Protective effects of selegiline against amyloid beta-induced anxiety-like behavior and memory impairment.

BACKGROUND: Alzheimer's disease (AD) is a complex and common neurodegenerative disorder. The present study aimed to investigate the potential effects of selegiline (SEL) on various aspects of memory performance, anxiety, and oxidative stress in an AD rat model induced by intracerebroventricular injection of amyloid beta1-42 (Aß1-42). METHODS: Oral administration of SEL at a dose of 0.5 mg/kg/day was performed for 30 consecutive days. Following the 30 days, several tests, including the open-field, elevated plus-maze, novel object recognition, Morris water maze, and passive avoidance learning were conducted to assess locomotor activity, anxiety-like behavior, recognition memory, spatial memory, and passive avoidance memory, respectively. RESULTS: The results indicate that the induction of AD in rats led to recognition memory, spatial memory, and passive avoidance memory impairments, as well as increased anxiety. Additionally, the AD rats exhibited a decrease in total antioxidant capacity and an increase in total oxidant status levels, suggesting an imbalance in oxidative-antioxidant status. However, the administration of SEL improved memory performance, reduced anxiety, and modulated oxidative-antioxidant status in AD rats. CONCLUSIONS: These findings provide evidence that SEL may alleviate anxiety-like behavior and cognitive deficits induced by Aß through modulation of oxidative-antioxidant status.

Cacao consumption improves passive avoidance memory impairment in a rat model of Alzheimer's disease: the role of hippocampal synaptic plasticity and oxidative stress.

Introduction: Alzheimer's disease (AD) causes progressive loss of cognitive function and synaptic plasticity, which is the most common form of dementia. The present study was designed to scrutinize the effects of cacao on passive avoidance memory function and to identify the roles of hippocampal synaptic plasticity and oxidative stress in an AD rat model induced by unilateral intracerebroventricular (UICV) injection of amyloid-beta (Aß). Methods: Oral administration of cacao (500 mg/kg/ day) was given for 2 consecutive months. A memory retention test was conducted 24 h after passive avoidance training was completed. Subsequently, the amplitude of population spike (PS) and slope of field excitatory postsynaptic potentials (fEPSPs) were assessed at hippocampal long-term potentiation (LTP) in perforant pathway-dentate gyrus (PP-DG) synapses. Moreover, total thiol group (TTG) and malondialdehyde (MDA) concentrations were evaluated in the plasma. Furthermore, compact Aß plaques were detected in the hippocampal DG by performing Congo red staining. Results: As a result of AD induction, passive avoidance memory was impaired; also, reduced fEPSP slopes, PS amplitudes, and content of TTG, and increase in MDA levels in the rats were observed. In contrast, cacao treatment ameliorated passive avoidance memory impairment, improved hippocampal LTP impairment, modulated oxidative-antioxidative status, and delayed Aß plaques production in AD rats. Disscussion: Conclusively, cacao alleviates Aß-induced cognitive deficit, probably by the amelioration of hippocampal LTP impairment, modulation of oxidative-antioxidative status, and inhibition of Aß plaque accumulation.

Ameliorative effects of thiamin on learning behavior and memory dysfunction in a rat model of hypothyroidism: implication of oxidative stress and acetylcholinesterase.

