Gastric ulcer disease is a common problem of the gastrointestinal tract, with increasing incidence and prevalence attributed to a loss of balance between aggressive and protective factors. Gastric ulcer is a chronic condition characterized by damage to the mucosal, submucosal, and muscular layers of the stomach, primarily caused by excessive secretion of gastric acid, pepsin, and other digestive enzymes. The role of antioxidants in promoting ulcer healing is well established. Magnesium (Mg), being a main macro element, exhibits various beneficial effects, including antioxidant, analgesic, anti-inflammatory, antidiabetic, antacid, anti-apoptotic, and free radical-scavenging properties. In this study, we investigated the effect of magnesium sulfate (MgSO4) on indomethacin-induced gastric ulcers in male Balb/c mice. The effect of orally administered MgSO4 (0.05, 0.1, and 0.2 g/kg) was assessed in both gastric ulcer and healthy mice. The animals were randomly assigned to 10 groups: healthy control; sham; MgSO4 alone at 0.05, 0.1, or 0.2 g/kg; gastric ulcer control (indomethacin, 18 mg/kg); MgSO4 at 0.05, 0.1, or 0.2 g/kg) plus indomethacin; and omeprazole (20 mg/kg) plus indomethacin. Treatment were administered intragastrically for 14 consecutive days. All mice underwent a 24-h fasting period before the final day of treatment. Six hours after the last dose, indomethacin was administered orally to induce gastric ulceration. The mice were then sacrificed for histopathological and biochemical assessments. Administration of MgSO4 significantly reduced the ulcerated area, decreased malondialdehyde (MDA) levels, and increased gastric antioxidative enzyme activity, consistent with histopathological evidence of mucosal protection. In ulcer-induced mice, MgSO4 significantly decreased the expression of Epidermal Growth Factor (EGF), 70-kDa Heat Shock Protein (HSP-70), and Spasmolytic Polypeptide (SP) expression in the gastric tissue. In conclusion, magnesium may act as an anti-ulcerogenic and gastroprotective agent in mice.

Introduction: Traumatic brain injury (TBI) encompasses a wide range of brain lesions caused by a blow to or severe impact on the head. Traumatic brain injuries are divided into four categories based on their symptoms and consequences: mild, moderate, severe, and very severe. Studies in animal models have shown that TBI leads to neurodegeneration, progressive brain atrophy, and changes in cerebrospinal fluid (CSF) composition. The aim of this study was to investigate the effect of CSF isolated from TBI victims on neurodegeneration and the differentiation of neural progenitor cells (NPCs). Methods: To achieve this goal, the expression of genes involved in NPC differentiation and the induction of tauopathy in these cells were examined. First, an animal model of craniocerebral trauma was created in rats, and CSF was collected. The collected CSF was then added to the NPC culture medium to study its effect on cell behavior. The cells were divided into three groups: NPC, NPC + EGF/bFGF, and NPC + EGF/bFGF + CSF. After seven days, the expression of Nestin, Pax6, Map2, and Tubb3 genes was measured by real-time PCR, and TAU expression was evaluated by immunocytochemistry. Results: A significant decrease in Nestin and Pax6 expression (P = 0.0001 for both) was observed in the experimental group. Map2 and Tubb3 expression increased (P = 0.0001 and P = 0.0002, respectively), indicating NPC differentiation. In addition, immunocytochemistry revealed elevated TAU protein levels (P = 0.05), consistent with tauopathy induction. Conclusion: We conclude that CSF obtained from TBI rats promotes neuronal differentiation but simultaneously exerts neurotoxic effects through tauopathy induction.

