In-vivo Antioxidant Effects of Emodin on Ischemia-Reperfusion Injury of Rat’s Skeletal Muscle

İngilizce (OpenAlex)

Background: Skeletal muscle ischemia-reperfusion (I/R) injury is a clinically significant condition characterized by oxidative stress, inflammation, and histological damage. Emodin, a natural anthraquinone derivative, has been shown to exert antioxidative, anti-inflammatory, and antiapoptotic effects in various organ systems, however its efficacy in skeletal muscle I/R injury remains unclear. This study aimed to evaluate the potential protective role of emodin in a rat model of skeletal muscle I/R injury using biochemical and histopathological assessments. Methods: Twenty-four male Wistar rats were randomly assigned to four groups: Sham (S), Emodin (E) (20 mg/kg intraperitoneal), Ischemia-Reperfusion (IR), and IR with E treatment (IR+E). Skeletal muscle I/R was induced by infrarenal aortic clamping for 45 minutes, followed by 120 minutes of reperfusion. Muscle tissue was analyzed for malondialdehyde (MDA) and glutathione (GSH) levels, as well as catalase (CAT) and superoxide dismutase (SOD) activities. Histopathological evaluation included semiquantitative scoring of muscle fiber disorganization, neutrophil infiltration, interstitial edema, and hemorrhage. Results: The IR group demonstrated significantly elevated MDA levels and decreased CAT activity compared with controls. E treatment markedly reduced MDA levels and partially restored CAT activity, while no significant changes were observed in SOD or GSH. Histopathological analysis showed severe disorganization, neutrophil infiltration, and edema in the IR group, which were notably attenuated by emodin, though not completely prevented. Conclusion: Emodin confers partial protection against skeletal muscle I/R injury, primarily by inhibiting lipid peroxidation and partially restoring CAT activity. This study provides the first in-vivo evidence of emodin's effects in skeletal muscle I/R, highlighting its potential as a tissue-specific antioxidant intervention and warranting further investigation of its mechanistic pathways.