[高血糖素对肺微血管内皮细胞损伤的保护机制]。

中国中西医结合杂志 Pub Date : 2017-04-01
Zhen-Ran Wang, Yang Li, Bo Tang
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引用次数: 0

摘要

目的探讨高血糖素对急性人肺微血管内皮细胞(hpmes)损伤的保护机制。方法不同浓度的LPS(0。01, 0。1、1。剂量为10 mg/L),诱导hpmec急性损伤。用Alpinetin(40、80、160、320 mg/L)干预hpmes模型(n =3)。选取正常hpmec作为对照组。检测细胞间细胞粘附分子-1 (ICAM-1)、TNF-α、APQ-1 mRNA和蛋白的表达。结果与对照组比较,模型组细胞中ICAM-1、TNF-a蛋白表达升高,APQ-1蛋白和mRNA表达降低,hpmec细胞的vi- ability降低(P
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Protection Mechanism of Alpinetin on Pulmonary Microvascular Endothelial Cells Injury].

Objective To explore the protection mechanisms about Alpinetin to acute human pulmonary microvascular endothelial cells ( HPMECs ) injury. Methods Different concentration of LPS (0. 01,0. 1 ,1. ,10 mg/L) was applied to the HPMECs to induce acute HPMECs injury. The HPMECs mod- els (n =3) were intervened by Alpinetin(40,80,160,320 mg/L) . Normal HPMECs were selected as control group. The viability of HPMECs was observed,mRNA and protein expression of intercellular cell adhesion molecule-1 (ICAM-1) ,TNF-α,APQ-1 were detected. Results Compared with control group, the protein expression of ICAM-1 , TNF-a were increased, the protein and mRNA expression of APQ-1 and the vi- ability of HPMECs were decreased in model group (P <0. 05). Compared with model group,ICAM-1 and TNF-α protein expressions were significantly inhibited in Alpinetin (80,160 mg/L) group, the mRNA and protein expression of APQ-1 and the viability of HPMECs were significantly increased (P <0. 05, P < 0. 01). Conclusion Alpenitin could protect the HPMECs injury by down-regulated protein expression of ICAM-1, TNF-α and up-regulated the mRNA and protein expression of APQ-1.

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