[1]严宁,杨春霞,马娟,等.β-谷甾醇对大鼠心肌缺血再灌注损伤和ERK1/2信号通路的影响[J].心血管病学进展,2020,(3):321-325.[doi:10.16806/j.cnki.issn.1004-3934.2020.03.026]
 YAN Ning,YANG Chunxia,MA Juan,et al.Effects of -sitosterolon Myocardial Ischemia-reperfusion Injury and ERK1/2 Signaling Pathway in Rats[J].Advances in Cardiovascular Diseases,2020,(3):321-325.[doi:10.16806/j.cnki.issn.1004-3934.2020.03.026]
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β-谷甾醇对大鼠心肌缺血再灌注损伤和ERK1/2信号通路的影响()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年3期
页码:
321-325
栏目:
论著
出版日期:
2020-03-25

文章信息/Info

Title:
Effects of -sitosterolon Myocardial Ischemia-reperfusion Injury and ERK1/2 Signaling Pathway in Rats
作者:
严宁13 杨春霞 1 马娟 2 齐国雪 1 杨立波13 马玉茹 1 马学平 1
(1.宁夏医科大学总医院心脏中心,宁夏 银川 7500042.宁夏医科大学研究生院,宁夏 银川 7500043.宁夏血管损伤与修复研究重点实验室,宁夏 银川 750004)
Author(s):
YAN Ning13 YANG Chunxia1 MA Juan2 QI Guoxue1 YANG Libo13 MA Yuru1 MA Xueping 1
(1.Department of Internal Medicine,Heart Centre,General Hospital of Ningxia Medical University, Yinchuan 750004, Ningxia,China 2.Graduate School, Ningxia Medical University,Yinchuan 750004,Ningxia,China3.Ningxia Key Laboratory of Vascular Injury and Repair Research, Ningxia Medical University,Yinchuan 750004, Ningxia,China)
关键词:
β-谷甾醇ERK1/2信号通路氧化应激炎症凋亡
Keywords:
β-sitosterol ERK1/2 signaling pathway Oxidative stress Inflammation Apoptosis
DOI:
10.16806/j.cnki.issn.1004-3934.2020.03.026
摘要:
目的 研究β-谷甾醇对大鼠心肌缺血再灌注损伤和ERK1/2信号通路的影响。方法 30只SD雄性大鼠随机分成3组:假手术组、模型组和β-谷甾醇处理组;采用HE染色观察大鼠心肌组织损伤,监测大鼠心脏指数(CI)、每搏量(SV)及每博指数(SI)等心肌功能指标的变化;采用酶联免疫吸附剂法(ELISA)测定大鼠血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、活性氧(ROS)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、白介素-1β(IL-1β)白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的含量;采用蛋白印记法(Western Blot)检测大鼠心脏组织中细胞外调节蛋白激酶(ERK1/2)、B淋巴细胞瘤-2(Bcl-2)和B淋巴细胞瘤-2结合蛋白X(Bax)的表达。结果 与假手术组相比,模型组大鼠心肌指标CI、SV和SI,血清中SOD水平及心脏组织中Bcl-2的表达均显著下降,血清中MDA、ROS、CK、CK-MB、IL-1β、IL-6、TNF-α和心脏组织中ERK1/2及Bax的表达显著上升(P<0.05);与模型组相比,β-谷甾醇处理组大鼠心肌指标CI、SV和SI,血清中SOD水平及心脏组织中Bcl-2的表达均显著上升,血清中MDA、ROS、CK、CK-MB、IL-1β、IL-6、TNF-α和心脏组织中ERK1/2及Bax的表达显著下降(P<0.05)。结论 β-谷甾醇可保护大鼠心肌缺血再灌注损伤,可能参与ERK1/2信号通路,缓解心肌缺血再灌注大鼠出现的氧化应激和炎症损伤,并抑制其心肌细胞的凋亡。
Abstract:
】Objective To study the effects o f β-sitosterol on myocardial ischemia-reperfusion injury and ERK1/2 signaling pathway in rats. Methods Thirty SD male rats were randomly divided into three groups, including sham operation group, model group and β-sitosterol group.The myocardial tissue injury in rats was observed by HE staining, and the myocardial function indexes of cardiac index (CI), stroke volume(SV) and stroke index(SI) were monitored.The contents of malondialdehyde(MDA),superoxide dismutase(SOD), reactive oxygen species(ROS), creatine kinase(CK), creatine kinase isoenzyme(CK-MB), interleukin-1β(IL-1β), interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) in serum were measured by enzyme-linked immunosorbent assay(ELISA). Western blot was used to detect the expression levels of extracellular regulated protein kinase(ERK1/2), B lymphocytoma-2(Bcl-2) and B lymphocytoma-2 binding protein X(Bax) in cardiac tissues. Results Compared with sham operation group, the myocardial indexes of CI, SV and SI, serum SOD level and Bcl-2 expression in cardiac tissues in model group were significantly decreased, and the levels of serum MDA, ROS, CK, CK-MB, IL-1β, IL-6 and TNF-α and the expression levels of ERK1/2 and Bax in cardiac tissues were significantly increased(P<0.05). Compared with model group, the myocardial indexes of CI, SV and SI, serum SOD level and Bcl-2 expression in cardiac tissues in β-sitosterol group were increased significantly, and the levels of serum MDA, ROS, CK, CK-MB, IL-1β, IL-6 and TNF-α and the expression levels of ERK1/2 and Bax in cardiac tissues were significantly decreased(P<0.05). Conclusions β-sitosterol can protect myocardial ischemia-reperfusion injury in rats, may participate in ERK1/2 signaling pathway, relieve oxidative stress and inflammatory injury in rats with myocardial ischemia-reperfusion, and inhibit the apoptosis of myocardial cells. ___________________________ 通讯作者:马学平,E-mail:2627337387@qq.com