BACKGROUND:Magnesium oxide nanoparticles (MgO-NPs) are currently utilized in antacid preparations, detoxifying agents, biomolecular detection, and diagnostics. These nanoparticles have been shown to attenuate apoptosis, inflammation, and oxidative stress. OBJECTIVE:This study aimed to assess the impact of MgO-NPs on varicocele-related testicular damage in adult Wistar rats. MATERIALS AND METHODS:Animals were randomly assigned to nine groups: normal control, sham-operated, three different doses of MgO-NPs alone (1.25, 2.5, and 5 mg/kg b.w./day, administered intragastrically), varicocele-induced control, and varicocele-induced rats treated with MgO-NPs. Thirty days post-treatment, blood and testicular tissue samples were collected for sperm profiling, biochemical assays, and histopathological evaluations. Sperm profiling included assessments of sperm abnormalities, total sperm count, motility, and viability. Biochemical analyses measured activities of catalase (CAT), glutathione peroxidase (GPX), superoxide dismutase (SOD), and malondialdehyde (MDA) levels. Histopathological evaluation was performed using hematoxylin-eosin (H&E) staining of testicular tissue and immunohistochemical analysis of aquaporin-9 (AQP9) expression. RESULTS:Administration of these NPs remarkably improved total sperm viability, count, and motility in varicocele-induced rats. Furthermore, treatment significantly elevated antioxidant status, reduced MDA levels, attenuated AQP9 immunoreactivity in testicular tissue, and restored architecture of testicular tissue. CONCLUSION:These findings suggest that MgO-NPs possess anti-infertility potential and may have clinical applications in the treatment of varicocele-related disorders.

This study aimed to determine the effects of exposure to sericin on serum GH, IGF-1 and antioxidant levels following parturition in mice. Forty pregnant female NMRI mice were allocated into four groups. In the control group, pregnant mice were given water as a placebo, whereas pregnant female mice in groups 2-4 were orally administered sericin (112.5, 225, and 450 mg/kg) on different days of gestation (5, 8, 11, 14, and 17). Following parturition, the open field test (OFT), forced swimming test (FST), tail suspension test (TST) and open field tests were used to evaluate depressive-like and antidepressant activity of sericin. At the end of the study, serum growth hormone (GH), insulin-like growth factor-1 (IGF-1), malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), and total antioxidant status (TAS) levels were determined. According to the results, sericin administration during pregnancy decreased immobility time in FST and TST, and increased the number of crosses in the OFT compared to the control group (P<0.05). Exposure to sericin significantly decreased serum MDA, while it increased SOD, GPx, and TAS levels compared with the control group (P<0.05). Also, sericin exposure during gestation significantly increased serum GH and IGF-1 levels compared to the control group (P<0.05). These results suggested pre-partum administration of sericin has antidepressant effect in postpartum mice.

Scopolamine-induced amnesia is associated with impairment of the cholinergic system and disruption of oxidative balance. Evidence supports the therapeutic potential of cilostazol (Cil), a phosphodiesterase-3 inhibitor, in individuals with mild cognitive impairment. An amnesic rat model was induced using scopolamine. To investigate the neuroprotective mechanisms of Cil, oral treatment with Cil and donepezil (DNP, positive control) was administered over three weeks. Behavioral assessments were conducted between days 14 and 21, followed by analysis of neurochemical alterations in hippocampal tissue. Scopolamine impaired learning and memory. Cil and DNP reduced escape latency and path length in scopolamine-exposed rats (P = 0.03-P < 0.001). Treated rats also spent more time in the target quadrant during the Morris water maze test (P = 0.03 and P < 0.001). In the passive avoidance test, both agents decreased dark compartment entries and duration, while increasing latency to enter and time in the light compartment (P = 0.04-P < 0.001). Cil and DNP also attenuated oxidative stress by reducing lipid peroxidation and enhancing antioxidant markers, including sulfhydryl groups and superoxide dismutase (SOD) activity (P = 0.04-P < 0.001). Scopolamine increased hippocampal acetylcholinesterase (AChE) activity and upregulated TNF-α and IL-1β mRNA expression. Both were suppressed following treatment with Cil and DNP (P = 0.02-P < 0.001). Additionally, Cil and DNP elevated hippocampal levels of sulfhydryl groups (P = 0.01-P < 0.001), SOD activity (P = 0.01-P < 0.001), and CHRM1 mRNA expression (P = 0.002 and P < 0.001). Collectively, these results support a potential role for Cil in mitigating scopolamine-induced cognitive impairment by restoring redox homeostasis, modulating AChE activity, and suppressing neuroinflammation.

