intervals (IPI) of 10, 20, 30, and 50 ms as a valid indicator of the short-term presynaptic facilitation and/or depression. In addition, PS amplitude and slope were taken as an index of long-term synaptic plasticity after application of High-frequency Stimulation (HFS) to induce LTP in the medial perforant-dentate gyrus pathway. 

No significant differences were noted amongst the experimental groups regarding fEPSP slope and paired-pulse indices as indicators of short-term plasticity. In contrast, fEPSP slope and PS amplitude significantly decreased following the application of HFS in Aβ-injected group. In addition, there was no significant difference between the control and sham-operated groups regarding the mentioned parameters. 

Findings of this study clearly demonstrated that microinjection of Aβ1-40 into the CA1 could impair LTP in dentate gyrus but could not modify short-term plasticity.

Klotho and dipeptidyl peptidase-4 (DPP4) are two proteins that modulate inflammatory pathways. We investigated the association between circulating klotho and DPP4 activity and their relationship with inflammatory cytokines, miR-29a, and miR-195 in Alzheimer disease (AD).

This study was conducted on 16 AD patients and 16 healthy age-matched controls. Plasma levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β, interleukin-6 (IL-6), klotho, and DPP4 were measured by enzyme-linked immunosorbent assay. Plasma expression of miR-29a and miR-195 were also measured and compared by a real-time polymerase chain reaction.

There was a significant increase in TNF-α (p=0.006), IL-1β (p=0.012), and IL-6 (p=0.012) levels in the AD subjects compared with controls. Also, we found a decrease in plasma levels of klotho and an increase in plasma levels of DPP4 in the AD group that was not significant compared with the controls. Lower expression of miR-29a (P=0.009) and higher expression of miR-195 (P=0.003) were observed in the AD group that was significant than controls. Further analysis showed a negative correlation between klotho and plasma levels of IL-6 (r=-0.58, p=0.01). Also, there was a positive correlation between plasma DPP4 activity and TNF-α levels (r=0.50, P=0.04) and IL-1β (r=0.62, P=0.01). Likewise, plasma klotho concentration showed a negative correlation with the age of AD subjects (r=-0.56, P=0.02).

TNF-α, IL-1β, and IL-6 are involved in AD pathophysiology, and dysregulation of DPP4 and klotho may be associated with the inflammatory response of AD. Down-regulation of miR-29a and up-regulation of miR‑195 indicated the role of miRNAs in the AD process.

Intrahippocampal amyloid β (Aβ) negatively affects synaptic plasticity with subsequent impairment of learning and memory. Trigonelline is an alkaloid commonly found in fenugreek seeds and coffee beans with neuroprotective property and a promising agent for management of neurodegenerative disorders like Alzheimer’s disease (AD). In the present study, the possible beneficial effect of trigonelline on the improvement of learning and memory and synaptic plasticity was evaluated in Aβ (1-40) rat model of AD. For modeling AD, aggregated A𝛽 (1-40) (10 𝜇g/2 𝜇l for each side) was bilaterally microinjected into the hippocampal CA1 area. Trigonelline was administered p.o. at a dose of 100 mg/kg. The results showed that trigonelline pretreatment of Aβ-microinjected rats ameliorates learning and memory deficit in passive avoidance task and spatial memory impairment in Morris water maze (MWM) paradigm. It also improved population spike (PS) amplitude and field excitatory post-synaptic potential (fEPSP) slope following application of high frequency stimulation (HFS) to induce long-term potentiation (LTP) in medial perforant-dentate gyrus pathway as an index of synaptic plasticity. Additionally, trigonelline mitigated hippocampal activity of acetylcholinesterase (AChE). In summary, trigonelline pretreatment of intrahippocampal Aβ-microinjected rats could ameliorate learning and memory impairment, partly through restoring hippocampal synaptic plasticity and AChE and it may be suggested as an adjunct and promising oral bioactive therapeutic agent that may prevent memory deterioration in AD.

In temporal lobe epilepsy (TLE), recurrent seizures accompany with cognitive deficit. In some patients, the current medications cannot provide satisfactory control of seizures, therefore new drugs that act through different mechanisms are required. In the present study, the useful effect of dipeptidyl peptidase-4 inhibitor was evaluated in experimental model of temporal lobe epilepsy in male rats.
In this study, the effects of administration of dipeptidyl peptidase-4 inhibitor, linagliptin, on seizures score according to Racine’s scores and learning and memory impairment induced by intrahippocampal injection of kainic acid (4 g) using Y-maze and passive avoidance test were studied in rats. Linagliptin thirty minutes before kainic acid injection was administrated intracerebroventricularly.
In this study, the kainic acid-induced recurrent seizures, reduced alternation level in Y-maze test (p The obtained data indicate that linagliptin in kainate rats mitigates seizure severity and develops short-term memory.

