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Functional roles of CCL5/RANTES in liver disease 被引量:2
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作者 Lili Chen Qianfei Zhang +2 位作者 Chang Yu Fang Wang Xiaoni Kong 《Liver Research》 2020年第1期28-34,共7页
Inflammation,which is mediated by leukocyte trafficking and activation,plays a prominent role in the pathogenesis of acute and chronic liver injury.Chemokines are critical mediators involved in the migration of leukoc... Inflammation,which is mediated by leukocyte trafficking and activation,plays a prominent role in the pathogenesis of acute and chronic liver injury.Chemokines are critical mediators involved in the migration of leukocytes into the diseased liver via binding to their G protein-coupled receptors.CeC motif ligand 5(CCL5)belongs to the CC-chemokine family and is secreted by several hepatic cell pop-ulations including hepatocytes,macrophages,hepatic stellate cells,and endothelial cells upon activation.CCL5 regulates the recruitment and migration of T cells(via CCR5)and NK cells(via CCR1).Moreover,CCL5 activates and stimulates T cell proliferation and cytokine production,sequentially regulating in-flammatory responses.Accumulating studies have identified crucial effects of CCL5 both in liver-disease patients and in experimental models,in which CCL5 is elevated and displays distinct effects according to pathological conditions.In this review,we discussed the crucial functions of CCL5 in liver diseases,including acute liver failure,hepatic ischemia-reperfusion injury,acute liver failure,acute and viral hepatitis,alcoholic liver disease,non-alcoholic fatty liver disease,fibrosis,and hepatocellular carcinoma.Continued understanding the roles of CCL5 in liver disease and their mechanisms of activation are indispensable for the development of effective clinical therapeutics. 展开更多
关键词 C-C motif ligand 5(ccl5) chemOkineS Liver injury HEPATITIS Alcoholic liver disease(ALD) Non-alcoholic fatty liver disease(NAFLD) FIBROSIS Hepatocellular carcinoma(HCC)
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热损伤血管内皮细胞对巨噬细胞极化的影响
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作者 张玲琴 谢建刚 +2 位作者 王倩梅 徐云云 黄杨 《中国急救医学》 CAS CSCD 2022年第6期521-525,共5页
目的探讨血管内皮细胞热损伤后培养上清对巨噬细胞极化的影响及机制。方法小鼠肺微血管内皮细胞系(MPVECs)给予40℃热刺激不同时间后,观察细胞状态和活力,ELISA检测培养上清中趋化因子5(CCL5)含量,选取合适的刺激时间;构建MPVECs热处理... 目的探讨血管内皮细胞热损伤后培养上清对巨噬细胞极化的影响及机制。方法小鼠肺微血管内皮细胞系(MPVECs)给予40℃热刺激不同时间后,观察细胞状态和活力,ELISA检测培养上清中趋化因子5(CCL5)含量,选取合适的刺激时间;构建MPVECs热处理上清与小鼠巨噬细胞系(RAW264.7)共培养体系,对照组予以正常培养3 h上清,处理组予以40℃处理3 h上清,干预组予以40℃处理3 h上清,同时加入Maraviroc,阻断CCL5/趋化因子5受体(CCR5)轴,培养6 h后流式细胞术观察巨噬细胞M1/M2极化,qPCR检测促炎相关细胞因子mRNA表达,ELISA检测培养上清细胞因子含量。结果MPVECs给予40℃热处理3 h细胞形态较完整,培养上清CCL5含量较高,适合用于刺激RAW264.7细胞;处理组、干预组予以不同处理后RAW264.7细胞M1极化明显上升(P<0.01),予以Maraviroc,阻断CCL5/CCR5轴,M1极化下降(P<0.01)。处理组、干预组予以不同处理后促炎细胞因子IL-1β、IL-6、TNF-α表达和培养上清含量均上升(P<0.05),阻断CCL5/CCR5途径明显减少IL-1β的表达(P<0.01)。结论血管内皮细胞受到热损伤时可以释放CCL5,通过CCL5/CCR5轴调控巨噬细胞向促炎的M1型极化并释放促炎细胞因子,靶向阻断CCL5/CCR5轴抑制巨噬细胞M1极化和相关促炎细胞因子分泌。 展开更多
关键词 热射病 趋化因子5(ccl5) 巨噬细胞 MARAVIROC
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