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

Abstract

Honokiol is one of the main active components of Magnolia officinalis, 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 (H 2 O 2)-induced DNA damage and mitochondrial dysfunction, while reducing reactive oxygen species (ROS) formation. The inhibitory effect of honokiol on H 2 O 2-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 cytochrome c release to the cytoplasm. Collectively, these results demonstrate that honokiol defends C2C12 myoblasts against H 2 O 2-induced DNA damage and apoptosis, at least in part, by preventing mitochondrial-dependent pathway through scavenging excessive ROS.

Activation of the Nrf2/HO-1 signaling pathway contributes to the protective effects of platycodin D against oxidative stress-induced DNA damage and apoptosis in C2C12 myoblasts

“…Therefore, the balance between the pro-apoptotic Bax member proteins against the anti-apoptotic Bcl-2 member proteins acts as a determinant that induces the activation of the caspase cascade upon initiation of the intrinsic apoptotic pathway. In the present study, the caspase-3 activity and degradation of PARP were obviously increased, and the Bax/Bcl-2 expression ratio was also enhanced in H 2 O 2 -treated C2C12 cells, both of which findings are consistent with previous studies (Siu et al 2009;Lee et al 2016;Choi 2018;Park et al 2019). However, these changes were all significantly blunted in the presence of platycodin D, indicating that platycodin D can protect C2C12 cell apoptosis by inhibiting the intrinsic apoptosis pathway activated by oxidative stress.…”

Induction of Apoptosis by Coptisine in Hep3B Hepatocellular Carcinoma Cells through Activation of the ROS-Mediated JNK Signaling Pathway

“…The comet assay was assessed to detect the DNA damage in individual cells, as previously describe [48]. In brief, the collected cells were mixed with 0.75% low-melting agarose (LMA).…”

Metabolic reprogramming as a novel therapeutic target for Coxsackievirus B3

“…To quantify MMP, cells were treated for 30 min at 37°C with 0.3 g/ml JC-1 (T3168; Invitrogen Life Technologies) and then processed for flow cytometry analysis as described before (Park et al 2020 ).…”