Neuroprotective Effect of Stemona tuberose Leaf Extract on MCAO/R-Induced Rats via P13K/Akt Signaling Pathway

Abstract

Background: Ischemic Stroke (IS) is a serious illness with great fatality and disability globally. The pathophysiological causes of IS are oxidative stress, apoptosis and neuroinflammation.Objectives: Cerebral Ischemia/Reperfusion Injury (CI/RI) is arecurrent pathological development resulting in IS. Stemona tuberose (ST), which comes under the Stemonaceae family, has been extensively involved in Chinese traditional medication to treat inflammatory disorders.Materials and Methods: The current study investigated this medicinal herbs Stemona tuberose leaf extract (STLE) for the first time concerning its neuroprotective activity inthe CI/RI ratsdeveloped by the MCAO/R technique. Rats were distributed into 5 sets; sham, MCAO/R-induced, MCAO/ R+STLE (25 mg/kg bw), MCAO/R + STLE (50 mg/kg bw) and MCAO/R+STLE (100 mg/kg bw). CI/RI triggered cerebral injury was evaluated using infarction volume, oxidative stress, histopathology, microglial polarization, neuroinflammation and apoptosis.Results: STLE could dose-dependably alleviate infarction volume, oxidative stress, histopathological changes, neuroinflammation and apoptosis while enhancing microglia/macrophages M1/M2 polarization in CI/RI rats. STLE exerts anti-apoptotic properties by the augmented Bcl-2/Bax proportion and diminished caspase-3 levels. STLE could modulate the microglia polarization from the phenotype M1 pro-inflammatory to the M2 anti-inflammatory potential.Conclusion: Furthermore, STLE showed promise in reducing CI/RI-induced apoptosis by modulating the P13K/Akt signaling pathway. These results demonstrate STLE's therapeutic promise in the management of ischemic stroke and associated neuroinflammatory diseases.

Keywords: Apoptosis; Ischemia-reperfusion; Ischemic stroke; Neuroinflammation; Oxidative stress; P13K/Akt signaling; Stemona tuberosa