Parisa Hasanein

This study aimed to evaluate the effects of ethanolic extract of dried Moringa oleifera leaves (MO) administered intragastrically at different doses for 30 days on diabetes-induced amnesia and hyperalgesia in rats, as well as to investigate the possible underlying mechanisms. Rats received MO extract (100, 200, and 400 mg/kg) or vehicle starting at the onset of hyperglycemia and continuing for 30 days. Passive avoidance learning (PAL) and memory tasks were used to assess memory, while formalin test was applied to analyze chemical hyperalgesia. Diabetes led to impairments in both phases of the PAL and memory test. MO (200 and 400 mg/kg) protected diabetic rats from learning and memory impairment and enhanced cognition of control animals. In the formalin test, MO at 200 and 400 ng/kg reversed chemical hyperalgesia of diabetic rats, while showing analgesic effects in healthy rats. The most significant hypoglycemic and antioxidant effects were shown with MO 400 mg/kg in diabetic animals. MO (200 and 400mg/kg) enhanced cognitive function and induced analgesia in diabetic rats, possibly by hypoglycemic and antioxidant mechanisms. Therefore, it may be a promising source for management of diabetic neurological complications that deserves notice and further studies.

Infertility affects around 15% of couples worldwide, with male factors being responsible for nearly half of these cases. Oxidative stress is a significant contributor to male infertility, leading to damaged sperm. This research examines the protective effects of Nacetylcysteine (NAC) on sperm exposed to hydrogen peroxide (H₂O₂) induced oxidative stress in rats. Sperm samples from adult male Wistar rats were divided into four groups: control, H₂O₂, NAC, and H₂O₂+NAC. Various parameters, including sperm viability, abnormal morphology, chromatin condensation, and plasma membrane integrity were evaluated after incubation using established assays. Exposure to H₂O₂ significantly decreased sperm viability, increased the rate of abnormal morphology, heightened chromatin condensation abnormalities, and compromised plasma membrane integrity. Treatment with NAC significantly ameliorated these effects, demonstrating its protective role against oxidative damage. NAC effectively counteracts oxidative damage in sperm, improving viability, morphology, chromatin integrity, and membrane integrity. These findings demonstrate the protective effects of NAC against oxidative stress-induced sperm damage under in vitro conditions, underscoring its potential as a subject for further investigation in the context of oxidative stress-related male infertility.

Background: DNA glycation, a process where Glc non-enzymatically binds to DNA, is implicated in various detrimental effects, including strand breaks, mutations, and altered gene expression. This damage is considered a significant contributor to the pathogenesis of diabetes mellitus and its associated complications. Consequently, there has been increasing interest in identifying antiglycation agents ...

Oxidative stress is part of the mechanisms involved in ethanol toxicity. We investigated effects of vitamins C (VC), E (VE) and the combination of VC+VE on chronic ethanol-induced toxicity in rat erythrocytes. The following groups were treated for 30 days: control (C), VC (200 mg/kg), VE (200 mg/kg), VC (200 mg/kg) + VE (200 mg/kg), ethanol 4 g/kg, ethanol + VC, ethanol + VE and ethanol + VC + VE. The doses of vitamins and ethanol were selected for per kilogram of animal’s body weight. Blood samples collected at the end of treatments were analyzed for erythrocyte osmotic fragility and plasma scavenging activity. The washed erythrocytes were used to determine superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and malondialdeyde (MDA). Ethanol induced erythrocyte fragility (p < 0.001) and increased lipid peroxidation (p < 0.001) in rat erythrocytes. Furthermore, there were significant decreases in plasma scavenging (p < 0.001), SOD (p < 0.001), CAT (p < 0.01) and GPx (p < 0.001) activities in erythrocytes of ethanol-treated animals. Although VC or VE alone restored all of ethanol-induced disturbances to near normal (p > 0.05) but there were still significant differences compared to control animals. Combination therapy completely corrected ethanol-induced erythrocyte fragility, lipid peroxidation and prooxidant/antioxidant imbalance. We showed the beneficial effects of VC and VE combination in decreasing erythrocyte fragility and lipid peroxidation in both ethanol and control groups. Therefore this combination treatment may provide a new potential alternative for prevention of ethanol toxicity which deserves consideration and further examination.

