安普克
CD11c公司
免疫印迹
巨噬细胞极化
富血小板血浆
化学
M2巨噬细胞
内科学
内分泌学
PI3K/AKT/mTOR通路
磷酸化
信号转导
细胞生物学
巨噬细胞
蛋白激酶A
生物
医学
血小板
生物化学
体外
基因
表型
作者
Ling‐Ying Shi,Yanhui Li,Jingjing Xu,Yu Zhang,Tingting Xie,Yubing Xu,Guiqiu Shan,Mou Zhou
出处
期刊:PubMed
日期:2023-10-01
卷期号:31 (5): 1486-1491
标识
DOI:10.19746/j.cnki.issn.1009-2137.2023.05.037
摘要
To investigate the role of platelet-rich plasma (PRP) in inducing the M2 macrophage polarization via regulating AMPK singling pathway.The expressions of M1 marker CD11c and M2 marker CD206 in macrophages of blank control group, LPS group, LPS+PRP group, and LPS+PRP+Compound C group were detected by flow cytometry. Western blot was used to observe the effects of PRP on the expression of AMPK-mTOR signaling pathway-related proteins at different times (12 h, 18 h and 24 h) after LPS treatment. RNA interference technology was used to silence the expression of AMPK in macrophages, and the expression of TGF-β protein was subsequently examined by Western blot.LPS significantly reduced the expression of CD206 and increased the expression of CD11c (P <0.05). After the addition of PRP, the expression of CD206 was significantly increased (P <0.05), while the expression of CD11c was significantly decreased (P <0.05). Compared with LPS group, PRP treatment significantly increased the expressions of p-AMPK and p-ULK1 proteins at 12 h, 18 h and 24 h, while significantly decreased the expression of p-mTOR protein (P <0.05). After the addition of AMPK inhibitor Compound C, the expression of CD206 was significantly reduced (P <0.05) and the expression of CD11c was significantly increased compared with LPS+PRP group (P <0.05). After silencing the expression of AMPK in macrophages, the promotion effect of PRP on TGF-β was significantly reduced (P <0.05).PRP can stimulate the transformation of macrophages to M2 type via AMPK signalling pathway.富血小板血浆通过调控AMPK信号通路刺激巨噬细胞向M2型转化的作用研究.研究富血小板血浆(PRP)通过调控AMPK信号通路刺激巨噬细胞向M2型转化的作用。.流式细胞术检测空白对照组、LPS处理组、LPS+PRP处理组及LPS+PRP+Compound C处理组巨噬细胞M1型标志物CD11c和M2型标志物CD206的表达。Western blot法检测经LPS处理后,不同处理时间(12 h、18 h和24 h)PRP对AMPK-mTOR信号通路相关蛋白的表达的影响。运用RNA干扰技术,沉默巨噬细胞AMPK的表达,Western blot法检测PRP对TGF-β表达的作用。.LPS能显著降低CD206的表达量并显著增加CD11c的表达量(P <0.05),而加入PRP后,CD206的表达量明显增加(P <0.05),CD11c的表达量则显著降低(P <0.05)。与LPS组对比,加入PRP干预12 h、18 h 和24 h后,p-AMPK和p-ULK1蛋白明显增加,p-mTOR蛋白则明显降低,均有统计学差异(P <0.05)。与LPS+PRP组 相比,加入Compound C后,CD206的表达量明显降低(P <0.05),而CD11c的表达量则显著增加(P <0.05)。沉默巨噬细胞中AMPK的表达后,PRP对TGF-β的促进作用显著降低(P <0.05)。.PRP可以通过调控AMPK信号通路刺激巨噬细胞向M2型转化。.
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