Resveratrol alleviates lysophosphatidylcholine-induced damage and inflammation in vascular endothelial cells

Chen,Jinsong; Cao,Xiaocheng; Cui,Yonghong; Zeng,Gaofeng; Chen,Jiaxian; Zhang,Guogang

doi:10.3892/mmr.2017.8300

Resveratrol alleviates lysophosphatidylcholine-induced damage and inflammation in vascular endothelial cells

Authors:
- Jinsong Chen
- Xiaocheng Cao
- Yonghong Cui
- Gaofeng Zeng
- Jiaxian Chen
- Guogang Zhang
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Affiliations: Department of Cardiovascular Medicine, Xiangya Hospital, Central South University, Kaifu, Changsha, Hunan 410008, P.R. China, Laboratory of Medicine, Medical College, Hunan Normal University, Changsha, Hunan 410016, P.R. China, Department of Cardiovascular Medicine, The Second Affiliated Hospital of South China University, Hengyang, Hunan 421001, P.R. China
Published online on: December 18, 2017 https://doi.org/10.3892/mmr.2017.8300
Pages: 4011-4018

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Abstract

The role of resveratrol (trans-3,5,4'-trihydroxystilbene; RES) in lysophosphatidylcholine (LPC)‑induced injury and inflammation in endothelial cells (regarded as an early event in arteriosclerosis) is unclear. The present study investigated whether RES reduces lactate dehydrogenase (LDH) activity and secretion of inflammatory cytokines such asinterleukin‑6 and tumor necrosis factor‑α, via the Toll‑like receptor (TLR)‑4/myeloid differentiation primary response gene 88 (MyD88)/nuclear factor (NF)‑κB signal transduction pathway in LPC‑induced damage and inflammation in human umbilical vein endothelial‑12 (HUVE‑12) cells. Using an ELISA and western blotting, the present study investigated the effects of RES on LDH activity and cytokine secretion. The effects of TLR‑4 short hairpin (sh)RNA and TLR‑4 cDNA transfection on NF‑κB activation during LPC‑induced damage and inflammation was also investigated in HUVE‑12 cells. The results demonstrated that RES significantly inhibited the effect of LPC on enzyme activity, pro‑inflammatory cytokine secretion, and expression of TLR‑4, MyD88 and NF‑κBp65 expression. In addition, RES and TLR‑4 shRNA transfection suppressed LPC‑induced injury and inflammation by blocking the TLR‑4/MyD88/NF‑κB signaling pathway Conversely, transfection with TLR‑4 cDNA enhanced LPC‑induced injury and inflammation, which abrogated the protective effects of RES. These data suggested that RES significantly suppressed LPC‑induced damage and inflammation, via suppression of the TLR‑4/MyD88/NF‑κB signaling pathway, which may provide a new mechanistic evidence for the treatment of arteriosclerosis by RES.

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