Regulation Mechanism of Shanjing Capsule on NF-B Signal Pathway in Myocardial Ischemia Rats

YU Dong-hua; LIU Shu-min; Wang Xiao-yang; DONG Pei-liang; ZHANG Ning; YU Chun-miao

doi:10.13422/j.cnki.syfjx.2017110151

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Regulation Mechanism of Shanjing Capsule on NF-B Signal Pathway in Myocardial Ischemia Rats

更新时间：2024-01-04

- Regulation Mechanism of Shanjing Capsule on NF-B Signal Pathway in Myocardial Ischemia Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 23, Issue 11, Pages: 151-157(2017)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2017110151
  CLC： R285.5
- Published：2017
- 稿件说明：
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YU Dong-hua, LIU Shu-min, Wang Xiao-yang, et al. Regulation Mechanism of Shanjing Capsule on NF-B Signal Pathway in Myocardial Ischemia Rats[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(11): 151-157.
DOI：

YU Dong-hua, LIU Shu-min, Wang Xiao-yang, et al. Regulation Mechanism of Shanjing Capsule on NF-B Signal Pathway in Myocardial Ischemia Rats[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(11): 151-157. DOI： 10.13422/j.cnki.syfjx.2017110151.

摘要

目的：探讨山精胶囊对心肌缺血大鼠能量代谢、氧自由基及细胞凋亡相关基因的作用及其机制。方法：选取Wista大鼠采用冠状动脉结扎法，建立慢性心肌缺血模型。将筛选出来的大鼠随机分为山精胶囊低、中、高剂量组（283.5，850.5，1 701.0 mg·kg-1）和阳性药组（心安胶囊324.0 mg·kg-1），假手术组和模型组灌胃给予同等剂量的0.9%的氯化钠注射液，给药10 d。紫外可见分光光度计检测血清及组织中乳酸（LD），游离脂肪酸（NEFA），丙二醛（MDA），超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GSH-Px），一氧化氮（NO）及三磷酸腺苷酶（ATP）水平；蛋白质免疫印迹（Western blot）法及逆转录聚合酶链反应（RT-PCR）法检测心肌组织中核转录因子-κB（NF-κB），半胱氨酸蛋白酶-3（Caspase-3），B细胞淋巴瘤/白血病-2（Bcl-2）及Bcl-2相关X蛋白（Bax）蛋白表达。结果：与假手术组比较，模型组大鼠LD，NEFA，MDA明显升高（P<0.05），NO，Na+-K+-ATP，Ca2+-ATP酶，SOD，GSH-Px明显降低（P<0.05），心肌NF-κB，Caspase-3，Bax mRNA及蛋白表达明显上调（P<0.05），Bcl-2 mRNA及蛋白表达明显下调（P<0.05）；与模型组比较，山精胶囊能显著降低LD，NEFA，MDA（P<0.05），NO，Na+-K+-ATP，Ca2+-ATP酶，SOD，GSH-Px显著升高（P<0.05），明显下调NF-κB，Caspase-3，Bax mRNA及蛋白表达（P<0.05），明显上调Bcl-2的mRNA及蛋白表达（P<0.05）。结论：山精胶囊可能通过调控NF-κB信号通路，提高心肌缺血大鼠清除氧自由基能力，改善心肌细胞能量代谢，调节凋亡相关蛋白和基因的表达，从而抑制了心肌细胞凋亡，减少缺血缺氧对心肌细胞的病理损害，起到保护心肌的作用。

Abstract

Objective: To explore the effect and mechanism of Shanjing capsule on energy metabolism

oxyradical and apoptosis-related genes in myocardial ischemia rats. Method: The chronic myocardial ischemia models were established with ligating coronary artery. Then the modeled rats were randomly divided into Shanjing capsule low dose

middle dose and high dose groups (283.5

850.5

1 701.0 mg·kg-1)

positive drug group (324.0 mg·kg-1). The rats in sham operation group and model group received equivalent amount of 0.9% Sodium Chloride Injection for 10 days. Then ultraviolet visible spectrophotometer was used to detect the content and activity of lactic acid (LD)

free fatty acids (NEFA)

malondialdehyde (MDA)

total superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px)

NO and ATP in serum and tissues. The expression levels of nuclear transcription factor-κB (NF-κB)

Caspase-3

B-cell lymphoma/leukemia-2(Bcl-2) and Bcl-2 associated X protein(Bax) in myocardial tissues were detected by Western blot and RT-PCR. Result: As compared with the sham operation group

contents of LD

NEFA

MDA were increased (P<0.05); levels of NO

Na+-K+-ATP

Ca2+-ATP enzyme

SOD and GSH-Px were decreased (P<0.05); the mRNA and protein expression of NF-κB

Caspase-3 and Bax in cardiomyocytes were up-regulated significantly (P<0.05)

while the mRNA and protein expression of Bcl-2 was decreased (P<0.05) in model group. As compared with the model group

Shanjing capsules could decrease the contents of LD

NEFA

MDA (P<0.05)

increase the levels of NO

Na+-K+-ATP

Ca2+-ATP enzyme

SOD and GSH-Px (P<0.05)

significantly down-regulate the mRNA and protein expression levels of NF-κB

Caspase-3

Bax in cardiomyocytes (P<0.05)

and up-regulate the mRNA and protein expression of Bcl-2 (P<0.05). Conclusion: Shanjing capsule could increase the ability of antioxidant and oxygen free radical scavenging in myocardial ischemia rats

improve energy metabolism of cardiomyocyte

regulate the expression of apoptosis related protein and genes by regulating the NF-κB signal pathway

which plays a role in myocardial preservation by inhibiting cardiomyocyte apoptosis and decreasing pathological lesion under cardiomyocyte ischemia and anoxia.

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