Background: Diabetes mellitus (DM) frequently leads to male infertility, with oxidative stress being a primary culprit in damaging testicular function. This damage may extend to key spermatogenic genes, including the sperm-specific cation channels CatSper1 and CatSper2, which are essential for male fertility. Materials and Methods: This study investigated the therapeutic potential of eugenol against testicular dysfunction in a streptozotocin (STZ)-induced diabetic rat model, focusing on glycemic control, oxidative stress, histopathology, and the expression of CatSper1 and CatSper2 genes. In this experimental study, 32 male Wistar rats were divided into control, diabetic, diabetic+eugenol (4 mg/kg/d, IP), and eugenol-only groups. Diabetes was induced with a single STZ injection (55 mg/kg). After 8 weeks of treatment, fasting blood glucose, serum oxidative stress markers (malondialdehyde [MDA], superoxide dismutase [SOD], glutathione peroxidase [GPx]), testicular histology, and CatSper1/2 mRNA expression were analyzed. Results: Eugenol treatment significantly attenuated hyperglycemia in diabetic rats (P<0.05). It also mitigated diabetes-induced testicular damage, as shown by histopathological improvement. Biochemically, eugenol reversed oxidative stress by lowering elevated MDA (P<0.05) and restoring depleted SOD and GPx activities (P<0.05). Crucially, diabetes profoundly downregulated CatSper1 and CatSper2 gene expression (P<0.000), and eugenol treatment significantly restored their mRNA levels (P<0.001). Conclusion: Eugenol exerts a multifaceted protective effect against diabetic testicular damage by improving glycemic control, reducing oxidative stress, preserving testicular architecture, and restoring the expression of the critical spermatogenic genes: CatSper1 and CatSper2. These findings highlight eugenol’s promise as a therapeutic adjunct for managing diabetic male infertility.

Carvacrol is a common ingredient in the pharmaceutical, cosmetic, and perfume industries. It possesses various pharmaceutical properties including pain relief, anti-cell death, antioxidant, anti-cancer, and anti-inflammatory effects. We investigated the protective impact of carvacrol on infertility caused by varicocele in rats. The animals were assigned to nine groups randomly: control, sham-operated, carvacrol alone at 10, 20, and 40 mg/kg b.w./day, varicocele-induced control, and varicocele-induced rats treated with carvacrol. After thirty days of treatment, the serum was collected to evaluate testosterone levels, and left epididymal sperm samples were obtained to assess sperm quality. Additionally, the left testis was removed for biochemical and histopathological evaluation. The findings demonstrated that carvacrol administration (20 and 40 mg/kg) notably improved sperm quality in rats with varicocele. Furthermore, carvacrol treatment (20 and 40 mg/kg) increased antioxidant levels, reduced MDA levels, decreased AQP9 expression in testicular tissue, and improved testicular tissue structure. Hence, carvacrol (20 and 40 mg/kg) may serve as a therapeutic agent for male reproductive system disorders, particularly varicocele-related infertility, due to its antioxidant properties and protective effects on testicular function.

