https://www.selleckchem.com/pr....oducts/ecc5004-azd50
The present results indicated that propofol pre-treatment inhibited CoCl2-induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders. Copyright © Han et al.The modification of proteins by small ubiquitin-like modifier (SUMO), known as SUMOylation, regulat
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