Targeting Mitochondrial Dysfunction in Rodent Model of Ischemic Stroke Role of Repurposed Drugs and Nutraceutical

Abstract

Disturbance in homeostatic mechanisms is concerned with numerous disease situations. Ischemic stroke is one of the conditions which is heterogenous multifactor disease condition comprises of both acute and chronic neuronal death consequences. Ischemic stroke is the severe clinical issue and is leading cause of death and disability worldwide. It has high prevalence and serious repercussion because of unmet therapeutic strategies which put enormous burden on society and contribute to increased disability-adjusted life years. Preclinically, various neuroprotective strategies have been studied efficiently that are ultimately failed in clinical setup due to absence of efficiency, restricted time window for treatment instigation, design and bioavailability issues and unresolved toxicities. newlineMitochondrial dysfunction is considered as important pathological hallmark of ischemic stroke. Mitochondria is the main organelle that regulates varied cellular and molecular functions. Mitochondria is important for the promotion of neural survival and neurological improvement after ischemic damage. Therefore, mitochondria represent a crucial drug target for stroke management. Understanding the mitochondrial mechanisms involved in neuronal death and survival following ischemic stroke may provide rationale design of novel therapeutic strategies in ischemic stroke. newline newline