Hypothyroidism causes learning and memory impairment. Considering the neuroprotective properties of thiamine (Vitamin B1), this study was conducted to investigate the effects of thiamine on acetylcholinesterase (AChE) activity, oxidative damage, and memory deficits in hypothyroid rats.In this study, 50 rats (21 days old) were randomly divided into 5 groups and treated with propylthiouracil (0.05% in drinking water) and thiamine (50, 100, and 200 mg/kg, oral) for 7 weeks. Following that, Morris water maze (MWM) and passive avoidance (PA) tests were performed. Finally, oxidative stress indicators and AChE activity were measured in brain tissue.Treatment of hypothyroid rats with thiamine, especially at 100 and 200 mg/kg, alleviated the ability to remember the location of the platform as reflected by less time spent and distance to reach the platform, during the MWM test (P < 0.05 to P < 0.001). In the PA test, the latency to enter the dark chamber and light stay time were increased in rats who received thiamine compared to the hypothyroid group (P < 0.05 to P < 0.001). In addition, thiamine increased the levels of total thiol groups and superoxide dismutase while decreasing the levels of malondialdehyde and AChE.Our results suggest that thiamine supplementation could effectively improve memory loss in a rat model of hypothyroidism. The positive effects of thiamin on the learning and memory of hypothyroid rats may be due to amelioration of redox hemostasis and cholinergic disturbance.

Effect of Duvelisib, a Selective PI3K Inhibitor on Seizure Activity in Pentylenetetrazole-Induced Convulsions Animal Model.

Epilepsy is one of the most common neurological diseases, which is caused by abnormal brain activity. A wide variety of studies have shown the importance of the phosphatidylinositol-3-kinase (PI3K) signaling pathway in epilepsy pathogenesis. Duvelisib (DUV) is a selective inhibitor of PI3K. The present study investigated the anticonvulsant potential of DUV in a rat model of pentylenetetrazole (PTZ)-induced convulsions. Male Wistar rats (200-250 g, 8 weeks old) were injected intraperitoneally (IP) with DUV at different doses of 5 and 10 mg/kg, or vehicle 30 minutes prior to PTZ (70 mg/kg, IP) treatment. Based on Racine's scale, behavioral seizures were assessed. The results showed that pretreatment with DUV prolonged the seizure stages according to the Racine scale, significantly decreased the duration of general tonic-clonic seizure and reduced the number of myoclonic jerks (P < .05). In conclusion, we found that PI3K antagonist DUV significantly reduced PTZ-induced seizures, indicating that DUV exerts an anticonvulsant effect by inhibiting PI3K signaling pathway.

Effect of Elettaria cardamomum L. on hormonal changes and spermatogenesis in the propylthiouracil-induced hypothyroidism male BALB/c mice.

INTRODUCTION: Spermatogenesis is significantly influenced by the thyroid gland. Thyroid disorders can be caused by a variety of factors. Traditionally, Ellettaria cardamomum has been used to treat a variety of ailments. The effects of E. cardamomum extract (ECE) on spermatogenesis in hypothyroid mice were investigated in this study. METHODS: In this study 42 male mice, weighing (25-35 g) were randomly divided in six groups: control group (taking normal saline, 0.5 mL/day, by oral gavage [P.O.]), hypothyroid group (taking 0.1% propylthiouracil in drinking water for 2 weeks), hypothyroid groups treated by levothyroxine (15 mg/kg/day, P.O.) and hypothyroid groups treated by ECE (100, 200 and 400 mg/kg/day, P.O.). After the end of experiments the mice were anaesthetised and blood samples were collected for hormonal analysis. RESULTS: The sperm count and microscopic studies of testes were done also. Our results showed that the T3 , T4 , testosterone levels and spermatogenesis in hypothyroid animals decreased and thyroid-stimulating hormone, follicle-stimulating hormone and luteinizing hormone increased compared with control group. Treatment by ECE reverse these effects in comparison with hypothyroid group. CONCLUSIONS: According to our findings, the ECE may stimulates thyroid gland function and increases testosterone and spermatogenesis.

Policosanol protects against Alzheimer's disease-associated spatial cognitive decline in male rats: possible involved mechanisms.