Objectives:Rosmarinic acid (RA) is a herbal compound with various antioxidant and anti-inflammatory effects. This study aimed to explore the anti-inflammatory and anti-apoptotic properties of RA in folic acid-induced renal injury. Materials and Methods:Thirty-six male C57/BL6 mice were randomly divided into six groups (N=6): Control (received normal saline), NaHCO3 (received NaHCO3 as folic acid solvent), FA (received folic acid (FA)(IP) to induce renal injury), RA (received 100 mg/kg RA), RA50-FA (received 50 mg/kg RA solution after folic acid injection), and RA100-FA (received 100 mg/kg RA after folic acid injection). For ten days, the treatment groups received RA by gavage. The effects of RA were assessed using H & E staining, biochemical tests, western blotting, and ELISA in the kidney tissues of the mice. Real-time RT-PCR was also performed to evaluate the expression changes of renal genes. Results:Our data showed that treatment by RA led to the over-expression of FoxO3 (P<0.05) and decrease in NFκB levels (P<0.01 and P<0.05) and expression of TNFα (P<0.05) and IL6 (P<0.001 and P<0.01). Other evaluations showed a decrease in p53 (P<0.01 and P<0.001), Bax/Bcl-2 ratio expression (P<0.01 and P<0.05), and Caspase-3 level (P<0.01 and P<0.05) compared to the folic acid group. Histological and biochemical results also confirmed the attenuation of tissue damage. Conclusion:This study revealed that RA's positive effects on folic acid-induced renal injury might result from the involvement of the FoxO3/NFκB pathway, thereby suppressing inflammation and apoptosis.

Objectives: Diabetes is a prevalent and chronic condition that has been found to have adverse effects on male fertility. Recent studies have explored the potential of eugenol in preventing diabetes-related complications. This research aimed to investigate whether eugenol has any protective effects against testicular tissue damage in diabetic rats induced by streptozotocin (STZ). Materials and Methods: In this experimental study, 32 male Wistar rats aged 8 weeks and weighing between 200-250 g were randomly divided into four groups: a control group, a diabetic group, a diabetic group treated with 4 mg/kg of eugenol, and a control group receiving the same dose of eugenol. Diabetes was induced in the appropriate groups using a 50 mg/kg intraperitoneal (IP) dose of STZ. The treatment lasted for eight weeks, after which testicular tissue samples were collected. Results: Histopathological analysis showed that eugenol treatment resulted in a notable decrease in testicular damage. The eugenoltreated group exhibited an elevation in the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) within the testicular tissue. The level of malondialdehyde (MDA) was significantly reduced in the eugenol-treated group. In terms of apoptosis, eugenol treatment led to decreased protein and mRNA expression of the pro-apoptotic protein BAX, a reduced BAX/BCL2 ratio, and decreased germ cell apoptosis (P < 0.01). Conversely, eugenol treatment increased the expression of the anti-apoptotic protein BCL2 at both the gene and protein levels. Conclusions: The administration of eugenol has the potential to mitigate testicular tissue damage in diabetic rats due to its antioxidant and anti-apoptotic properties.

Background: Diabetes mellitus (DM) is a metabolic disorder that can impair male reproductive function by inducing oxidative stress, testicular damage, and hormonal imbalance. Eugenol, a bioactive component of clove, has shown antioxidant and protective effects in various tissues. This study aimed to investigate the effects of eugenol on testicular histology, spermatogenesis, sperm parameters, and reproductive hormone levels in streptozotocin-induced diabetic rats. Materials and Methods: Thirty-two adult Wistar rats were randomly divided into 4 groups (each with 8 rats): Control, diabetic control, diabetic+eugenol (4 mg/kg/d via gavage for 8 weeks), and eugenol alone. Diabetes was induced with a single intraperitoneal injection of streptozotocin (55 mg/kg). Fasting blood glucose and serum insulin levels of the rats were monitored during the study. At the end of the study, testicular tissues were collected for histopathology and Johnsen scoring. Also, epididymal sperm were analyzed for count, morphology, and motility. Serum testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels were also measured by ELISA. Results: Diabetic rats exhibited significant hyperglycemia, reduced serum insulin, disrupted testicular architecture, decreased Johnsen scores, reduced seminiferous tubule diameter and epithelial thickness, impaired sperm parameters, and lower reproductive hormone levels (P<0.05). Eugenol treatment significantly ameliorated fasting blood glucose; improved insulin levels; restored testicular histology; increased Johnsen scores; and enhanced sperm count, motility, and morphology. Furthermore, serum testosterone, LH, and FSH levels were significantly elevated in the diabetic+eugenol group compared to diabetic controls (P<0.05), approaching levels observed in healthy controls. Conclusion: Eugenol effectively mitigates diabetes-induced testicular damage, improves spermatogenesis, and restores reproductive hormone levels in diabetic rats. These findings suggest that eugenol may have therapeutic potential for protecting male reproductive function under diabetic conditions.

