桃红四物汤对人脑微血管内皮细胞OGD损伤的保护作用及机制

季兆洁; 韩岚; 吴欢茹; 郭栋栋; 彭代银

doi:10.13422/j.cnki.syfjx.20180627

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桃红四物汤对人脑微血管内皮细胞OGD损伤的保护作用及机制

药理 | 更新时间：2024-01-04

- 桃红四物汤对人脑微血管内皮细胞OGD损伤的保护作用及机制
- Protective Effect and Mechanism of Taohong Siwutang on OGD-induced Injury of Human Brain Microvascular Endothelial Cells
- 中国实验方剂学杂志 2018年24卷第7期页码：95-100
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金项目（81473387）;国家自然科学基金青年基金项目（81503291）;安徽中医药大学2016年青年科学研究基金项目（2016qn013）
- DOI：10.13422/j.cnki.syfjx.20180627
  中图分类号： R285
- 纸质出版日期：2018
- 稿件说明：
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季兆洁, 韩岚, 吴欢茹, 等. 桃红四物汤对人脑微血管内皮细胞OGD损伤的保护作用及机制[J]. 中国实验方剂学杂志, 2018,24(7):95-100.

JI Zhao-jie, HAN Lan, WU Huan-ru, et al. Protective Effect and Mechanism of Taohong Siwutang on OGD-induced Injury of Human Brain Microvascular Endothelial Cells[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(7): 95-100.
季兆洁, 韩岚, 吴欢茹, 等. 桃红四物汤对人脑微血管内皮细胞OGD损伤的保护作用及机制[J]. 中国实验方剂学杂志, 2018,24(7):95-100. DOI： 10.13422/j.cnki.syfjx.20180627.

JI Zhao-jie, HAN Lan, WU Huan-ru, et al. Protective Effect and Mechanism of Taohong Siwutang on OGD-induced Injury of Human Brain Microvascular Endothelial Cells[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(7): 95-100. DOI： 10.13422/j.cnki.syfjx.20180627.

摘要

目的：通过建立糖氧剥夺（OGD）诱导的人脑微血管内皮细胞（h-BMECs）损伤模型，观察桃红四物汤对细胞的保护作用及机制。方法：体外建立人脑微血管内皮细胞糖氧剥夺损伤模型，随机分为正常组、模型组、桃红四物汤高、中、低质量浓度组（0.8，0.4，0.2 g ·L-1）和阳性药尼莫地平组。噻唑蓝（MTT）比色法检测h-BMECs细胞活性，酶联免疫吸附法（ELISA）测定细胞上清液中乳酸脱氢酶（LDH）水平、细胞中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性，采用蛋白免疫印迹法（Western blot）检测内皮细胞血管内皮生长因子（VEGF）和缺氧诱导因子-1α（HIF-1α）表达水平。结果：桃红四物汤可显著提高拟缺血损伤的人脑微血管内皮细胞活性，降低LDH漏出率（P<0.05，P<0.01），改善细胞形态，降低MDA水平（P<0.05），增强SOD活性（P<0.05，P<0.01）。增加内皮细胞VEGF和HIF-α蛋白的表达（P<0.05，P<0.01）。结论：桃红四物汤对拟缺血损伤人脑微血管内皮细胞具有保护作用，其机制与增强细胞抗氧化能力，通过HIF-α途径增强VEGF表达有关，显示中药组方可发挥整体调节的治疗优势。

Abstract

Objective: To investigate the mechanism that Taohong Siwutang (TST) protectshuman brain cerebral microvascular endothelial cells (h-BMECs) injury induced by oxygen-glucose deprivation (OGD). Method: Theh-BMECs injury models were induced by OGD

and then the cells were randomly divided into six groups:normal control group

model group

TST high

middle and low dose (0.8

0.4

0.2 g ·L-1) groups and nimodipine group.3-(4

5-dimethyl-2-thiazolyl)-2

5-diphenyl-2-H-tetrazolium bromide(MTT)staining was employed to assay the activities of h-BMECs; the content of superoxide dismutase(SOD)

malonaldehyde(MDA)in cells

andlactate dehydrogenase (LDH)in cell supernatantwere determined by enzyme-linked immunosorbent assay (ELISA); and the expression levels of hypoxia inducible factor-1α (HIF-α) andvascular endothelial growth factor (VEGF)were detected by Western blot. Result: TST could significantly improve the activities of mimic ischemia injured hMBECs

decrease LDH leakage rate

improve the morphology of h-MBECs obviously

reduce MDA level

enhance SOD activity

and up-regulate the protein expression levels of VEGF and HIF-α. Conclusion: TST has protective effects on OGD-injured h-BMECs

and its mechanism may be related to enhancing the antioxidant capacity

and up-regulating the expression of VEGF and HIF-α

showing the advantages of compound Chinese medicine in integrative regulation.

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