Effect of Resveratrol in Regulating TRPC1/STIM1-mediated SOCC to Inhibit Atherosclerosis

LIU Hai-mei; YAN Fu-man; XU Jin-wen; ZHOU Le-quan; WU Zhi-xue; ZHANG Ren; LIU Na

doi:10.13422/j.cnki.syfjx.2018040096

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Effect of Resveratrol in Regulating TRPC1/STIM1-mediated SOCC to Inhibit Atherosclerosis

更新时间：2024-01-04

- Effect of Resveratrol in Regulating TRPC1/STIM1-mediated SOCC to Inhibit Atherosclerosis
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 4, Pages: 96-102(2018)
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- DOI：10.13422/j.cnki.syfjx.2018040096
  CLC： R285.5
- Published：2018
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LIU Hai-mei, YAN Fu-man, XU Jin-wen, et al. Effect of Resveratrol in Regulating TRPC1/STIM1-mediated SOCC to Inhibit Atherosclerosis[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(4): 96-102.
DOI：

LIU Hai-mei, YAN Fu-man, XU Jin-wen, et al. Effect of Resveratrol in Regulating TRPC1/STIM1-mediated SOCC to Inhibit Atherosclerosis[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(4): 96-102. DOI： 10.13422/j.cnki.syfjx.2018040096.

摘要

目的：研究白藜芦醇通过调节瞬时受体电位通道蛋白1（transient receptor potential channel protein 1，TRPC1）及基质交互分子1（stromal interaction molecule 1，STIM1）介导的钙库操纵性钙通道（store-operated calcium channel，SOCC）发挥抗动脉粥样硬化（atherosclerosis，AS）的具体机制。方法：雌性C57BL/6J小鼠卵巢去势后高脂饮食建立AS模型，分为空白组，模型组，白藜芦醇低、中、高剂量组（50，100，150 mg·kg-1），雌激素组（0.3 mg·kg-1）。高脂喂养16周后，收集血清检测各组小鼠血清中血脂4项及Ca2+水平；油红O染色从形态学观察动脉粥样硬化斑块形成；蛋白免疫印迹法（Western blot）检测小鼠胸主动脉TRPC1，STIM1及内皮型一氧化氮合成酶（endothelial nitric oxide synthase，eNOS）蛋白表达水平；实时荧光定量PCR法（Real-time PCR）检测小鼠胸主动脉血管中TRPC1与STIM1 mRNA信号表达。结果：与模型组相比，白藜芦醇高剂量组及雌激素组小鼠血清总胆固醇（TC），甘油三酯（TG），低密度脂蛋白（LDL）均降低（P<0.05），但高密度脂蛋白表达（HDL）升高，血清Ca2+浓度下降；油红O染色提示，与空白组相比，模型组AS病理改变明显，内膜增厚，不完整，连续性被破坏，有较明显的脂质斑块；补充白藜芦醇或雌激素后，动脉管壁AS病理改变明显减轻，脂滴明显减少。Western blot结果显示，补充白藜芦醇中、高剂量及雌激素后，与模型组相比，TRPC1与STIM1蛋白表达明显减少，而eNOS蛋白表达增加（P<0.05）；通过Real-time PCR检测发现，与模型组相比，白藜芦醇中、高剂量组及雌激素组TRPC1与STIM1 mRNA基因表达的水平明显降低（P<0.05）。结论：白藜芦醇可通过下调TRPC1及STIM1基因表达及蛋白水平，抑制SOCC介导的Ca2+内流，增加eNOS蛋白表达及活性，发挥抗动脉粥样硬化的作用。

Abstract

Objective: To study the anti-atherosclerosis (AS) mechanism of resveratrol (RES) by regulating store-operated calcium channel (SOCC) induced by transient receptor potential channel protein 1 (TRPC1) and stromal interaction molecule 1 (STIM1). Method: Atherosclerosis model was established with female C57BL/6J mice that were fed with high-fat diet after ovariectomy

and then the mice were divided into control group

model group

low-dose resveratrol group

medium-dose resveratrol group

high-dose resveratrol group(50

100

150 mg·kg-1) and estradiol (E2) group(0.3 mg·kg-1). After 16 weeks

serum was collected

and the lipid level and Ca2+ concentration were detected. The morphological changes were measured by oil red O staining. The protein expressions of TRPC1

STIM1 and endothelial nitric oxide synthase (eNOS) were detected by Western blot and Real-time PCR. The activity of eNOS was measured by enzyme-linked immunosorbent assay(ELISA). Result: Compared with model group

total cholesterol(TC)

triglyceride(TG)

low density lipoprotein(LDL) were decreased

while the high density lipoprotein(HDL) was increased in supplementary high-dose resveratrol or estrogen groups (P<0.05). The pathological changes in the model group were obvious compared with control group

after supplementation with RES or estrogen

the pathological changes were significantly reduced in thoracic aorta. Western blot and Real-time PCR results showed that in model group

the protein expressions of TRPC1 and STIM1 were increased

while the protein expression of eNOS was decreased (P<0.05); in supplementary high-dose resveratrol or estrogen group

these changes were reversed (P<0.05). Conclusion: RES could down-regulate TRPC1 and STIM1 gene and protein expressions

inhibit SOCC-mediated Ca2+ influx

increase eNOS expression and resist atherosclerosis.

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