RATIONALE: Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by cognitive decline and synaptic failure. OBJECTIVE: The present study was designed to explore the possible protective effects of policosanol (PCO) on spatial cognitive capacity, long-term potentiation (LTP) induction, oxidant/antioxidant status, and Aß plaques formation in an AD rat model induced by intracerebroventricular (ICV) injection of Aß1-40. METHODS: Healthy adult male Wistar rats were randomly divided into control, sham (ICV injection of 5 µl phosphate-buffered saline), AG (50 mg/kg; P.O., as PCO vehicle), PCO (50 mg/kg; P.O.), AD model (ICV injection of 5 µl Aß), AD + AG (50 mg/kg; P.O.), and AD + PCO (50 mg/kg; P.O.). Treatments were performed for eight consecutive weeks. At the end of the treatment course, spatial learning and memory functions, hippocampal long-term potentiation (LTP) induction, malondialdehyde (MDA), and total thiol group (TTG) levels, as well as the formation of Aß plaques, were examined. RESULTS: The results showed that injection of Aß reduced spatial learning and memory abilities in the Barnes maze test, which was accompanied by decreases in field excitatory postsynaptic potential (fEPSP) slope, population spike (PS) amplitude, and TTG level and increases in Aß plaque accumulation and MDA content. In contrast, PCO treatment improved all the above-mentioned changes in the Aß-infused rats. CONCLUSIONS: The results suggest that amelioration of hippocampal synaptic plasticity impairment, modulation of oxidant/antioxidant status, and inhibition of Aß plaque formation by PCO may be the mechanisms behind its protective effect against AD-associated spatial cognitive decline.

The Protective Effects of Policosanol on Learning and Memory Impairments in a Male Rat Model of Alzheimer's Disease.

Alzheimer's disease (AD), the most common form of dementia, is characterized by a progressive decline in cognitive performance and memory formation. The present study was designed to investigate the effect of policosanol (PCO) on cognitive function, oxidative-antioxidative status, and amyloid-beta (Aß) plaque formation in an AD rat model induced by intracerebroventricular (ICV) injection of Aß1-40. Healthy adult male Wistar rats were randomly divided into seven groups: control, sham (5 µL, ICV injection of phosphate-buffered saline), AD model (5 µL, ICV injection of Aß), acacia gum (50 mg/kg, 8 weeks, gavage), PCO (50 mg/kg, 8 weeks, gavage), AD + acacia gum (50 mg/kg, 8 weeks, gavage), and AD + PCO (50 mg/kg, 8 weeks, gavage). During the ninth and tenth weeks of the study, the cognitive function of the rats was assessed by commonly used behavioral paradigms. Subsequently, oxidative-antioxidative status was examined in the serum. Moreover, compact Aß plaques were detected by Congo red staining. The results showed that injection of Aß impaired recognition memory in the novel object recognition test, reduced the spatial cognitive ability in the Morris water maze, and alleviated retention and recall capability in the passive avoidance task. Additionally, injection of Aß resulted in increased total oxidant status, decreased total antioxidant capacity, and enhanced Aß plaque formation in the rats. Intriguingly, PCO treatment improved all the above-mentioned neuropathological changes in the Aß-induced AD rats. The results suggest that PCO improves Aß-induced cognitive decline, possibly through modulation of oxidative-antioxidative status and inhibition of Aß plaque formation.

Maternal long-term inhalation exposure to perchloroethylene and prenatal teratogenicity: morphometric, hormonal, and histological study.

Some commonly used chemicals have teratogenic effects. Perchloroethylene (PCE) is a liquid that is widely used in various industries and drying clothes. In this study, the teratogenic effects of PCE in rat embryos were investigated. In this experimental study, 32 adult Wistar female rats in the weight range of 230-250 g were used. Female rats were randomly divided into 4 groups (n = 8). Control group (without PCE inhalation), experimental group G(I) (exposed to PCE 18 days prior to mating), experimental group G(II) (exposed to PCE 18 days after mating) and experimental group G(III) (exposed to PCE 18 days before and 18 days after mating). Pregnant rats were anesthetized on the 18th day of gestation and then serum and embryos were removed for the required studies. Embryos were examined for number, weight, sex, morphometric parameters of organs, and tissue samples were prepared for histological studies. Serum isolated from dams were evaluated for sexual and gonadal hormones. The results of this study showed that PCE has teratogenic effects on rat embryos. Infertility and reduced birth rate were other effects of PCE in rats. PCE has teratogenic effects and impairs the reproductive system of rats.

