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High glucose‑induced upregulation of CD36 promotes inflammation stress via NF‑κB in H9c2 cells.
Molecular Medicine Reports ( IF 3.4 ) Pub Date : 2021-09-07 , DOI: 10.3892/mmr.2021.12404
Baosheng Han 1 , Jianzhong Wang 1 , Jiawei Wu 1 , Fang Yan 1 , Yaru Wang 1 , Jun Li 2
Affiliation  

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.

中文翻译:

高糖诱导的 CD36 上调通过 H9c2 细胞中的 NF-κB 促进炎症应激。

心脏炎症在糖尿病性心肌病的进展中起重要作用。CD36(分化簇 36)介导多种疾病状态下的炎症应激。本研究调查了高糖 (HG) 诱导的 H9c2 细胞中 CD36 的表达,CD36 上调是否促进炎症应激及其潜在机制。HG 在细胞中以时间依赖性方式诱导 CD36 表达,在 CD36 敲除或用 N-乙酰半胱氨酸或 MitoTEMPO 处理后被阻断。通过 HG 刺激 H9c2 细胞,CD36 向细胞膜的易位在 72 小时增加。此外,CD36 敲除抑制 HG 诱导的活性氧 (ROS) 生成、肿瘤坏死因子-α、白细胞介素 (IL)-6 和 IL-1β 表达以及核因子 (NF)-κB 通路激活。更远,CD36 敲除逆转了由 HG 引起的代谢重编程、脂质积累和 AMP 激活的蛋白激酶活化。上述数据表明,HG 诱导的 CD36 上调通过 H9c2 细胞中的 NF-κB 促进炎症应激,由代谢重编程、脂质积累和增强的 ROS 生成介导。
更新日期:2021-09-07
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