Naringin Prevents Diabetic-Induced Dysmetabolism in Male Wistar Rats by Modulating GSK-3 Activities and Oxidative Stress-Dependent Pathways.

Type 2 diabetes mellitus (T2DM), characterized by insulin resistance and glucose dysmetabolism, is a major metabolic disorder accompanied with health and financial burden. Recently, research findings showed that orange peel extract (OPE) has health benefits such as improved insulin sensitivity and glucose metabolism. The present study aimed at establishing the role of naringin from OPE on T2DM-induced glucose and lipid dysmetabolism. Thirty male (30) Wistar rats were randomized into five groups: control, diabetes, diabetes + naringin, diabetes + orange peel, and diabetes + metformin. Oral administration was once per day for 28 days. After 28 days of treatment, naringin ameliorated the diabetes-induced increase in blood sugar, homeostatic model assessment (HOMA) IR, triglyceride, total cholesterol, triglyceride/high density lipoprotein, total cholesterol/high density lipoprotein, triglyceride glucose index, glucose synthase kinase-3, lactate, lactate dehydrogenase, malondialdehyde, c-reactive protein, and tumor necrosis factor α compared with the diabetic untreated animals. Furthermore, naringin reversed diabetes-induced decrease in serum insulin, HOMA B, HOMA S, quantitative insulin-sensitivity check index, high-density lipoprotein, total antioxidant capacity, superoxide dismutase, catalase, glucose transporter-4, and hepatic glycogen. This study showed that naringin prevented diabetes-induced dysglycemia and dyslipidemia via glucose synthase kinase-3 and oxidative stress-dependent pathways.

Naringin from sweet orange peel improves testicular function in high fat diet-induced diabetic rats by modulating xanthine oxidase/uric acid signaling and maintaining redox balance.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a metabolic disorder affecting many organs, including the testis. Naringin from orange peel extract (OPE) is a flavanone with fertility-enhancing properties. Hence, this study was designed to establish the effect of naringin on T2DM-induced testicular dysfunction. Thirty male (30) Wistar rats were randomized into five groups control, diabetes, diabetes + naringin, diabetes + OPE, and diabetes + metformin. The administrations were via the oral route and lasted for 28 days. RESULTS: Naringin ameliorated T2DM-induced increase in FBS and decrease in serum insulin. It also abrogated T2DM-induced decrease in sperm quality, gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone, testosterone, estradiol, prolactin, catalase, superoxide dismutase, and total antioxidant capacity. Furthermore, naringin prevented a T2DM-induced increase in malonaldehyde, tumor necrosis factor-alpha, C-reactive protein, xanthine oxidase (XO), and uric acid (UA), it was accompanied by the restoration of normal testicular histoarchitecture. CONCLUSIONS: Naringin prevented T2DM-induced testicular dysfunction by modulating XO/UA and restoring redox balance. Also, while the animals treated with OPE exhibited better ameliorative effects than their counterparts treated with naringin, the findings from this study showed that naringin would be a promising supplement for treating T2DM-induced male infertility.

Hepatoprotective potential of Tamarindus indica following prenatal aluminum exposure in Wistar rat pups.

Over time, the use of plant-derived agents in the management of various human health conditions has gained a lot of attention. The study assessed the hepatoprotective potential of ethyl acetate fraction Tamarindus indica leaves (EFTI) during prenatal aluminum chloride exposure. Pregnant rats were divided into 5 groups (n = 4); Group I rats were administered 2 ml kg-1 of distilled water (negative control), Group II rats received only 200 mg kg-1 aluminum chloride (positive control), Group III rats were administered 200 mg kg-1 aluminum chloride and 400 mg kg-1 EFTI, Group IV rats were administered 200 mg kg-1 aluminum chloride and 800 mg kg-1 EFTI, Group V rats were administered 200 mg kg-1 aluminum chloride and 300 mg kg-1 Vit E (comparative control). On postnatal day 1, the pups were euthanized, and liver tissues were harvested for the biochemical study (tissue levels of malondialdehyde, caspase-3, tumor necrosis factor-alpha, aspartate aminotransferase, alkaline phosphatase, and alanine aminotransferases) and the liver histological examination. The administration of EFTI was marked with significant improvement in the tissue levels of malondialdehyde, caspase-3, tumor necrosis factor-alpha, aspartate aminotransferase, alkaline phosphatase, and alanine aminotransferases. There was a marked improvement in histopathological changes associated with prenatal aluminum chloride exposure. In conclusion, the administration of EFTI was protective during prenatal aluminum chloride exposure of the liver in Wistar rats, and is mediated by the anti-lipid peroxidative, antiapoptotic, and anti-inflammatory activity of EFTI.

