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.