Mechanism of Total Flavonoids from Jinhe Yangxin Prescription on Myocardial Ischemia Injury Based on Oxidative Stress and NLRP3 Inflammasome

CHENG Yan-gang; LI Guo-yan; LIU Yan; ZHAO Jian-bin; LI Fei-he; LI Hui-feng; TAN Jin-yan; YANG Bing-you; PEI Miao-rong

doi:10.13422/j.cnki.syfjx.20181728

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Mechanism of Total Flavonoids from Jinhe Yangxin Prescription on Myocardial Ischemia Injury Based on Oxidative Stress and NLRP3 Inflammasome

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- Mechanism of Total Flavonoids from Jinhe Yangxin Prescription on Myocardial Ischemia Injury Based on Oxidative Stress and NLRP3 Inflammasome
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 18, Pages: 93-100(2018)
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- DOI：10.13422/j.cnki.syfjx.20181728
  CLC： R285.5
- Published：2018
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CHENG Yan-gang, LI Guo-yan, LIU Yan, et al. Mechanism of Total Flavonoids from Jinhe Yangxin Prescription on Myocardial Ischemia Injury Based on Oxidative Stress and NLRP3 Inflammasome[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(18): 93-100.
DOI：

CHENG Yan-gang, LI Guo-yan, LIU Yan, et al. Mechanism of Total Flavonoids from Jinhe Yangxin Prescription on Myocardial Ischemia Injury Based on Oxidative Stress and NLRP3 Inflammasome[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(18): 93-100. DOI： 10.13422/j.cnki.syfjx.20181728.

摘要

目的：研究锦鹤养心方总黄酮提取物对盐酸异丙肾上腺素（ISO）诱导的小鼠心肌缺血损伤保护作用，并初步探讨其作用机制。方法： 108只SPF级KM小鼠随机分为正常组，模型组，阳性药组（盐酸普萘洛尔，33 mg·kg-1），总黄酮提取物高、中、低剂量组（4.4，2.2，1.1 g·kg-1），给药组连续给药7 d，各组于第5天开始，除正常组外，其余各组小鼠均于给药1 h后皮下注射ISO 20 mg·kg-1，正常组小鼠皮下注射等剂量生理盐水，连续注射3 d，制备心肌缺血模型。造模24 h后取材，记录各组小鼠第1次注射ISO前及最后1次注射24 h后心电图；测定各组小鼠的心脏指数；用2，3，5-氯化三苯基四氮唑（TTC）染色法测定心肌缺血面积；试剂盒检测血清中肌酸激酶同工酶（CK-MB），心肌钙蛋白I （cTnI），乳酸脱氢酶（LDH），丙氨酸氨基转移酶（ALT），天门冬氨酸氨基转移酶（AST），超氧化物歧化酶（SOD），丙二醛（MDA），白细胞介素-6（IL-6），肿瘤坏死因子-α（TNF-α），白细胞介素-1β（IL-1β）的含量；苏木素-伊红（HE）染色观察心肌组织病理形态学变化；蛋白免疫印迹法（Western blot）测定小鼠心肌组织核苷酸结合寡聚化结构域样受体蛋白3（NLRP3），凋亡相关斑点样蛋白（ASC）和半胱氨酸天冬氨酸蛋白酶-1（Caspase-1）蛋白的表达。结果：与正常组比较，模型组小鼠Ⅱ导联心电图ST段位移增加（P<0.01），血清CK-MB，cTnI，ALT，AST，LDH，MDA，IL-6，TNF-α，IL-1β含量及心脏指数水平显著升高，SOD的含量显著降低（P<0.01），心肌缺血面积显著增加（P<0.01），心肌组织损伤明显，NLRP3，ASC，Caspase-1蛋白表达显著升高（P<0.01）；与模型组比较，锦鹤养心方总黄酮各剂量组小鼠Ⅱ导联心电图ST段位移降低（P<0.05，P<0.01），血清CK-MB，cTnI，ALT，AST，LDH，MDA，IL-6，TNF-α，IL-1β含量及心脏指数水平降低，SOD的含量升高（P<0.05，P<0.01），心肌缺血面积降低（P<0.05，P<0.01），心肌缺血损伤明显减轻，NLRP3，ASC，Caspase-1蛋白表达降低（P<0.05，P<0.01）。结论：锦鹤养心方总黄酮对心肌缺血损伤具有保护作用，且呈现一定的量效关系，该作用可能与提高机体抗氧化活性，减少氧化应激损伤，抑制NLRP3炎性小体活化有关。

Abstract

Objective: To investigate the underlying mechanism of the total flavonoids from Jinhe Yangxin prescription (FJYP) on myocardial ischemia (MI) injury induced by isoproterenol (ISO) in mice. Method: Totally 108 SPF KM mice were randomly divided into blank group

model group

positive group (propranolol hydrochloride

33 mg·kg-1)

high-dose FJYP group (4.4 g·kg-1)

middle-dose FJYP group (2.2 g·kg-1)

and low-dose FJYP group (1.1 g·kg-1). All mice were administrated with drugs for 7 days

except for the blank group. All mice were injected subcutaneously with ISO on the 5th

6th and 7th day to establish the MI model. The electrocardiogram test was conducted in anesthetized mice before the first injection and after the final injection with ISO. The heart weight index (HWI) was determined. Triphenyltetrazolium chloride(TTC)staining was performed to determine the area of MI. Creatine kinase isoenzyme MB(CK-MB)

cardiac troponin I(cTnI)

lactate dehydrogenase(LDH)

alanine aminotransferase(ALT)

aspartate aminotransferase(AST)

superoxide dismutase(SOD)

malondialdehyde(MDA)

interleukin-6(IL-6)

tumor necrosis factor-α(TNF-α) and IL-1β levels in serum were measured using commercial kits

and the pathological changes of myocardial tissues were observed by hematoxylin-eosin (HE) staining. Western blot analysis was used to detect the expression levels of nucleotide binding oligomeric domain-like receptor protein 3(NLRP3)

apoptosis related speckle(ASC)

Caspase-1. Result: Compared with the blank group

ST-segment was significantly elevated in model group (P<0.01). The heart weight index

CK-MB

cTnI

ALT

AST

LDH

MDA

IL-6

TNF-α and IL-1β in serum were significantly increased

and serum SOD activity was significantly decreased (P<0.01); the MI area was increased (P<0.01). The expression levels of NLRP3

ASC

Caspase-1 were all increased (P<0.01). Compared with the model group

FJYP could effectively decrease the change of ST-segment (P<0.05

P<0.01). The heart weight index

CK-MB

cTnI

ALT

AST

LDH

MDA

IL-6

TNF-α

IL-1β and the MI area of mice decreased

while the serum SOD content increased (P<0.05

P<0.01); and the pathological damages induced by ISO were significantly alleviated in FJYP treatment group; and the expression levels of NLRP3

ASC

Caspase-1 were also decreased (P<0.05

P<0.01). Conclusion: FJYP plays a protective role in myocardial ischemia in mice

the protective effect and mechanism may be related to increase of antioxidant ability

reduction of oxidant damage and inhibition of the NLRP3 inflammasome activation.

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