Phlogacanthus thyrsiflorus Nees. modulates hepatic and renal apoptosis via attenuation of oxidative stress in alloxan-administered mice

摘要

Abstract An endeavor has been made in this study to assess the effect of Phlogacanthus thyrsiflorus on hyperglycemia-induced oxidative stress along with apoptosis in liver?and kidney?of alloxan-administered mice. To analyze the effect of Phlogacanthus thyrsiflorus on oxidative stress in kidney?and liver?of diabetic mice. Furthermore, we have also examined the effect of Phlogacanthus thyrsiflorus on apoptosis in diabetic mice. Following preparation of methanolic flower extract (MFE), preliminary phytochemical screenings and acute toxicity test were carried out for MFE. Lipid peroxidation and protein carbonyl assays were determined to check the MDA level and oxidative damage in tissues of groups normal control mice (NCM), diabetic control mice (DCM), ascorbic acid–treated diabetic mice (D?+?AA), and MFE-treated diabetic mice (D?+?MFE). Histological and ultrastructural studies were conducted to evaluate any changes in tissues as well as sub-cellular organelles. The effects of MFE on caspase 3 and Bcl-2 expression in alloxan-induced diabetic mice were studied and compared against the diabetic control group of mice. Upon treatment with MFE, the diabetic mice manifested a notable depletion of malondialdehyde (MDA) and protein carbonyl levels. The ultrastructural studies divulged the capability of MFE to reinstate morphological and cellular alterations as contemplated in alloxan-induced diabetic mice. On apoptosis, the effect of MFE showed the downregulation of cysteine-dependent aspartate specific protease (caspase) 3, whereas upregulation of B-cell lymphoma-2 (Bcl-2) protein and the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL) assay illustrated a few apoptotic cells. It can be put forward that methanolic flower extract of Phlogacanthus thyrsiflorus treatment can exert hepatoprotective and nephroprotective effect via regulating hyperglycemia-induced oxidative stress and apoptosis in alloxan-administered diabetic mice.