Effect of amitriptyline on learning and memory consolidation in the male Wistar rats with an experimental model of pentylenetetrazole-induced seizure

Abstract Amitriptyline (AMT) was developed for the treatment of chronic and neuropathic pain. There is also evidence it may be useful in the treatment of neurodegenerative disorders. In this regard, the effect of on the experimental model of seizures and memory impairment caused by seizures in rats is investigated in the present study. Seizures in Wistar rats (200-250 g) were induced by pentylenetetrazole (PTZ, 60 mg/kg, intraperitoneally (i.p.)). The anticonvulsant effect of AMT (10 and 20 mg/kg, i.p.) was evaluated in the seizure model. The effect on memory was assessed using passive avoidance (PA) learning and memory test. After behavioral tests, the animals underwent deep anesthesia and were put down painlessly. Animal serum was isolated for oxidant/antioxidant assays (malondialdehyde (MDA), and glutathione peroxidase (GPx)). Intraperitoneal injection of AMT decreased the mean number of myoclonic jerks and generalized tonic-clonic seizure (GTCS) duration and increased the mean latency of myoclonic jerk and GTCS compared to the PTZ group. Moreover, in the PA test, AMT caused a significant increase in retention latency (RL) and total time spent in the light compartment (TLC) compared to the PTZ group. Biochemical tests showed that AMT was able to significantly increase GPx serum levels and significantly reduce MDA serum levels compared to the PTZ group. Overall, this study suggests the potential neuroprotective effects of the AMT drug in a model of memory impairment caused by seizures via the mechanism of inhibition of the oxidative stress pathway.

Protective efficacy of dark chocolate in letrozole-induced ovary toxicity model rats: hormonal, biochemical, and histopathological investigation.

OBJECTIVE: To assess the protective effect of dark chocolate (DC) on the letrozole-induced rat model of polycystic ovary syndrome (PCOS). METHODS: In this experimental study, 32 female Wistar rats, weighing (200 ± 20) g, were randomly categorized into 4 groups including control, letrozole (1 mg·kg·d), metformin (500 mg·kg·d) along with letrozole, and DC (500 mg·kg·d) along with letrozole for 28 d by oral gavage. Twenty-four hours after the last supplementation, direct blood sampling was taken from the heart to obtain blood serum for evaluation of sex hormones and gonadotropins, oxidative parameters, inflammatory cytokines, and ovarian tissue was examined for histology. RESULTS: The DC treatment significantly improved PCOS signs, as demonstrated by the significant restoration of ovarian morphology and physiological functions as compared with the letrozole group. DC treatment also decreased ovarian interleukin-1ß and tumor necrosis factor-α levels and improved total oxidative/antioxidative status as compared with the letrozole group. CONCLUSIONS: Treating the animals with DC could alleviate the PCOS symptoms and reduced the toxic effects of letrozole in the ovary. This effect may mediate through antioxidant and antiinflammatory properties.

Anticonvulsant activity of oxaprozin in a rat model of pentylenetetrazole-induced seizure by targeting oxidative stress and SIRT1/PGC1α signaling.