D-ribose-L-cysteine exhibits neuroprotective activity through inhibition of oxido-behavioral dysfunctions and modulated activities of neurotransmitters in the cerebellum of Juvenile mice exposed to ethanol.

Alcohol exposure to the cerebellum has been known to trigger cerebellar dysfunctions through several mechanisms. This present study was designed to evaluate the repealing effect of D-ribose-L-cysteine (DRLC) on alcohol-induced cerebellar dysfunctions in juvenile BALB/c mice. The animals were randomly divided into 4 groups (n = 10 per group). Mice were given oral administration of normal saline (control), DRLC (100 mg/kg, p.o), ethanol (0.2 mL of 10% w/v), or DRLC (100 mg/kg, p.o) + ethanol (0.2 mL of 10% w/v). On day 29 of the study (i.e., 24 h after the administration of the last respective doses), neurochemical quantification of the respective levels of serotonin and dopamine, lipid peroxidation, total antioxidant, superoxide dismutase, and glutathione peroxidase in the cerebellar tissues of the mice were analyzed. Compared with the saline-treated group, the studied neurochemical indices were modulated across the various experimental groups. The administration of ethanol significantly modulates the levels of monoamine neurotransmitters (serotonin and dopamine) as well as contents of total antioxidants, activities of superoxide dismutase, and glutathione peroxidase, with a concurrently increased level of lipid peroxidase in the cerebellar tissue of the mice. DRLC significantly reverses these effects in the DRLC + ethanol co-treated group. Combined exposure to DRLC + ethanol counteracts the deleterious effect of ethanol in the cerebellum of juvenile BALB/c mice via monoamine neurotransmitter, lipid peroxidation, total antioxidant status, superoxide dismutase, and glutathione peroxidase action pathways. Therefore, DRLC could be a pharmacologic or therapeutic agent in attenuating the deleterious effects of alcohol on the cerebellum.

Neurobehavioral and Immunohistochemical Studies of the Cerebral Cortex Following Treatment with Ethyl Acetate Leaf Fraction of Tamarindus indica During Prenatal Aluminum Chloride Exposure in Wistar Rats.

Purpose: The recent increase in aluminum exposure and its effect on the development of the brain call for serious attention. The study investigated the behavioral and immunohistochemical changes in the cerebral cortex of Wistar rats following prenatal co-administration of ethyl acetate leaf fraction of Tamarindus indica (EATI) and aluminum chloride (AlCl3). Methods: Pregnant Wistar rats were divided into 5 groups (n=4). Group I (negative control), Group II-V were experimental groups treated with 200 mg/kg of AlCl3 s/c. Group III and IV received an additional 400 mg/kg and 800 mg/kg of EATI respectively, while Group V received an additional 300 mg/kg of Vitamin E for 14 days (prenatal days 7-21) via the oral route. The pups were then exposed to cliff avoidance, negative geotaxis, and elevated plus maze (EPM) test on the post-natal day (PoND) 4-6, 7-10, and 18 respectively. On PoND 21 pups were sacrificed, and the skull dissected to remove the brain. The harvested brain tissues were processed for Cresyl fast (CF) and glial fibrillary acid protein (GFAP). Results: The study showed that EATI administration during AlCl3 exposure was associated with significant improvement in sensory-motor development. The EPM, CF, and GFAP results revealed significant improvement in anxiety-like behavior, motor activities, GFAP expression, pyramidal cell count, and Nissl staining following prenatal EATI administration during AlCl3 exposure. Conclusion: The present study concludes that EATI was associated with some protective potential during prenatal AlCl3 exposure in Wistar rats.