Bee venom ameliorates oxidative stress and histopathological changes of hippocampus, liver and testis during status epileptics.

The unrelenting progression of neurodegenerative diseases has a negative impact on affected individuals, their families, and society. Recurrent epileptic seizures are the hallmark of epilepsy, and treating it effectively remains difficult. Clarify and understanding effects of the antiepileptic drugs (AEDs) in epilepsy by comparing the therapeutic effects between rats receiving valproic acid (VPA) and Bee venom (BV) was aimed throughout the present study. Four male Wistar rat groups were included: control, epileptic group receiving pilocarpine (PILO), epileptic group treated with VPA and BV respectively. Cognitive functions were assessed by evaluating latency time in hot plate, despair swim test, grooming, rearing and ambulation frequency in the open field. BV has ameliorative effect on electrolytes balancing, assured by decreasing lipid peroxidation, nitric oxide and increasing catalase, superoxide dismutase and glutathione peroxidase activities. BV enhanced restoration of liver functions indicated by alanine transaminase (ALT) and aspartate transaminase (AST), total proteins, and albumin; hormonal parameters total and free testosterone, follicle stimulating hormone (FSH) and Luteinizing hormone (LH) were preserved by BV with great recovery of hippocampus, liver and testicular histopathology and ultrastructure comparing with the epileptic rats. The present findings suggested that BV and its active components offer fresh options for controlling epilepsy and prospective methods via minimize or manage the severe consequences.

Isatin Counteracts Diethylnitrosamine/2-Acetylaminofluorene-Induced Hepatocarcinogenesis in Male Wistar Rats by Upregulating Anti-Inflammatory, Antioxidant, and Detoxification Pathways.

Hepatocellular carcinoma (HCC) represents around 85% of all known types of liver cancers and is estimated to be the fifth most common cause of cancer-related death worldwide. The current study assessed the preventive efficacy of isatin on diethylnitrosamine (DENA)/2-acetylaminofluorene (2-AAF)-induced hepatocarcinogenesis in male Wistar rats and investigated the underlying cellular and molecular mechanisms. HCC was initiated by intraperitoneal injection of DENA (150 mg/kg/week) for two weeks, followed by oral 2-AAF (20 mg/kg) every other day for three successive weeks. Oral isatin or vehicle (control) was administered at 25 mg/kg for 20 weeks during and following HCC induction. Isatin ameliorated the deleterious effects of DENA/2-AAF on liver function as evidenced by reduced serum levels of AST, ALT, total bilirubin, albumin, and liver tumor biomarkers (CA19.9 and AFP) compared to control DENA/2-AAF-treated rats. Histopathological evaluations demonstrated that isatin-mediated protection against hepatocarcinogenesis was accompanied by a decline in hepatic lipid peroxidation, a marker of oxidative stress, and enhanced antioxidant capacity, as evidenced by increased glutathione and superoxide dismutase expression. Isatin treatment also upregulated expression of the major stress-response transcription factor Nrf2 and the detoxifying enzymes NAD(P)H quinine oxidoreductase and glutathione-S-transferase alpha 2 and downregulated expression of the proliferation marker Ki67. Moreover, isatin significantly reduced the DENA/2-AAF-induced decrease in hepatic expression of anti-apoptotic Bcl2 and the DENA/2-AAF-induced increases in pro-inflammatory and pro-apoptotic factors (TNF-α, NF-κB p50, NF-κB p65, p53, and caspase 3). Thus, it can be concluded that isatin may protect against chemically induced hepatocarcinogenesis by enhancing cellular antioxidant, anti-inflammatory, and detoxification mechanisms, in part through upregulation of the Nrf2 signaling pathway.