The effect of oxaprozin (OXP) on an experimental model of seizures in rats was investigated in this study. Seizures in Wistar rats (200-250 g) were induced by pentylenetetrazole (PTZ, 60 mg/kg). The anticonvulsant effect of OXP (100, 200, and 400 mg/kg, intraperitoneally) was evaluated in a seizure model. After behavioral tests, the animals underwent deep anesthesia and were put down painlessly. Animal serum was isolated for antioxidant assays (nitric oxide (NO) and glutathione (GSH)). The animals' brains were also isolated to gauge the relative expression of genes in the oxidative stress pathway (sirtuin 1 (Sirt1) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (Pgc1α)). Intraperitoneal injection of OXP increased the mean latency of myoclonic jerks and generalized tonic-clonic seizure (GTCS) and decreased the number of myoclonic jerks and GTCS duration compared with the PTZ group. Biochemical tests showed that pretreatment with OXP was able to restore GSH serum levels and reverse the augmented NO serum levels caused by PTZ induction to the normal level. The quantitative polymerase chain reaction results also revealed that OXP counteracts the negative effects of PTZ by affecting the expression of the Sirt1 and Pgc1α genes. Overall, this study suggests the potential neuroprotective effects of the nonsteroidal, anti-inflammatory OXP drug in a model of neural impairment caused by seizures via the mechanism of inhibition of the oxidative stress pathway.

Nonsteroidal Anti-inflammatory Drug Oxaprozin is Beneficial Against Seizure-induced Memory Impairment in an Experimental Model of Seizures in Rats: Impact On Oxidative Stress and Nrf2/HO-1 Signaling Pathway.

There is substantial evidence that anti-inflammatory agents and antioxidants have neuroprotective properties and may be useful in the treatment of neurodegenerative disorders. In this regard, the effects of oxaprozin (OXP) (a nonsteroidal anti-inflammatory drug) on the experimental model of seizure and memory impairment caused by seizures in rats were investigated in the present study. Seizures in male Wistar rats (200-250 g, 8 weeks) were induced by pentylenetetrazol (PTZ, 60 mg/kg). The anticonvulsant effects of OXP (100, 200, and 400 mg/kg, administered intraperitoneally) were evaluated in the seizure model. The effect on memory was assessed using the passive avoidance (PA) test. After behavioral tests, the animals underwent deep anesthesia and were euthanized painlessly. Animal serum was isolated for antioxidant assays (MDA and GPx). The animals' brains (hippocampus) were also isolated to gauge the relative expression of genes in the oxidative stress pathway (Nrf2/HO-1). Intraperitoneal injection of OXP decreased the mean score on the Racine scale compared to the PTZ group. Moreover, in the PA test, OXP caused a significant increase in retention latency (RL) and total time spent in the light compartment (TLC) compared to the PTZ group. Biochemical tests showed that OXP was able to significantly increase GPx serum levels and significantly reduce MDA serum levels compared to the PTZ group. Quantitative polymerase chain reaction (qPCR) results also revealed that OXP counteracted the negative effects of PTZ by significantly increasing the expression of the Nrf2 and Hmox1 genes. Overall, this study suggests the potential neuroprotective effects of the nonsteroidal anti-inflammatory drug OXP in a model of memory impairment caused by seizures via inhibition of the oxidative stress pathway.

Treatment with human umbilical cord blood serum in a gentamicin-induced nephrotoxicity model in rats.

Sold under the brand name of Garamycin, gentamicin (GM) is an antibiotic in the category of aminoglycoside, that although does have many antibacterial properties, owing to several side effects, its consumption is confined. The current study is aimed at gauging the protective influences of human umbilical cord blood serum (hUCBS) on nephrotoxicity which is induced by GM. In this regard, in the present experimental design, twenty-eight male Wistar rats with the weights of 220 ± 20 g were categorized randomly into 4 groups of seven. The groups included GM (100 mg/kg), control as well as hUCBS at doses of one and two percent together with GM (100 mg/kg) for ten days in an intraperitoneal manner. Blood sampling was collected from the heart directly 24 h after the final injection for obtaining blood serum; the parameters of C-reactive protein (CRP), total oxidant status (TOS), interleukin (IL)-6, lactate dehydrogenase (LDH), total antioxidant capacity (TAC), creatinine (Cr), blood urea nitrogen (BUN), blood serum glutathione (GSH) were gauged in blood serum samples to evaluate renal function. Moreover, for histology, an examination of kidney tissue was performed. In comparison to those of the GM group, in the treatment group, hUCBS significantly decreased the levels of BUN, Cr, LDH, TOS, IL-6, and the CRP levels, and significantly increased the TAC and GSH levels. It was revealed that the treatment of the animals with hUCBS culminates in the reduction of GM' toxic impacts on the kidney.

