AbstractThe present study aims to evaluate the cytoprotective efficacy of Khamira, a traditional Unani formulation, in an in vitro model of chemically induced toxicity. Specifically, the protective potential of Khamira was assessed against Isoproterenol (ISO)-induced cytotoxicity using SVEC endothelial cells. Cell viability assays demonstrated that Khamira is non-toxic up to a concentration of 20 mg/mL, beyond which significant cytotoxicity was observed. ISO exposure at 150 µM resulted in moderate lethality, with higher concentrations inducing marked toxicity and cellular apoptosis. In wound healing (scratch) assays, cells co-treated with 5 mg/mL Khamira showed enhanced wound closure compared to those treated with 10 mg/mL, indicating a dose-dependent effect on cellular migration and repair. The experimental design employed a co-treatment model to simulate a therapeutic scenario. Reactive oxygen species (ROS) analysis revealed that Khamira may contribute to maintaining redox homeostasis, likely through modulation of endogenous antioxidant systems. Upregulation of superoxide dismutase 2 (SOD2) further suggests a potential influence on oxidative stress-responsive signaling pathways, influencing either upstream signaling events or acting post-ROS generation. These preliminary findings support the potential of Khamira as a cytoprotective agent in oxidative stress-induced cellular injury. However, further mechanistic investigations and comprehensive in vivo studies are warranted to substantiate its therapeutic potential and clarify its role in cellular protection and tissue regeneration.
M. Abdul Kareem (Thu,) studied this question.