天然产物研究与开发 ›› 2024, Vol. 36 ›› Issue (8): 1401-1408.doi: 10.16333/j.1001-6880.2024.8.014

• 开发研究 • 上一篇    下一篇

原花青素对大鼠运动性心肌损伤的保护作用及机制研究

任   鹏1,林丹丹2,聂   煜3,王一峰4,董诗稳1*,王博源1*   

  1. 1玉溪师范学院体育学院,玉溪 653100;2云南农业大学;3云南财经大学,昆明 650500;4长春科技学院军事体育部,长春 130600
  • 出版日期:2024-08-28 发布日期:2024-08-29
  • 基金资助:
    云南省教育厅科学研究基金(2023J0995)

Protective effect of oligomeric proanthocyanidins on the exercise-induced myocardial injury in rat and its mechanism

REN Peng1,LIN Dan-dan2,NIE Yu3,WANG Yi-feng4,DONG Shi-wen1 *,WANG Bo-yuan1 *   

  1. 1School of Physical Education,Yuxi Normal University,Yuxi 653100,China;2Yunnan Agricultural University;3Yunnan University of Finance and Economics,Kunming 650500,China;4Departmtent of Military Physical Education ,Changchun Sci-Tech University,Changchun 130600,China
  • Online:2024-08-28 Published:2024-08-29

摘要:

该文研究了原花青素(oligomeric proanthocyanidins,OP)对长时间、大强度运动导致的心肌损伤的保护作用及其潜在机制。Wistar大鼠进行连续6周过量游泳运动训练,其中2组大鼠每天分别灌胃50 mg/kg OP(OP50组)和100 mg/kg OP(OP100组),模型组(model,Mod)灌胃等体积生理盐水,正常组(normal,Nor)作为对照。结果表明,Mod组血清中运动性心肌损伤标记物乳酸脱氢酶(lactate dehydrogenase,LDH)、肌酸激酶(creatine kinase,CK)及心肌肌钙蛋白I(cardiac troponin,cTnI)显著升高,心肌组织出现明显病理形态,呈现明显炎性细胞浸润;OP50及OP100组中LDH、CK及cTnI显著下调,心肌组织病理变化明显减轻(P<0.05)。心肌组织中,Mod组丙二醛(malondialdehyde,MDA)明显上升,抗氧化物酶谷胱甘肽(glutathione,GSH)及超氧化物歧化酶(superoxide dismutase,SOD)下降,核因子E2相关因子2(nuclear factor erythroid-2 related factor 2,Nrf2)/血红素加氧酶-1(hemeoxygenase-1,HO-1)(Nrf2/HO-1)抗氧化应激信号通路中关键蛋白的表达量显著下降;OP50及OP100组中MDA含量显著下调,GSH及SOD显著上调,Nrf2/HO-1通路中蛋白表达量显著增多(P<0.05)。Mod组血清及心肌中炎症指标肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)和白细胞介素-1β(interleukin-1β,IL-1β)含量明显上升,硫氧还蛋白互作蛋白/NOD样受体热蛋白结构域相关蛋白3(thioredoxin-interacting protein/NOD-like receptor thermal protein domain associated protein 3,TXNIP/NLRP3)炎症反应信号通路中关键蛋白的表达量显著上升;OP50及OP100组中炎症因子含量均显著下调,OP100组中TXNIP/NLRP3通路中蛋白表达量显著降低(P<0.05)。综上所述,补充OP对大鼠运动性心肌损伤具有明显的保护作用,且这种保护机制与增强心肌Nrf2/HO-1抗氧化通路及抑制TXNIP/NLRP3炎症反应信号通路有关。

关键词: 原花青素, 运动性心肌损伤, 氧化应激, Nrf2/HO-1抗氧化通路, 炎症反应, TXNIP/NLRP3促炎通路

Abstract:

The protective effects of oligomeric proanthocyanidins (OP) on myocardial injury induced by long-time and intensive exercise and its potential mechanisms were investigated in this study.Wistar rats were subjected to six consecutive weeks of excessive swimming exercise training,in which two groups were gavaged with 50 mg/kg OP (OP50 group) and 100 mg/kg OP (OP100 group) daily,respectively,the model group (Mod) received an equal volume of saline,and the normal group (Nor) was used as control.Results showed that the serum levels of lactate dehydrogenase (LDH),creatine kinase (CK) and cardiac troponin (cTnI),the common markers of exercise-induced myocardial injury,were significantly elevated in the Mod group,and myocardial tissues showed obvious pathological morphology,and a marked inflammatory cell infiltration.In the OP50 and OP100 groups,LDH,CK and cTnI were significantly down-regulated,and the pathological changes in myocardial tissue were significantly reduced (P<0.05).In the Mod group,malondialdehyde (MDA) increased significantly in the myocardial tissues,the antioxidant enzymes glutathione (GSH) and superoxide dismutase (SOD) decreased,and the nuclear factor E2 related factor 2 (Nrf2) / heme oxygenase-1 (HO-1) (Nrf2/HO-1) signaling pathway was inhibited.In the OP50 and OP100 groups,the level of GSH and SOD was significantly up-regulated,and the expression of proteins in the Nrf2/HO-1 pathway was significantly increased (P<0.05).The levels of inflammatory indicators,tumor necrosis factor-α(TNF-α),interleukin-6 (IL-6) and interleukin-1β (IL-1β),were significantly increased in the Mod group,and the expression of key proteins in the thioredoxin-interacting protein/NOD-like receptor thermal protein domain associated protein 3 (TXNIP/NLRP3) inflammatory response signaling pathway was significantly increased.The levels of the inflammatory factors were significantly down-regulated in both the OP50 and OP100 groups,and the expression of proteins in the TXNIP/NLRP3 pathway was significantly decreased in the OP100 group (P<0.05).In summary,OP supplementation has a significant protective effect on exercise-induced myocardial injury in rats,and this protective mechanism is involved in enhancing the myocardial Nrf2/HO-1 antioxidant pathway and inhibiting the TXNIP/NLRP3 inflammatory response signaling pathway.

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中图分类号:  R873