Protective effects of the fruit extract of raspberry (Rubus fruticosus L.) on pituitary-gonadal axis and testicular histopathology in streptozotocin induced diabetic male rats.

OBJECTIVE: Protective effects of raspberry (Rubus fruticosus L.) fruit extract on pituitary-gonadal axis and testicular tissue in diabetic male rats, were investigated. MATERIALS AND METHODS: Sixty male rats were divided into control, sham (saline treated), streptozotocin (STZ)-diabetic, and STZ-diabetic animals treated with 50, 100 and 200 mg/kg/day of raspberry extract. After 4 weeks, blood samples were obtained and left testes were removed and prepared for histopathological studies. Serum levels of Luteinizing hormone (LH), Follicle stimulating hormone (FSH), testosterone, Nitric oxide (NO), and malondialdehyde (MDA), as well as superoxide dismutase (SOD) and catalase (CAT) activity level were assayed. Sperm number and motility in the epididymis samples were measured. Data were analyzed using ANOVA (one-way analysis of variance). RESULTS: Serum levels of LH, FSH and MDA significantly increased in diabetic rats, however, treatment with the extract significantly reversed the alterations. Serum levels of testosterone and NO, activity of SOD and CAT, and sperm number and motility significantly decreased and severe destruction of testicular histology was observed in diabetic animals while treatment with the extract significantly reversed the pathologic alterations observed in diabetic rats. According to the results, 100 and 200 mg/kg of the extract were able to effectively reverse the diabetes complications. CONCLUSION: Our findings demonstrated that the fruit extract of raspberry has protective effects on male reproductive system in diabetic rats partially due to its improving effects on NO system, and SOD and CAT activity.

Effects of vanillic acid on Aß1-40-induced oxidative stress and learning and memory deficit in male rats.

Alzheimer's disease (AD) is a neurodegenerative disease, in which the accumulation of ß-amyloid (Aß) peptide in the extracellular space causes a progressive reduction in cognitive performance. Aß stimulates active oxygen species generation leading to oxidative stress and neural cell death. Vanillic Acid (VA) is the oxidant form of vanillin widely found in vanilla beans. VA has many properties, such as suppressing apoptosis and eliminating the harmful effects of oxidative stress in animal models. The VA effects on impaired learning and memory in Aß rats were assessed. Forty adults male Wistar rats were assigned to the following five groups in random: the control, sham (received saline (vehicle) via intracerebroventricular (ICV) injection), Aß (received Aß1-40 via ICV injection), VA (50 mg/kg by oral gavage once a day through four weeks), and Aß + VA (50 mg/kg) groups. Open field test, novel object recognition (NOR) test, Morris water maze (MWM) test, and passive avoidance learning (PAL) task were performed, and finally, we determined the malondialdehyde (MDA), total antioxidant capacity (TAC) and total oxidant status (TOS) levels. Aß decreased the cognitive memory in NOR, spatial memory in MWM, and passive avoidance memory in PAL tests. In contrast, VA improved learning and memory in the treated group. Aß significantly increased MDA and TOS and decreased TAC levels, whereas VA treatment significantly reversed TAC, TOS and MDA levels. In conclusion, VA decreased the Aß effects on learning and memory by suppressing oxidative stress and can be regarded as a neuroprotective substance in AD.

Vanillic acid attenuates amyloid ß1-40-induced long-term potentiation deficit in male rats: an in vivo investigation.