Oxidative stress induced by proinflammatory cytokines such as IL-1β plays a major role in β-cell destruction in diabetes type 1. Salvianolic acid B (Sal B) is a polyphenolic compound with antioxidant and protective effects. Thus, objective of this study was to assess the protection exerted by Sal B on isolated rat islets exposed to IL-1β and to investigate an underlying mechanism in vitro.
Isolation of pancreatic islets was done by using the collagenase digestion method. Isolated rat islets were divided into 6 groups including: 1. control, 2. interleukin-1β treated, 3 and 4. interleukin-1β treated Sal B, 5 and 6. interleukin-1β treated Sal B PKB and PI3K inhibitors. Interleukin-1β (1 U/ml) was used to induce cytotoxicity after pretreatment with two doses of Sal B (50 μM and 100 μM) and application of each inhibitors was before Sal B.
IL-1β significantly decreased insulin secretion from isolated islets. Pretreatment with Sal B ameliorated the effect of IL-1β on glucose stimulated insulin secretion in a concentration dependent manner. Inhibitors of PKB and PI3K both abolished these improving effect of Sal B.
Sal B that has antioxidant, anti inflammatory and anti apoptotic properties, provided resistance to pancreatic β-cell dysfunction from cytokine in part via PI3K/Akt pathway. The findings represent that it is a promising agent for prevention of β-cell dysfunction in type 1 diabetes.

Diabetes as a metabolic disorder can cause memory and learning impairment. In recent years, the effect of plant extracts on the treatment of diabetes mellitus has been raised. The purpose of this study was to determine the effect of isorhmnetin administration on learning and memory disability in an experimental model of streptozotocin-induced diabetes mellitus in rats.
In the present study, for inducing diabetes, streptozotocin was administered at a dose of 60 mg/kg (intraperitoneal) in male rats. Intraperitoneal injection of isorhmnetin (10 mg/kg) was performed after induction of diabetes (10 mg/kg) for 12 weeks. Control groups also received relevant doses. Y-maze and passive avoidance tests were used for assessing of learning and memory ability. The serum glucose and body weight were determined before and 12 weeks after diabetic development.
Behavior data showed that compared to control rats, alternation percentage in Y-maze task (p
This study reveals that isorhmnetin administration to diabetic rats attenuates learning and memory impairment.

Epilepsy as a chronic neurological disorder causes inherent seizures and learning and memory failure. Since there is no acceptable control of seizures in some patients with the current recommended drug therapy, new medications with different mechanisms of action are needed. Here, the beneficial effect of hepatocyte growth factor (HGF) was evaluated in an experimental model of temporal lobe epilepsy in male rats.
In the present study, effects of intracerebroventricular administration of HGF (6 µg) thirty minutes before intrahippocampal injection of kainic acid (4 µg) on spontaneous seizures and learning and memory impairment were assessed in rats. As positive control group, valproic acid (200 mg/kg) was injected intraperitoneally.
Behavior data showed that the kainate rats exhibited spontaneous seizures, lower spontaneous alternation score in Y-maze task (p
This study revealed that HGF administration to kainate-injected rats attenuates seizure scores and improves learning and memory.

Alzheimer’s disease (AD) is a neurodegenerative disorder which is associated with extracellular accumulation of amyloid beta (Aβ) plaques. AD is accompanied by mitochondrial dysfunction and energy metabolism reduction. Fibroblast growth factor 21 (FGF21) is an endogenous polypeptide which its beneficial effects have been demonstrated on mitochondrial function, energy metabolism regulation and neuroprotection.
The present study was performed to investigate the effect of pretreatment with different concentrations of FGF21 [100,200 and 400 nM] on SH-SY5Y cells as a cellular model of AD induced by Ab(1-42). For induction of cellular model of AD. Ab(1-42) [20 µM] was added to SH-SY5Y cell medium. Cell viability (MTT assay) and mitochondrial membrane potential changes (Rhodamine 123 fluorescence intensity) were measured using microplate reader.
The results of this study showed that Ab(1-42) enhances cell damage (p
Taken together, the results of this study suggest that FGF21 prevents cell death induced by Ab(1-42) in SH-SY5Y cells. It seems that the beneficial effects of FGF21 are mediated through mitochondrial membrane potential maintenance.

Alzheimer’s disease (AD) is a neurodegenerative disorder specified by deposition of b-amyloid (Ab) and neuronal loss that leads to learning and memory disturbances. One of the most important causes of AD is glutamate-dependent excitotoxicity in brain regions that is vulnerable to AD. According to previous reported results, it was revealed that riluzole, as a glutamate release inhibitor, could improve learning and memory in an experimental model of AD. The aim of this study was to determine the effects of riluzole on Hippocampal astrogliosis and amyloidosis in a rat model of AD.
In the present study, the effects of riluzole administration at a dose of 10 mg/kg/day p.o. on hippocampal glial fibrillary acid protein (GFAP) as an astrogliosis marker and inducible nitric oxide synthase (iNOS) level in Ab (25-35)-injected rats was evaluated.
The results showed that in Ab (25–35)-injected rats, the intrahippocampal GFAP (p This study indicates that in rat model of AD, riluzole is able to attenuate NO synthesis with reducing hippocampal iNOS level, probably through inhibition of glutamatergic signaling pathway.