Objective(s): Recent studies have increasingly focused on applying nanotechnology to treat neurodegenerative diseases. In this study, we compared the effects of the monoterpene linalool and linalool-loaded chitosan nanoparticles on key pathological features of Alzheimer’s disease (AD), including oxidative stress, neuroinflammation, neuronal death, amyloid plaque deposition, alterations in tryptophan metabolism, and memory deficit in a rat model of AD. Materials and Methods: An intracerebroventricular injection of Aβ42 (10 µg) was used to induce the AD model. Linalool (25 mg/kg) and nano-linalool (25 mg/kg) were administered orally once daily for 30 consecutive days. Results: Both linalool and nano-linalool significantly reduced malondialdehyde levels and enhanced superoxide dismutase activity in the hippocampus. They also decreased the mRNA levels of monocyte chemoattractant protein-1, inhibited the up-regulation of beta-secretase, reduced amyloid plaque deposition, and attenuated pyramidal neuron death in the CA1 region. Additionally, treatment with both compounds down-regulated indoleamine 2,3-dioxygenase, lowered kynurenine levels, and increased serotonin concentrations in the hippocampus. Although both treatments improved learning and spatial memory in Aβ-injected rats, nano-linalool’s effectiveness was more significant than that of linalool in modulating the molecular, biochemical, and histological parameters.Conclusion: Encapsulating linalool in chitosan nanoparticles enhances its effectiveness in improving molecular, biochemical, and histological changes in the hippocampus of rat models of AD.

Background: Liver disorders associated with type II diabetes result in cellular death, highlighting the importance of exploring protective mechanisms such as apoptosis to mitigate tissue damage. Antioxidant agents are promising options to address this issue, and plant secondary metabolites, such as the alkaloids of Peganum harmala, are considered among the most effective factors for treating liver disorders. Objectives: This study aimed to examine apoptosis, along with biochemical and histopathological parameters, in the liver of diabetic Wistar rats using methanolic extracts of P. harmala from seeds and leaves. Methods: Peganum harmala was collected from Zahedan. Phytochemical analysis of the leaf and seed extracts was conducted via high-performance liquid chromatography (HPLC) and DPPH tests. Sixty-four male Wistar rats (250 - 300 g) were organized into eight groups of eight individuals. Diabetes was induced by a 70 mg/kg streptozotocin (STZ) injection. The treatment groups were administered 150 mg/kg of leaf or seed extracts, or 6.5 mg/kg of harmine, a P. harmala alkaloid, daily for four weeks. Samples were then collected from anesthetized rats for biochemical, histopathological, and flow cytometry analyses. Results: The results indicated that methanolic extracts of P. harmala seed reduced plasma cholesterol and triglyceride levels in both healthy and diabetic groups. Biochemical tests also demonstrated that the seed extracts and harmine significantly reduced the plasma levels of liver enzymes. The leaf extracts and harmine significantly reduced apoptosis among diabetic groups, while seed extracts induced more apoptosis. The group treated with the seed extracts showed significant levels of healing and recovery in the liver tissue in histopathological evaluations. Conclusions: The significant antioxidant characteristics of the seed extract of P. harmala suggest its potential as a hypoglycemic medicine to moderate complications associated with diabetes.