Objectives: Alzheimer disease (AD) is a neurodegenerative disorderliness that involves deductible progressive cognition function caused by amyloid-beta (Aß) peptide accumulation in the interstitial space. The increase of Aß stimulates all kinds of active oxygen and causes oxidative stress and apoptosis. In this investigation, we researched the neuroprotective impacts of vanillic acid (VA) on the Aß-induced (Aß1-40) long-term potentiation (LTP) of the hippocampus - a commonly probed synaptic plasticity model that happens at the same time as memory and learning - in the AD rats.Methods: Forty-five male Wistar rats were categorized into five groups (n = 8 rats/group, 200-220 g), and studied as control (standard diet), sham (vehicle), VA (50 mg/kg), Aß and Aß + VA (50 mg/kg) groups. In vivo electrophysiological recordings were implemented after the stereotaxic surgery to gauge the excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the dentate gyrus of the hippocampus. By the stimulation at high-frequency of the perforate pathway, long-term potentiation (LTP) was induced. To assess the plasma levels of malondialdehyde (MDA) and total thiol group (TTG), blood samples were garnered.Results: In the Aß-injected rats, EPSP slope, and PS amplitude were significantly reduced after the induction of LTP. Thus, the findings demonstrate that VA decreases the impacts of Aß on LTP; also, the treatments through VA neuroprotective against the negative effects of Aß on the synaptic plasticity of the hippocampus can decrease the MDA levels and also increase the TTG levels significantly.Discussion: Therefore, based on this experiment on male rats, VA has neuroprotective effects and antioxidants benefits against the Aß-mediated inhibition of long-term potentiation.

Ameliorative effects of endurance training and Matricaria chamomilla flowers hydroethanolic extract on cognitive deficit in type 2 diabetes rats.

Diabetes mellitus is mainly associated with degeneration of the central nervous system, which eventually leads to cognitive deficit. Although some studies suggest that exercise can improve the cognitive decline associated with diabetes, the potential effects of endurance training (ET) accompanied by Matricaria chamomilla (M.ch) flowers extract on cognitive impairment in type 2 diabetes has been poorly understood. Forty male Wistar rats were randomized into 5 equal groups of 8: healthy-sedentary (H-sed), diabetes-sedentary (D-sed), diabetes-endurance training (D-ET), diabetes-Matricaria chamomilla. (D-M.ch), and diabetes-endurance training-Matricaria chamomilla. (D-ET-M.ch). Nicotinamide (110 mg/kg, i.p.) and Streptozotocin (65 mg/kg, i.p.) were utilized to initiate type 2 diabetes. Then, ET (5 days/week) and M.ch (200 mg/kg body weight/daily) were administered for 12 weeks. After 12 weeks of the experiment, cognitive functions were assessed using the Morris Water Maze (MWM) test and a passive avoidance paradigm using a shuttle box device. Subsequently, using crystal violet staining, neuron necrosis was examined in the CA3 area of the hippocampus. Diabetic rats showed cognitive impairment following an increase in the number of necrotic cells in region CA3 of the hippocampal tissue. Also, diabetes increased serum levels of lipid peroxidation and decreased total antioxidant capacity in serum and hippocampal tissue. ET + M.ch treatment prevented the necrosis of neurons in the hippocampal tissue. Following positive changes in hippocampal tissue and serum antioxidant enzyme levels, an improvement was observed in the cognitive impairment of the diabetic rats receiving ET + M.ch. Therefore the results showed that treatment with ET + M.ch could ameliorate memory and inactive avoidance in diabetic rats. Hence, the use of ET + M.ch interventions is proposed as a new therapeutic perspective on the death of hippocampal neurons and cognitive deficit caused by diabetes.

Human umbilical cord blood serum attenuates gentamicin-induced liver toxicity by restoring peripheral oxidative damage and inflammation in rats.

