Robinin attenuates cardiac oxidative stress-induced endoplasmic reticulum-dependent apoptosis through AKT/GSK3β pathway.

ABSTRACT: Myocardial injury is a pathological condition often resulting from excessive β-adrenergic stimulation, such as that induced by isoproterenol (ISO), a β-adrenergic agonist that increases reactive oxygen species (ROS) production, leading to endoplasmic reticulum (ER) stress, apoptosis, and impaired survival signaling. This study investigated Robinin's (Rob) ability to mitigate ISO-induced myocardial damage in H9c2 cardiomyocytes and male Sprague-Dawley rats. ISO-induced damage was assessed through histology, oxidant/antioxidant assays, cardiac marker enzyme assays, and molecular analyses, including PCR and Western blotting. Rob treatment significantly reduced ISO-induced ROS generation and apoptosis, while preserving cell morphology and survival. Rob also modulated ER stress and apoptosis-re

SUBMITTER: Abhirami N 

PROVIDER: S-EPMC12528489 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature