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Abstract Title:

Honokiol ameliorates oxidative stress-induced DNA damage and apoptosis of c2c12 myoblasts by ROS generation and mitochondrial pathway.

Abstract Source:

Anim Cells Syst (Seoul). 2020 ;24(1):60-68. Epub 2019 Dec 28. PMID: 32158617

Abstract Author(s):

Cheol Park, Sung Hyun Choi, Jin-Woo Jeong, Min Ho Han, Hyesook Lee, Su Hyun Hong, Gi-Young Kim, Sung-Kwon Moon, Wun-Jae Kim, Yung Hyun Choi

Article Affiliation:

Cheol Park


Honokiol is one of the main active components of, and has been demonstrated to have multiple pharmacological activities against a variety of diseases. Recently, this phenolic compound is known to have antioxidant activity, but its mechanism of action remains unclear. The purpose of the current study was to evaluate the preventive effects of honokiol against oxidative stress-induced DNA damage and apoptosis in C2C12 myoblasts. The present study found that honokiol inhibited hydrogen peroxide (HO)-induced DNA damage and mitochondrial dysfunction, while reducing reactive oxygen species (ROS) formation. The inhibitory effect of honokiol on HO-induced apoptosis was associated with the up-regulation of Bcl-2 and down-regulation of Bax, thus reducing the Bax/Bcl-2 ratio that in turn protected the activation of caspase-9 and -3, and inhibition of poly (ADP-ribose) polymerase cleavage, which was associated with the blocking of cytochromerelease to the cytoplasm. Collectively, these results demonstrate that honokiol defends C2C12 myoblasts against HO-induced DNA damage and apoptosis, at least in part, by preventing mitochondrial-dependent pathway through scavenging excessive ROS.

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