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Hexarelin对H2O2诱导的大鼠胸主动脉内皮细胞损伤的抑制作用及其机制

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第1期
页码:
51-55
栏目:
基础研究
出版日期:
2010-10-27

文章信息/Info

Title:
Hexarelin protects rat thoracic aorta endothelial cells from H2O2-induced damage in vitro
作者:
张晓卉1; 张改改2; 刘越1; 马骁3; 尹新华1
哈尔滨医科大学：1.附属一院心内八科，3.附属二院消化内科，黑龙江 哈尔滨 150000；2.清华大学附属一院干部病房，北京 100016
Author(s):
ZHANG Xiao-hui1;  ZHANG Gai-gai2;  LIU Yue1;  MA Xiao3;  YIN Xin-hua1
1.Department of Cardiology, First Hospital, 3.Department of Digestive Disease, Second Hospital;2.Department of Cardiology, First Hospital, Qinghua University, Beijing 100016, China
关键词:
Hexarelin; H2O2; 内皮细胞
Keywords:
hexarelin;  H2O2;  endothelial cell
分类号:
R972.4
DOI:
-
文献标识码:
A
摘要:
目的: 观察人工合成的生长激素释放肽hexarelin对H2O2诱导的大鼠胸主动脉内皮细胞损伤是否有抑制作用及可能的机制。方法: 体外原代培养的大鼠胸主动脉内皮细胞，随机分为对照组、H2O2组及H2O2+10-5 mmol/L hexarelin组和H2O2+10-7 mmol/L hexarelin组，通过光镜和电镜观察各组细胞的形态学变化。采用MTT比色法检测各组细胞活力的变化；用比色法检测内皮细胞培养上清液中乳酸脱氢酶（LDH）的含量；用硝酸还原酶法检测内皮细胞培养上清液中一氧化氮（NO）的含量。结果: 光镜和电镜观察发现，H2O2可以诱导大鼠胸主动脉内皮细胞损伤及凋亡；而Hexarelin能减轻H2O2所诱导的内皮细胞损伤及凋亡。MTT比色法检测发现，H2O2能使内皮细胞的活力由(0.39±0.03)下降为(0.23±0.04)(P<0.01)；而1×10-5和1× 10-7 mmol/L hexarelin能减轻H2O2对内皮细胞活力的影响，内皮细胞的活力分别由（0.23±0.04）变为（0.30±0.02）和（0.29±0.02）(P<0.01)。H2O2能诱导内皮细胞产生LDH，由(31.11±4.97)U/L上升为(157.48±7.33)U/L(P<0.01)；而1×10-5和1×10-7 mmol/L hexarelin能减少LDH的生成，由［(157.48±7.33)U/L下降为(55.12±6.11) U/L和(94.48±4.07) U/L(P<0.01)。另外，H2O2能引起NO生成减少，由（29.38±6.14）μmol/L降为 （17.24±7.51）μmol/L(P<0.01)，而hexarelin能逆转H2O2引起的内皮细胞NO生成的减少，由(17.24±7.51)μmol/L变为(35.95±4.89)μmol/L和(19.73±2.50)μmol/L(P<0.01)。结论: Hexarelin能够抑制H2O2所诱导的大鼠胸主动脉内皮细胞的损伤及其凋亡，其机制可能与hexarelin抑制氧化应激反应及促进NO的产生有关。
Abstract:
AIM: To observe whether hexarelin, a synthetic growth hormone-releasing peptide, protects rat thoracic aorta endothelial cells from H2O2-induced damage and to elucidate its mechanism. METHODS: Cultured endothelial cells from rat thoracic aorta were divided randomly into four groups: control group, H2O2 group, H2O2+10-5 mmol/L hexarelin group and H2O2+10-7 mmol/L hexarelin group. The morphology of endothelial cells was observed by contrast phase microscope and transmission electron microscope and cell viability was detected by MTT assay. Levels of lactate dehydrogenase (LDH) and nitrogen monoxidum (NO) were measured by supernatant. RESULTS: Contrast phase microscope and transmission electron microscope showed that H2O2 induced apoptosis of endothelial cells but hexarelin reversed the damage. H2O2 decreased endothelial cell viability (P<0.01), whereas 1×10-5 mmol/L/1×10-7 mmol/L hexarelin reversed the damage (P<0.01). H2O2 increased LDH release (P<0.01) but 1×10-5 mmol/L/1×10-7 mmol/L hexarelin decreased the LDH release (P<0.01). Compared with that in control group, H2O2 caused the reduction of NO (P<0.01), but 1×10-5 mmol/L/1×10-7 mmol/L hexarelin increased the NO. CONCLUSION: Hexarelin protects rat thoracic aorta endothelial cells from H2O2-induced damage and apoptosis, possibly through inhibiting the oxidative stress by increasing the NO levels.

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备注/Memo

备注/Memo:
收稿日期：2009-12-12.通讯作者：尹新华，教授，主要从事心血管疾病的诊断与治疗 Email: harbin0910@yahoo.com 作者简介：张晓卉，硕士生Email：maxiao19830522@163.com
更新日期/Last Update: 2010-10-27