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异常黑胆质成熟剂治疗下抑制核因子κB通路可保护大鼠心肌缺血/再灌注损伤

Inhibition of nuclear factor kappa B pathway protects myocardial ischemia/reperfusion injury in rats under treatment with abnormal savda munziq.

作者信息

Maimaitiaili Abudunaibi, Li Junhong, Aibibula Aili, Abudureheman Mulati

机构信息

Department of Cardiac Surgery, The First Affiliated of Xinjiang Medical UniversityUrumqi 830011, P. R. China.

出版信息

Am J Transl Res. 2018 Jan 15;10(1):77-85. eCollection 2018.

Abstract

OBJECTIVE

Uighur medicine Fufang Munziq granule (Munziq) [corrected] shows cardioprotective effect in myocardial ischemia/reperfusion injury (IRI) in animal models, but the molecular mechanism of this effect is not clear. The present study investigates the regulation of nuclear factor kappa B (NF-kappa B) pathway by Fufang Munziq granule (Munziq) in IRI rat models.

METHODS

Male Sprague-Dawley rats were divided into three groups: the NF-κB gene knockout group (n = 5); the NF-κB transgenic group (n = 8); and the control group (n = 5). All rats were treated with Fufang Munziq granule (Munziq) [corrected] for 21 days before underwent IRI surgical procedure. Blood and tissue samples were collected for the RT-PCR, ELISA, western blot and other examination.

RESULTS

Expression of NF-κB p65mRNA and protein were down-regulated in the NF-κB knockout rats but up-regulated in the transgenic rats comparing with the controls (P<0.05). The upstream NF-κB kinase expressions, the downstream inflammatory cytokines, and the myocardial injury markers were all changed in accordance with the NF-κB gene modification (all values <0.05). AMSq treatment relieved IRI in the NF-κB knockout rats.

CONCLUSION

Inhibition on NF-κB signaling pathway may alleviate IRI in rats under Fufang Munziq granule (Munziq) [corrected] treatment.

摘要

目的

维吾尔药复方木尼孜其颗粒(木尼孜其)在动物模型的心肌缺血/再灌注损伤(IRI)中显示出心脏保护作用,但其作用的分子机制尚不清楚。本研究探讨复方木尼孜其颗粒(木尼孜其)对IRI大鼠模型中核因子κB(NF-κB)信号通路的调控作用。

方法

将雄性Sprague-Dawley大鼠分为三组:NF-κB基因敲除组(n = 5);NF-κB转基因组(n = 8);对照组(n = 5)。所有大鼠在接受IRI手术前均用复方木尼孜其颗粒(木尼孜其)治疗21天。采集血液和组织样本进行RT-PCR、ELISA、western blot等检测。

结果

与对照组相比,NF-κB基因敲除大鼠中NF-κB p65mRNA和蛋白表达下调,而转基因大鼠中表达上调(P<0.05)。上游NF-κB激酶表达、下游炎性细胞因子和心肌损伤标志物均随NF-κB基因改变而变化(所有P值<0.05)。木尼孜其治疗可减轻NF-κB基因敲除大鼠的IRI。

结论

抑制NF-κB信号通路可能减轻复方木尼孜其颗粒(木尼孜其)治疗下大鼠的IRI。

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