参考文献/References:

[1]王颖. 微小RNA参与心肌缺血再灌注损伤的作用机制及研究进展[J]. 心血管病学进展,2017,38(4):434-438.

[2]Wang EW,Han YY,Jia XS. PAFR-deficiency alleviates myocardial ischemia/reperfusion injury in mice via suppressing inflammation, oxidative stress and apoptosis[J]. Biochem Biophys Res Commun,2018,495(4):2475-2481.

[3] Rajavel T ,Packiyaraj P,Suryanarayanan V,et al. β-Sitosterol targets Trx/Trx1 reductase to induce apoptosis in A549 cells via ROS mediated mitochondrial dysregulation and p53 activation[J]. Sci Rep,2018,8(1):2071.

[4] Liu N,Kong T,Chen X,et al. Ubiquitin-specific protease 14 regulates LPS-induced inflammation by increasing ERK1/2 phosphorylation and NF-κB activation[J]. Mol Cell Biochem,2017,431(1-2):87-96.

[5] Cavalcante R,Sotomi Y,Zeng Y,et al. Coronary bypass surgery versus stenting in multivessel disease involving the proximal left anterior descending coronary artery[J]. Heart,2017,103(6):428-433.

[6] Yao BJ ,He XQ,Lin YH,et al. Cardioprotective effects of anisodamine against myocardial ischemia/reperfusion injury through the inhibition of oxidative stress, inflammation and apoptosis[J]. Mol Med Rep,2018,17(1):1253-1260.

[7] Tocmo R ,Liang D,Lin Y,et al. Chemical and biochemical mechanisms underlying the cardioprotective roles of dietary organopolysulfides[J]. Front Nutr,2015,2:1.

[8] Zhao Q,Liu Z,Huang B,et al. PEDF improves cardiac function in rats subjected to myocardial ischemia/reperfusion injury by inhibiting ROS generation via PEDF R[J]. Int J Mol Med,2018,41(6):3243-3252.

[9] Zhou Z,Ma S,Liu J,et al. Protective effects of endogenous carbon monoxide against myocardial ischemia-reperfusion injury in rats[J] .Sheng Li Xue Bao,2018,70(2):115-122.

[10] Zervou S ,Whittington HJ,Ostrowski PJ,et al. Augmentation of creatine kinase in vitro protects against simulated ischaemia reperfusion injury[J]. Heart,2017,103(5):141-144.

[11] Zhai M,Li B,Duan W,et al. Melatonin ameliorates myocardial ischemia reperfusion injury through SIRT3-dependent regulation of oxidative stress and apoptosis[J]. J Pineal Res,2017,63(2):12419.

[12] Liu H,Jing X,Dong A,et al. Overexpression of TIMP3 protects against cardiac ischemia/reperfusion injury by inhibiting myocardial apoptosis through ROS/Mapks pathway[J]. Cell Physiol Biochem,2017,44(3):1011-1023.

[13] Yuan X,Xiang Y,Zhu N,et al. Salvianolic acid A protects against myocardial ischemia/reperfusion injury by reducing platelet activation and inflammation[J]. Exp Ther Med,2017,14(2):961 -966.

[14] Lim W,Park S,Bazer FW,et al. Apigenin reduces survival of choriocarcinoma cells by inducing apoptosis via the PI3K/AKT and ERK1/2 MAPK pathways[J]. J Cell Phys,2016,231(12):2690-2699.

[15] Fan Y,Yang F,Cao X,et al. Gab1 regulates SDF-1-induced progression via inhibition of apoptosis pathway induced by PI3K/AKT/Bcl-2/BAX pathway in human chondrosarcoma[J]. Tumor Biol,2016,37(1):1141-1149.

备注/Memo

备注/Memo:
收稿日期:2019-11-18 通讯作者:马学平,E-mail:2627337387@qq.com
更新日期/Last Update: 2020-05-20