High glucose-induced upregulation of CD36 promotes inflammation stress via NF-κB in H9c2 cells

Cardiac inflammation serves an important role in the progression of diabetic cardiomyopathy. CD36 (cluster of differentiation 36) mediates inflammation stress in a variety of disease states. The present study investigated CD36 expression in high glucose (HG)-induced H9c2 cells, whether CD36 upregulation promotes inflammatory stress, and its potential mechanism. HG induced CD36 expression in a time-dependent manner in cells, which was blocked following CD36 knockout or treatment with N-acetylcysteine or MitoTEMPO. CD36 translocation to the cell membrane was increased at 72 h by HG stimulation of H9c2 cells. Moreover, CD36 knockout inhibited HG-induced reactive oxygen species (ROS) generation, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β expression, and nuclear factor (NF)-κB pathway activation. Further, CD36 knockout reversed metabolic reprogramming, lipid accumulation and AMP-activated protein kinase activation caused by HG. The aforementioned data suggest that HG-induced upregulation of CD36 promotes inflammatory stress via NF-κB in H9c2 cells, mediated by metabolism reprogramming, lipid accumulation and enhanced ROS generation.