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κ-阿片受体激活后通过caveolin-eNOS途径抑制由软脂酸钠诱导的内皮损伤(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2017年第4期
页码:
394-398
栏目:
基础研究
出版日期:
2017-02-25

文章信息/Info

Title:
κ-opioid receptor activation inhibits endothelial injury induced by sodium palmitate via caveolin-eNOS pathway
作者:
杨 帆; 张淑苗; 李 娟; 周亚光; 田 心; 王渊博; 贾 敏;  樊 荣; 裴建明
第四军医大学基础医学部生理学教研室、细胞生物学国家重点学科，陕西 西安 710032
Author(s):
YANG Fan;  ZHANG Shu-miao;  LI Juan;  ZHOU Ya-guang;  TIAN Xin;  WANG Yuan-bo;  JIA Min;  FAN Rong;  PEI Jian-ming
Department of Physiology & National Key Discipline of Cell Biology, Fourth Military Medical University, Xi’an 710032, Shaanxi, China
关键词:
κ-阿片受体; 高脂血症; caveolin-1; 内皮型一氧化氮合酶
Keywords:
κ-opioid receptor;  Hyperlipidemia;  caveolin-1;  eNOS
分类号:
R589.2
DOI:
-
文献标识码:
A
摘要:
目的 探讨κ-阿片受体在对抗软脂酸钠（sodium palmitate,SP）诱导的人脐静脉内皮细胞（HUVECs）损伤中的作用及其作用机制。方法 体外培养HUVECs并分为6组即正常对照组、κ-阿片受体激动剂U50,488H组、SP组、SP+U50,488H组、SP+U50,488H+κ-阿片受体阻断剂nor-BNI组、SP+U50,488H+eNOS抑制剂L-NAME组。检测各组细胞生存率、测定各组caveolin-1、eNOS的蛋白表达水平，以及NO的产生及细胞凋亡情况。结果 与正常对照组相比，SP组细胞的生存率明显降低（P<0.01），caveolin-1的蛋白表达显著增加（P<0.01），eNOS的活性明显受到抑制（P<0.05），NO生成量大幅下降（P<0.01），细胞凋亡显著增加（P<0.01）；而κ-阿片受体激动剂U50,488H可以显著抑制SP的上述作用，使细胞生存率升高（P<0.01）， caveolin-1的蛋白表达均显著降低（P<0.05或P<0.01），eNOS的蛋白表达显著增加（P<0.05），NO生成量显著增多（P<0.01），细胞凋亡明显减少（P<0.01）。U50,488H的作用可被κ-阿片受体阻断剂nor-BNI或NO合酶抑制剂L-NAME所阻断（P<0.05或P<0.01）。结论 激活κ-阿片受体能够抑制软脂酸钠诱导的内皮损伤，其机制可能与下调caveolin-1表达，增强eNOS活性有关。
Abstract:
AIM To investigate the effect of κ-opioid receptor activation on sodium palmitate (SP)-induced human umbilical vein endothelial cells (HUVECs) injury and the underlying mechanism. METHODS HUVECs were divided into 6 groups: control group, U50,488H group (a selective κ-opioid receptor agonist), SP group, SP+U50,488H group, SP+U50,488H+nor-BNI (a selective κ-opioid receptor antagonist) group and SP+U50,488H+L-NAME (an eNOS inhibitor). Caveolin-1 and eNOS protein expressions were detected by Western blot, respectively. Cell survival rate was assayed by cell counting kit (CCK-8), apoptotic cells were determined by flow cytometry and NO production was analyzed by nitric oxide assay kit. RESULTS Compared with the control group, SP group showed a lower cell survival rate (P<0.01), significantly higher caveolin-1 protein expression (P<0.01), impaired eNOS activity (P<0.05), reduced NO production (P<0.01) and increased cell apoptosis (P<0.01). SP-induced HUVECs injury was ameliorated by U50,488H, as evidenced by a higher cell survival rate (P<0.01), reduced caveolin-1 protein expression (P<0.01), restored eNOS expression (P<0.05), increased NO production (P<0.01) and lower cell apoptosis (P<0.01). The protective effect of U50,488H against SP-induced HUVECs injury was abolished by nor-BNI or L-NAME. CONCLUSIONκ-opioid receptor activation protects HUVECs against SP-induced injury by down-regulation of caveolin-1 and up-regulation of eNOS activity.

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备注/Memo

备注/Memo:
收稿日期：2016-11-09.基金项目：国家自然科学基金项目资助（81270402），陕西省科技统筹创新工程计划项目（2016KTCL03-11），陕西省自然科学基础研究计划（2016JM3022） 通讯作者：裴建明，教授，主要从事心血管生理研究 Email：jmpei8@fmmu.edu.cn 作者简介：杨帆，硕士生 Email:283139896@qq.com 共同第一作者：张淑苗，高级实验师Email：topsniper@126.com
更新日期/Last Update: 1900-01-01