ABSTRACT Selenium (Se) is an essential trace element with well‐documented health benefits, including antioxidative, anti‐inflammatory, antiapoptotic, and anticarcinogenic properties. Selenium nanoparticles (nano‐Se) represent an advanced Se delivery system characterized by superior bioavailability and a reduced risk of Se‐related toxicity. This study investigates the protective efficacy of nano‐Se against cadmium chloride (CdCl 2 )‐induced infertility in adult male Wistar rats. The experimental design involved random allocation of the rats into nine groups: a healthy control group, a vehicle control group, three groups receiving nano‐Se alone at 0.05, 0.1, and 0.2 mg/kg b.w./day, a group exposed to CdCl 2 to induce infertility, and three CdCl 2 ‐exposed groups treated with nano‐Se. After 30 days of treatment, the animals were euthanized for biochemical and histopathological assessments. The findings revealed that nano‐Se administration ameliorated the detrimental effects of treatment CdCl 2 on serum testosterone levels. Additionally, nano‐Se significantly reduced malondialdehyde levels and enhanced the activity of antioxidant enzymes in testicular homogenates. Histological analyses further demonstrated that nano‐Se preserved the structural integrity of testicular tissue in the CdCl 2 ‐induced fertility model. Nano‐Se modulated apoptotic pathways, as evidenced by the suppression of Bax expression and upregulation of Bcl 2 expression in testicular tissue. Furthermore, nano‐Se mitigated the overexpression of aquaporin‐9 in CdCl 2 ‐exposed rats. Collectively, these results provide robust biochemical, histological, and biochemical evidence supporting the potential therapeutic utility of nano‐Se in mitigating testicular dysfunction.

Background: Neural progenitor cells (NPCs) in specific regions of the adult brain hold promise for treating central nervous system (CNS) disorders and degenerative diseases, such as Parkinson's and Alzheimer's. Rosa damascena, enriched with flavonoids, offers restorative, inhibitory, and protective advantages against nerve damage. Objectives: This study investigates the neuroprotective effects of R. damascena essential oil (ESO) on NPCs exposed to ethanol (ETH)-induced toxicity. Methods: The study involved two phases: The NPCs were isolated from the brains of young Wistar rats and cultured following standard protocols. Differentiation into mature neural cells (NCs) was induced by withdrawing supportive factors. MTT assays were used to determine effective ETH and ESO doses, followed by assessments of their impact on NPCs and NCs. Gene expression analysis of neuroepithelial stem cell protein (Nestin), Sex determining region Y-box 2 (Sox2), and Paired Box 6 (Pax6) was conducted using real-time PCR during the NPC phase, while class III β-tubulin (Tuj1) and microtubule associated protein 2 (Map2) were evaluated during the NC stage. TAU protein expression was analyzed via immunocytochemistry (ICC). Results: The ETH exposure significantly reduced cell viability in a dose- and time-dependent manner (24, 48, 72 hours), while treatment with 200 µM ESO significantly improved survival in NPCs and NCs (P < 0.001). Additionally, ESO reduced TAU protein expression in NCs exposed to ETH. The NPCs treated with ETH + ESO showed increased expression of Nestin, Sox2, and Pax6 compared to the ETH-only group (P < 0.01). Similarly, Tuj1 and Map2 expression levels were significantly higher in the ETH + ESO group compared to ETH-treated NCs (P < 0.01). Conclusions: The ESO demonstrates significant neuroprotective properties, mitigating ETH-induced toxicity in NPCs and NCs. These findings highlight its potential as a therapeutic agent for reducing neurodegenerative damage and supporting nervous system function.

