Up-regulation of oxidative stress and inflammation in the brain of albino wistar rats following sub-acute administration of Synclisia scabrida root extract

Objective: Synclisia scabrida is a medicinal plant used over the years for the treatment ofseveral medical conditions yet there is paucity of information on its systemic and organspecific toxicity. Consequently, sub-acute neurotoxicity of root extract of Synclisia scabridawas evaluated in albino Wistar rats. Methods: Thirty male albino rats with average weightof 140g were randomized into 5 groups consisting of 6 rats in each group. Group 1 was thecontrol while 50 mg/kg, 100 mg/kg, 200 mg/kg and 400 mg/kg of the root extract wereadministered to Groups 2, 3, 4 and 5 respectively for 28 days. Malondialdehyde,glutathione, nitric oxide, protein, tumour necrosis factor-α, acetylcholine, catalase andacetylcholinesterase levels were measured in brain homogenates. Body weight of theanimals and histology of the hippocampus and cerebral cortex were evaluated. Results:Root extract of Synclisia scabrida was observed to increase malondialdehyde concentrationand decrease antioxidants biomarkers when compared with the control. Significantly(p<0.05) increased TNF-α concentration and acetylcholinesterase activity caused by theextract when compared with the control was observed. The concentration of acetylcholinesignificantly decreased in Synclisia scabrida treated groups in comparison with the control.The histomorphology of the hippocampus and cerebral cortex revealed pyknotic pyramidalneurons in Synclisia scabrida treated rat relative to the control with normal pyramidalneurons. The body weight of the extract treated groups were significantly decreased whencompared to the control Group. Conclusion: The study has demonstrated that the rootextract of Synclisia scabrida induces and up-regulates oxidative stress and inflammation inthe brain of male albino Wistar rat coupled with reduced acetylcholine concentration hencethe extract possesses neurotoxic potentials.

Pleiotropic attenuating effect of Ginkgo biloba against isoprenalineinduced myocardial infarction via improving Bcl-2/mTOR/ERK1/2/Na^(+) , K^(+) -ATPase activities

Objective:Myocardial infarction(MI)is linked to an imbalance in the supply and demand of blood oxygen in the heart muscles.Beta-blockers and calcium antagonists are just two of the common medications used to treat MI.However,these have reportedly been shown to be either ineffective or to have undesirable side effects.Extract of Ginkgo biloba leaves(GBE),a Chinese herbal product offers special compatibility benefits in therapeutic settings relating to inflammatory diseases and oxidative stress.In order to better understand how GBE affects MI in rats insulted by isoprenaline(ISO),the current study was designed.Methods:The heart weight index,serum lipid profile,cardiac marker enzymes,endogenous antioxidants[catalase(CAT),superoxide dismutase(SOD),glutathione(GSH),nitrites and malondialdehyde(MDA)],inflammatory mediators[tumour necrosis factor alpha(TNF-a)and interleukin-6(IL-6)],immunohistochemical expressions of B-cell lymphoma factor-2(Bcl-2),extracellular signal-regulated kinase(ERK1/2),and mammalian target of rapamycin(mTOR)and histopathological analysis were used to assess the cardioprotective properties of GBE.Results:The findings showed that GBE effectively attenuated myocardial infarction by boosting the body’s natural antioxidant defense system and reducing the release of inflammatory cytokines as well as heart injury marker enzymes.The expression of Bcl-2,ERK1/2 and mTOR was increased while the histomorphological alterations were reversed.Conclusion:The cardioprotective effects of GBE may be due to a mechanism involving increased Bcl-2/mTOR/ERK1/2/Na^(+),K^(+)-ATPase activity.