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硫化氢通过 p38MAPK 通路改善 ox-LDL 诱导的 THP-1 单核细胞中 Lp-PLA 的表达水平。

Hydrogen sulfide improves ox‑LDL‑induced expression levels of Lp‑PLA in THP‑1 monocytes via the p38MAPK pathway.

机构信息

Department of Cardiology Laboratory, First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China.

Department of Cardiology Laboratory, Huazhong University of Science and Technology Tongji Medical College First Clinical College, Wuhan, Hubei 430000, P.R. China.

出版信息

Mol Med Rep. 2021 May;23(5). doi: 10.3892/mmr.2021.11997. Epub 2021 Mar 24.

DOI:10.3892/mmr.2021.11997
PMID:33760156
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7974332/
Abstract

Hydrogen sulfide (HS) exerts an anti‑atherosclerotic effect and decreases foam cell formation. Lipoprotein‑associated phospholipase A2 (Lp‑PLA) is a key factor involved in foam cell formation. However, the association between HS and Lp‑PLA expression levels with respect to foam cell formation has not yet been elucidated. The present study investigated whether HS can affect foam cell formation and potential signalling pathways via regulation of the expression and activity of Lp‑PLA. Using human monocytic THP‑1 cells as a model system, it was observed that oxidized low‑density lipoprotein (ox‑LDL) not only upregulates the expression level and activity of Lp‑PLA, it also downregulates the expression level and activity of Cystathionine γ lyase. Exogenous supplementation of HS decreased the expression and activity of Lp‑PLA induced by ox‑LDL. Moreover, ox‑LDL induced the expression level and activity of Lp‑PLA via activation of the p38MAPK signalling pathway. HS blocked the expression levels and activity of Lp‑PLA induced by ox‑LDL via inhibition of the p38MAPK signalling pathway. Furthermore, HS inhibited Lp‑PLA activity by blocking the p38MAPK signaling pathway and significantly decreased lipid accumulation in ox‑LDL‑induced macrophages, as detected by Oil Red O staining. The results of the present study indicated that HS inhibited ox‑LDL‑induced Lp‑PLA expression levels and activity by blocking the p38MAPK signalling pathway, thereby improving foam cell formation. These findings may provide novel insights into the role of HS intervention in the progression of atherosclerosis.

摘要

硫化氢 (HS) 具有抗动脉粥样硬化作用，并可减少泡沫细胞的形成。脂蛋白相关磷脂酶 A2 (Lp-PLA) 是参与泡沫细胞形成的关键因素。然而，HS 与 Lp-PLA 表达水平与泡沫细胞形成之间的关系尚未阐明。本研究探讨了 HS 是否可以通过调节 Lp-PLA 的表达和活性来影响泡沫细胞的形成及其潜在的信号通路。使用人单核细胞 THP-1 细胞作为模型系统，观察到氧化型低密度脂蛋白 (ox-LDL) 不仅上调了 Lp-PLA 的表达水平和活性，还下调了胱硫醚 γ 裂解酶的表达水平和活性。外源性补充 HS 可降低 ox-LDL 诱导的 Lp-PLA 的表达和活性。此外，ox-LDL 通过激活 p38MAPK 信号通路诱导 Lp-PLA 的表达水平和活性。HS 通过抑制 p38MAPK 信号通路阻断 ox-LDL 诱导的 Lp-PLA 的表达水平和活性。此外，HS 通过阻断 p38MAPK 信号通路抑制 Lp-PLA 活性，并通过油红 O 染色显著减少 ox-LDL 诱导的巨噬细胞中的脂质积累。本研究结果表明，HS 通过阻断 p38MAPK 信号通路抑制 ox-LDL 诱导的 Lp-PLA 表达水平和活性，从而改善泡沫细胞的形成。这些发现可能为 HS 干预动脉粥样硬化进展的作用提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/7815fb658bd9/mmr-23-05-11997-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/517d0c25027f/mmr-23-05-11997-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/5b7d40a8c5db/mmr-23-05-11997-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/c6524257f200/mmr-23-05-11997-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/7815fb658bd9/mmr-23-05-11997-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/517d0c25027f/mmr-23-05-11997-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/5b7d40a8c5db/mmr-23-05-11997-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/c6524257f200/mmr-23-05-11997-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed7/7974332/7815fb658bd9/mmr-23-05-11997-g03.jpg

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