Today, with the prevalence of metabolic diseases such as diabetes, which can be caused by insulin resistance, the need for targeted drug delivery seems essential. Using Nano crystals that contain antioxidant materials such as Umbelliprenin and are surface modified may be a solution to this problem. This study aims to investigate the IR/PDK1 pathway in the presence of cellulose nano-crystal surface-modified with cetyltrimethylammonium bromide containing Umbelliprenin (UCC-NCs delivery system). The UCC-NCs delivery system was synthesized and characterized by FTIR and zeta-potential methods. Forty-two Wistar male rats (aged 12 weeks, 250-300 g) were divided into seven groups of six. After induction of diabetes with a single dose of intraperitoneal injection of STZ (60 mg.kg- 1), the treatment groups were treated orally with doses of 5 and 10 mg.kg- 1UM and Nano crystals. After the treatment period, the rats were anesthetized, and blood was taken from the rats' retro-orbital plexus area, and their serum glucose, total cholesterol (TC), triglyceride, and HDL levels were measured. RNA was extracted from the tissue samples, and cDNA was synthesized, and the expression of IR and PDK1 genes was examined by real-time. Pathological changes were evaluated in the prepared sections. The results showed that Nano crystals were much better and more effective than UM in improving glucose and blood factors. Gene expression analysis showed a significant increase in the expression of IR and PDK1 genes in the groups receiving Nano crystals compared to UM. Therefore, nano crystals were probably able to prevent hyperglycemia by activating the IR/PDK1 pathway through anti-inflammatory and antioxidant properties. It is suggested that this drug delivery system be further tested for metabolic diseases such as diabetes.

BACKGROUND:Molybdenum, as a trace element, exhibits various pharmacological properties, including antioxidant, anti-inflammatory, and free radical-scavenging activities. This study aimed to evaluate the effects of sodium molybdate on neurotoxicity induced by beta-amyloid (Aβ) in adult male Wistar rats. METHODS:Forty-eight rats were randomly divided into eight groups: Healthy control group, Experimental groups receiving sodium molybdate (0.1, 0.2, and 0.4 mg/kg intragastrically daily), Alzheimer's control group (intrahippocampal injection of Aβ bilaterally), and Alzheimer's experimental groups receiving sodium molybdate (0.1, 0.2, and 0.4 mg/kg intragastrically daily) for 30 consecutive days following Aβ injection. Histopathological changes in the hippocampus were assessed using Hematoxylin and Eosin staining, and amyloid plaques were evaluated via Congo Red staining. The expression levels of GFAP and S100 proteins were investigated by immunohistochemistry, and changes in the expression level of Bax/Bcl2 ratio were evaluated by Real-time PCR in the hippocampus. FINDINGS:Our results revealed a dose-dependent attenuation of neuronal degeneration, and reduced amyloid plaque formation in the Alzheimer's experimental groups following sodium molybdate administration. Treatment with sodium molybdate at doses of 0.2 and 0.4 mg/kg significantly reduced the levels of both S100 and GFAP proteins (P < 0.05 and P < 0.001 respectively) compared to the Alzheimer's control group. Furthermore, sodium molybdate administration at a dose of 0.1 mg/kg significantly reduced the Bax/Bcl2 expression ratio (P < 0.05), with greater reductions observed at 0.2 and 0.4 mg/kg doses (P < 0.01). CONCLUSION:The results of this study suggest that sodium molybdate may exert protective effects against neurological disorders caused by Aβ in a rat model of Alzheimer's disease.

This study investigated the effect of sericin consumption during gestation on the neurodevelopmental reflexes, motor behaviour and biochemical profiles of mice offspring. Forty pregnant NMRI mice were randomly assigned into four groups: a control group and three experimental groups that received sericin (112.5, 225 and 450 mg/kg) via oral administration on Days 5, 8, 11, 14 and 17 of gestation. Then, neurodevelopmental reflex tests included ambulation, hindlimb foot angle, hindlimb suspension, surface righting, front-limb suspension, grip strength and negative geotaxis were assessed. Additionally, blood samples were collected to evaluate biochemical parameters, including serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant capacity (TAC), growth hormone (GH) and insulin-like growth factor (IGF) levels. The findings revealed that prenatal sericin exposure improved ambulation scores, reduced hindlimb foot angle and increased hindlimb suspension scores (p < 0.05). Sericin administration led to an increase in grip strength and front-limb suspension scores (p < 0.05). Furthermore, sericin administration decreased serum and brain MDA levels while increasing serum and brain SOD, GPx and TAC levels (p < 0.05). Sericin exposure also increased serum GH and IGF levels (p < 0.05). The results indicated that maternal sericin consumption during gestation had a positive impact on offspring's motor skills and antioxidant status.