Anxiety and stress are considered as universal psychiatric exhibitions of the present societies and lifestyles. Several experiments have been conducted to examine natural anxiolytic agents to find out an alternative to synthetic anxiolytic drugs. The present study investigated the anxiolytic effects of cinnamaldehyde (Cin) on mice behavior in the elevated plus maze (EPM) and open field (OF) tests. Sixty male Swiss mice, weighing 20–30 g, were divided into six groups including: acute stress + mazola oil; chronic stress + oil; acute stress + Cin (20 mg/kg); chronic stress + Cin; non-stress + oil; and non-stress + Cin groups. The groups were administered for seven days (once a day). The acute stress + Cin group showed a meaningful rise in the percentage of entries into the open arms compared to the acute stress + oil group (p <.05). The percentage of time spent in the open arms in the chronic stress + Cin group was significantly higher compared to the chronic stress + oil group (p < .01). The percentage of entries into the open arms increased significantly (p < .01) in the chronic stress + Cin group in comparison with the chronic stress + oil group. The Cin treated groups showed significant increases in the time spent in the center area and in the number of entries into the center area compared with the oil treated groups in OF test. The number of entries into the arms (total activity), as well as locomotor activity was not significant among groups. The results of the present study indicated that Cin, as a natural product, might have anxiolytic effects in mice behavior in the EPM and OF tests.

The kidney is one of the main organs affected by nickel toxicity. We investigated the protective effects of carnosine on nickel-induced oxidative stress in kidney of rats. Animals received NiSO₄ (20 mg·kg⁻¹·day⁻¹ intragastrically) and (or) carnosine (10 mg·kg⁻¹·day⁻¹ intragastrically) for 21 days and then were evaluated for biochemical, molecular, and histopathological alterations. Nickel caused an increase in renal levels of malondialdehyde and a decrease in reduced glutathione, catalase, and superoxide dismutase levels and total antioxidant capacity. Carnosine prevented the prooxidant and antioxidant imbalance induced by nickel. Nickel-treated rats showed an increase in serum creatinine, urea, and uric acid with a concomitant decrease in albumin. Nickel markedly accumulated in kidney of exposed rats, but its concentration was effectively reduced by carnosine treatment. Carnosine corrected the biochemical abnormalities and the elevated renal TNF-α and IL-6 levels in the nickel-treated group. It also attenuated nickel-induced abnormalities in renal architecture. Although carnosine showed antioxidant and anti-inflammatory effects in renal tissue of nickel-exposed rats, we cannot clearly attribute the protective effect of carnosine to these effects. Instead, the beneficial effect of carnosine observed in the current study may be due to chelation between nickel and carnosine. Thus, carnosine may represent a therapeutic option to protect against nickel-induced nephrotoxicity that deserves further consideration and examination.

Lead affects multiple organ systems including testis. We investigated the effects of ferulic acid (FA) on lead-induced oxidative stress and spermatogenesis suppression in rats. Animals received lead acetate (500 mg/L in drinking water) and/or FA (50 mg/kg, i.g.) for eight weeks. Lead increased testicular malondialdehyde (MDA) and nitrite levels and decreased glutathione (GSH) content and catalase (CAT) activity. Lead decreased testis weight and testosterone level. Sperm parameters decreased in lead group. FA ameliorated the decreased testis weight, serum testosterone as well as sperm count, viability, motility and normal morphology in lead group. FA improved antioxidant capacity as well as sperm count, viability, motility and normal morphology. FA decreased Johnsen's mean testicular biopsy score (MTBS) criteria by restoring degeneration, atrophy and tubular disarrangement. FA also normalised spermatogonia, spermatocytes and spermatids numbers in lead group and led to increases in number of Leydig and Sertoli cells. FA showed beneficial effects in lead-induced testicular oxidative stress and spermatological disorders, through inhibiting lipid peroxidation and enhancing antioxidant defence systems. The positive effects of FA on Leydig cells may be involved in restoring testosterone levels in lead group. FA can be considered a potential candidate to protect testis against the deleterious effect of lead intoxication.