Gentamicin (GM) is an aminoglycoside antibiotic that despite its antibacterial effects, its use is restricted due to numerous side effects. The umbilical cord serum contains various biomolecules that have protective impacts on the damaged tissues. The aim of this study was to gauge the protective effect of human umbilical cord blood serum (hUCBS) on GM-induced hepatotoxicity. In this experimental study, 28 male Wistar rats, weighing 220 ± 20 g, were randomly categorized into 4 groups including control, GM (100 mg/kg), hUCBS at doses of 1 and 2% along with GM (100 mg/kg) for 10 days, intraperitoneally. Twenty-four hours after the last injection, direct blood sampling was taken from the heart to obtain blood serum and liver enzymes, inflammatory cytokines and liver tissue were examined for histology. GM causes necrosis and inflammation in liver tissue. Liver enzyme and inflammatory cytokine levels were significantly increased in the GM group. Human umbilical cord blood serum significantly decreased liver enzyme and inflammatory cytokines levels in the experimental groups compared to the GM group. GM causes liver damage such as the inflammation and necrosis in liver tissue. Treating the animals with hUCBS reduced the toxic effects of GM in the liver.

The effects of concurrent treatment of silymarin and lactulose on memory changes in cirrhotic male rats.

Introduction: Chronic liver disease frequently accompanied by hepatic encephalopathy (HE). Changes in the permeability of the blood-brain barrier in HE, make an easier entrance of ammonia among other substances to the brain, which leads to neurotransmitter disturbances. Lactulose (LAC), causes better defecation and makes ammonia outreach of blood. Silymarin (SM) is a known standard drug for liver illnesses. The purpose of this research was to determine the results of LAC and SM combined treatment, on the changes in memory of cirrhotic male rats. Methods: The cirrhotic model established by treatment with thioacetamide (TAA) for 18 weeks. Cirrhotic rats randomized to four groups (n = 7): TAA group (received drinking water), LAC group (2 g/kg/d LAC in drinking water), SM group (50 mg/kg/d SM by food), SM+ LAC group (similar combined doses of both compounds) for 8 weeks. The control group received drinking water. The behavior examined by wire hanging (WH), passive avoidance (PA), and open field (OF) tests. Results: Our findings showed that treatment with SM+LAC effectively increased PA latency, compared with the control group. The results showed that the administration of LAC and SM+LAC affected the number of lines crossed, the total distance moved and velocity in the OF tests. Conclusion: SM and LAC have anti-inflammatory effects that are memory changing. It may be due to their useful effects. These results indicated that SM+LAC restored memory disturbance and irritated mood in the cirrhotic rats. Comparable neuroprotection was never previously informed. Such outcomes are extremely promising and indicate the further study of SM+LAC.

Attenuating properties of Rubus fruticosus L. on oxidative damage and inflammatory response following streptozotocin-induced diabetes in the male Wistar rats.

PURPOSE: Diabetes mellitus is a prevalent metabolic disorder that entails numerous complications in various organs. In current era, different types of diseases are being treated by the applications of herbs. The present study is aimed at investigating the anti-inflammatory and antioxidant effects of the Rubus fruticosus hydroethanolic extracts (RFHE) in the streptozotocin (STZ)-induced diabetic rats. METHODS: At this experimental research, male Wistar rats with the weight of 220 ± 20 g, were categorized randomly into five groups of vehicles as control, STZ (60 mg kg- 1 of body weight, intraperitoneally (i.p.)) and RFHE (50, 100 and 200 mg kg- 1, i.p.). In the last stage (end of week 4) of the experiment, after being euthanized, the blood samples of the rats were collected for measuring malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS) as well as inflammatory markers like tumor necrosis factor (TNF)-α, interleukin (IL)-6 and C-reactive protein (CRP). RESULTS: Data from this study was revealed that diabetes causes oxidative damage and consequently the serum level of inflammatory markers rises. RFHE was shown to be significantly correlated with lowering the level of MDA, TNF-α, IL-6 and CRP of diabetic rats. Moreover, RFHE significantly elevated the GSH and TAS serum levels in diabetic rats when compared with STZ group. CONCLUSIONS: RFHE might have anti-diabetic properties; this outcome may be mediated by high antioxidant and anti-inflammatory effects.