Cinnamaldehyde attenuates TNF- α induced skeletal muscle loss in C2C12 myotubes via regulation of protein synthesis, proteolysis, oxidative stress and inflammation

Arch Biochem Biophys. 2024 Feb 8:109922. doi: 10.1016/j.abb.2024.109922. Online ahead of print.ABSTRACTInflammation is the primary driver of skeletal muscle wasting, with oxidative stress serving as both a major consequence and a contributor to its deleterious effects. In this regard, regulation of both can efficiently prevent atrophy and thus will increase the rate of survival (Meng and Yu, 2010) [1]. With this idea, we hypothesize that preincubation of Cinnamaldehyde (CNA), a known compound with anti-oxidative and anti-inflammatory properties, may be able to prevent skeletal muscle loss. To examine the same, C2C12 post-differentiated myotubes were treated with 25ng/ml Tumor necrosis factor-alpha (TNF-α) in the presence or absence of 50μM CNA. The data showed that TNF-α mediated myotube thinning and a lower fusion index were prevented by CNA supplementation 4 h before TNF-α treatment. Moreover, a lower level of ROS and thus maintained antioxidant defense system further underlines the antioxidative function of CNA in atrophic conditions.CNA preincubation also inhibited an increase in the level of inflammatory cytokines and thus led to a lower level of inflammation even in the presence of TNF-α. With decreased oxidative stress and inflammation by CNA, it was able to maintain the intracellular level of injury markers (CK, LDH) and SDH activity of mitochondria. In addition, CNA modulates all five proteolytic systems (cathepsin-L, UPS (atrogin-1), calpain, LC3, beclin) simul...
Source: Archives of Biochemistry and Biophysics - Category: Biochemistry Authors: Source Type: research