Context: Drug-induced liver injury is a significant worldwide clinical problem. Rosmarinic acid (RA), a natural phenol, has antioxidant effects. Objective: The effects of RA against acetaminophen (N-acetyl-p-amino-phenol (APAP))-induced oxidative damage and hepatotoxicity in rats were investigated. Materials and methods: Male Wistar rats were pretreated with RA (10, 50 and 100 mg/kg, i.g.) for one week. On day 7, rats received APAP (500 mg/kg, i.p.). Then aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin, total protein, malondialdehyde (MDA), glutathione (GSH), total antioxidant capacity (TAC), glutathione S-transferase (GST), cytochrome CYP450 and histopathological changes were determined. Results: APAP-induced oxidative stress in liver by a significant increase in the level of MDA (7.6 ± 0.21 nmol/mg) as well as a decrease in the contents of TAC (1.75 ± 0.14 μmol/g), GSH (1.9 ± 0.22 μmol/g) and GST) 3.2 ± 0.28 U/mg). RA treatment decreased MDA (4.32 ± 0.35 nmol/mg) but increased the contents of TAC (3.51 ± 0.34 μmol/g), GSH (3.42 ± 0.16 μmol/g) and GST (5.71 ± 0.71 μmol/g) in APAP group. RA 100 mg/kg decreased ALT (91.5 ± 1.5 U/L), AST (169 ± 8.8 U/L) and CYP450 (3 ± 0.2 nmol/min/mg) in APAP group. Histologically RA attenuated hepatic damage by decreasing necrosis, inflammation, and haemorrhage in liver sections of APAP group. Discussion and conclusions: This is the first report that oral administration of RA dose-dependently elicited significant hepatoprotective effects in rats through inhibition of hepatic CYP2E1 activity and lipid peroxidation. RA-protected hepatic GSH and GST reserves and total tissue antioxidant capacity.

Objectives: Ethanol consumption induces neurological disorders including cognitive dysfunction. Oxidative damage is considered a likely cause of cognitive deficits. We aimed to investigate the effects of rosmarinic acid (RA) in different doses for 30 days on chronic ethanol-induced cognitive dysfunction using the passive avoidance learning (PAL) and memory task in comparison with donepezil, a reference drug. We also evaluated the levels of superoxide dismutase (SOD), catalase (CAT), and lipid peroxidation in hippocampus as possible mechanisms. Methods: Memory impairment was induced by 15% w/v ethanol (2 g/kg, i.g.) administration for 30 days. RA (8, 16, and 32 mg/kg, i.g.) or donepezil (2 mg/kg, i.g.) was administered 30 minutes before ethanol. The acquisition trial was done 1 hour after the last administration of RA and donepezil. At the end, animals were weighed and hippocami were isolated for analyzing of oxidant/antioxidant markers. Results: Ethanol caused cognition deficits in the PAL and memory task. While RA 16 and 32 mg/kg improved cognition in control rats, it prevented learning and memory deficits of alcoholic groups. RA 8 mg/kg did not influence cognitive function in both control and alcoholic rats. RA 32 mg/kg had comparable effects with donepezil in prevention of acquisition and retention memory impairment. The higher doses of RA not only prevented increased lipid peroxidation and nitrite content but also decreased SOD, CAT, GSH, and FRAP levels in alcoholic groups and exerted antioxidant effects in non-alcoholic rats. Discussion: We showed that RA administration dose-dependently prevented cognitive impairment induced by chronic ethanol in PAL and memory and disturbed oxidant/antioxidant status as a possible mechanism. The antioxidant, anticholinesterase, and neuroprotective properties of RA may be involved in the observed effects. Therefore, RA represents a potential therapeutic option against chronic ethanol-induced amnesia which deserves consideration and further examination.