Cerebral ischemia is one reason for death and loss of movement ability of people, which imposes a large and significant cost on the global health system. Niosomes, as useful tools, can increase drug delivery to the brain. The purpose of this research is to investigate the effect of niosomes containing saponin (NS) on strokeinduced damage in the hippocampus of an animal model. The physicochemical characteristics of nanocarriers, such as zeta potential, size, and release test were investigated after the fabrication of thin film method. In this study, Wistar rats were divided into five experimental groups including sham group, stroke group, stroke group with empty niosome injection, stroke group with saponin injection, and stroke group with niosome saponin injection. The study examined various aspects of ischemia including stroke volume, blood-brain barrier (BBB) damage, neurological defects, levels of inflammatory cytokines, and cellular damage in the hippocampus. The findings indicate that NS, with a size of 85.92nm, zeta potential of -34.7 mv, and an entrapment efficiency (EE%) of 85.70% effectively reduced stroke volume, cerebral edema, BBB damage, expression level of TNF-alpha, and NF-kB genes and inflammation in hippocampal cells. Additionally, NS improved sensory and motor performance in rats. These results demonstrate that NS can mitigate stroke-induced damage in the hippocampus of the rat model by effectively crossing the BBB.

Berberine which is the major active component of Berberis vulgaris, has been widely used in traditional medicine and has an antioxidant activity against oxidative stress. Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in reproductive-aged women. PCOS is often associated with a metabolic syndrome. In the present study, the effect of berberine on letrozole-induced PCOS was investigated in adult female Wistar rats. The rats were randomly divided into 8 groups: normal control, berberine (25, 50 and 100 mg/kg intragastrically, daily) alone, PCOS control rats (letrozole, 1 mg/kg, intragastrically, daily), berberine (25, 50 and 100 mg/kg intragastrically, daily) together with (letrozole 1 mg/kg, intragastrically, daily), and treatment was performed accordingly. Administration of berberine was started 30 minutes before the first dose of letrozole and continued up to 28 days. The animals were euthanized 24 hours after the last dose of the treatment. Antioxidant activity was tested by measuring the activity of superoxide dismutase, catalase and glutathione peroxidase enzymes as well as the amount of malondialdehyde in ovarian tissue homogenates. The findings of the present study showed that berberine increases antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase and decreases malondialdehyde levels. The results of this study suggest that berberine treatment may be beneficial in letrozole-induced PCOS in rats.

Polycystic ovary syndrome (PCOS) is a disease associated with inflammation and the follicular fluid of this patient contains proinflammatory cytokines. Abdominal obesity (AO) is also linked to increased levels of proinflammatory cytokines. This study investigated the induction of inflammation and decidualization of in vitro cultured endometrial stromal cells (ESCs) obtained from women with a normal uterus using the follicular fluid of PCOS and non-PCOS patients with or without abdominal obesity. Forty patients under 35 years old, referred to the Royan Institute, were divided into four groups: PCOS with AO, PCOS without AO, non-PCOS with AO, and non-PCOS without AO. Follicular fluid samples were added to the culture medium of ESCs for each group. The rate of decidualization was measured by examining decidual markers. The study also investigated morphological changes in uterine endometrial cells, cell migration rates, and gene expression across all groups. We found that the non-PCOS group without AO had the highest decidualization potential and the highest expression of decidualization markers (P ≤ 0.05). Groups with an inflammatory phenotype of PCOS or abdominal obesity showed the highest expression of decidual pathway markers. The expression levels of inflammatory and proliferative markers in the PCOS group with AO were significantly higher than in the other groups (P ≤ 0.05). The inflammatory profile present in the follicular fluid may trigger the decidualization process. Consequently, in the future, follicular fluid could be utilized as a natural supplement with human cells to promote decidualization and enhance endometrial receptivity in assisted reproductive technology.