Temporal lobe epilepsy (TLE) is a chronic neurological disorder with spontaneous recurrent seizures and abnormal intracranial waves. Since the role of oxidative stress in the occurrence of epilepsy is inevitable, it seems that the use of antioxidants can prevent some of the complications resulting from this disease. This study was designed to assess the protective effect of carvacrol on seizure behavior and intracranial electroencephalographic (iEEG) recordings.
In this study, male Wistar rats were randomly allocated into four groups: Sham-operated, carvacrol (10 mg/kg) pretreated-sham-operated, kainic acid (0.8 μg/μl), and carvacrol (10 mg/kg) pretreated-kainic acid. In this study, we evaluated the status epilepticus and spontaneous seizures according to Racine΄s scores and recorded iEEG for investigating the antiepileptic effect of carvacrol in kainite-injected rats.
The seizures behavior (status epilepticus and spontaneous seizures) appeared in kainite-injected rats and iEEG amplitude increased as compared to sham group (p
Collectively, the results of this study indicate that carvacrol is able to prevent some of the epilepsy disease complications in an experimental model of temporal lobe epilepsy.

Alzheimer’s disease (AD) is a disorder with multiple pathophysiological causes, destructive outcomes, and no available definitive cure. Pelargonidin (Pel), an anthocyanin derivative, is an estrogen receptor agonist with little estrogen side effects. This study was designed to assess Pel memory enhancing effects on the a rat Amyloid Beta25-35 (Aβ) intrahippocampal microinjections model of AD in the passive avoidance task performance paradigm and further evaluate the potential estrogen receptor role on the memory-evoking compound. Equally divided rats were assigned to 5 groups of sham, Aβ intrahippocampal microinjected, Pel pretreated (10 mg/kg; P.O), α estrogen antagonist intra-cerebrovascular (i.c.v.) microinjected, and β estrogen antagonist (i.c.v) microinjected animals. Intrahippocampal microinjections of Aβ were adopted to provoke AD model. Passive avoidance task test was also used to assess memory performance. Pel pretreatment prior to Aβ microinjections significantly improved step-through latency (P

Parkinson's disease (PD) is a neurodegenerative disease with selective damage of mesencephalic dopaminergic neurons. Due to the protective, anti-inflammatory, and antioxidant effect of Hypericum perforatum (HP), this study was undertaken to assess dose-dependent effect of HP hydroalcoholic extract on motor imbalance following intrastriatal injection of 6-hydroxydopamine in the rat.
In this experimental research, male Wistar rats (n=35) were equally divided into sham, 6-hydroxydopamine (OHDA)-lesioned, and HP extract-treated lesion groups. Model of PD was induced by microinjecting 12.5 microgram of 6-OHDA dissolved in saline-ascorbate solution into the left striatum. Treated lesion groups received HP extract at doses of 50, 100, and 200 mg/kg/day p.o. started one week before the surgery for 1 week post-surgery. After 1 week, ipsilateral and contralateral rotations induced by apomorphine were counted and net scores were obtained.
In the 6-OHDA-lesioned group, the dopaminergic agonist apomorphine induced contralateral rotational behavior (P
Oral administration of HP extract at doses of 100 and 200 mg/kg could reduce motor imbalance and attenuate forced biased rotational behavior in 6-OHDA-induced model of PD.

Parkinson’s disease (PD) is a common neurological disorder due to degeneration of dopaminergic neurons within pars compacta of substantia nigra (SNC). With regard to protective effect of Malva sylvestris (MS), this study was conducted to evaluate the effect of aquaeous extract of this plant in an experimental model of PD induced by 6-hydroxydopamine (6-OHDA).
Rats were divided into sham-operated, MS-treated sham-operated, lesioned and MS-treated lesioned groups. The hemi-PD early model was induced by unilateral intrastriatal injection of 6-OHDA (12.5 µg/5µl of saline-ascorbate, left side). The treated groups received aquaeous extract of MS (i.p.) at a dose of 100 mg/kg once a day for one week at an interval of 24 h till 1 h pre-surgery. One week after surgery, the animals were tested for rotational behavior by apomorphine for an hour and the number of dopaminergic neurons in the SNC was counted.
After one week, apomorphine caused a significant contralateral turning (P Intraperitoneal administration of aquaeous extract of Malva sylvestris could reduce motor asymmetry and has not neuroprotective effect against 6-OHDA toxicity in an experimental model of PD.