引用本文:王宏1,刘丽2,郭美珺1,刘学永2.黄葵素通过核因子κB信号改善老年糖尿病大鼠心肌缺血再灌注的研究[J].世界中医药,2024,(12):. |
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黄葵素通过核因子κB信号改善老年糖尿病大鼠心肌缺血再灌注的研究 |
Total flavones of Abelmoschus manihot Ameliorate Myocardial Ischemia-reperfusion Injury in Elderly Diabetic Rats via NF-κB Signaling Pathway |
投稿时间:2023-12-13 |
DOI:10.3969/j.issn.1673-7202.2024.12.009 |
中文关键词: 黄葵素 老年糖尿病大鼠 心肌缺血再灌注 心肌损伤 心功能 氧化应激 凋亡 核因子κB信号通路 |
English Keywords:Total flavones of Abelmoschus manihot Elderly diabetic rats Myocardial ischemia-reperfusion Myocardial injury Cardiac function Oxidative stress Apoptosis Nuclear factor-κB signaling pathway |
基金项目:河北省中医药管理局科研计划项目(2022289) |
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中文摘要: |
目的:探讨黄葵素对糖尿病心肌缺血再灌注老年大鼠的影响及其作用机制。方法:将老年大鼠按照简单随机法分为假手术组(只穿线不结扎)、模型组(构建糖尿病心肌缺血再灌注模型)、黄葵素低剂量组(75 mg/kg的黄葵素)、黄葵素高剂量组(150 mg/kg的黄葵素)、抑制剂组(10 mg/kg的核因子κB抑制剂BAY11-7082),高剂量+抑制剂组(150 mg/kg的黄葵素+10 mg/kg BAY11-7082)。观察比较大鼠心功能指标、心肌梗死面积、血清指标含量、心肌细胞凋亡率、心肌组织相关蛋白表达。结果:与模型组比较,黄葵素低剂量、黄葵素高剂量组、抑制剂组、高剂量+抑制剂组大鼠心肌梗死面积、心肌肌钙蛋白T(cTnT)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、丙二醛(MDA)、原位末端转移酶标记法(Tunel)阳性细胞率、磷酸化核因子κB(p-NF-κB p65)、裂解胱天蛋白酶-3(Cl-caspase-3)、Bcl-2相关X蛋白(Bax)水平均显著降低(均P<0.05),左室射血分数(LVEF)、核因子κB抑制蛋白(IκBα)、B淋巴细胞瘤-2基因(Bcl-2)水平均显著升高(均P<0.05);与高剂量组比较,高剂量+抑制剂组大鼠心肌梗死面积、cTnT、CK-MB、LDH、MDA、Tunel阳性细胞率、p-NF-κB p65、Cl-caspase-3、Bax水平均显著降低(均P<0.05),LVEF、IκBα、Bcl-2水平均显著升高(均P<0.05)。结论:黄葵素可能通过调节核因子κB信号抑制心肌细胞凋亡、氧化应激改善糖尿病心肌缺血再灌注老年大鼠心功能。 |
English Summary: |
To investigate the effects of total flavones of Abelmoschus manihot(TFA) on myocardial ischemia-reperfusion injury in elderly diabetic rats and reveal the potential mechanism.Methods:The simple random method was used to assign elderly rats into sham(threading without ligature),model(diabetic myocardial ischemia-reperfusion),low-and high-dose(75 and 150 mg/kg,respectively) TFA,inhibitor [10 mg/kg nuclear factor κB(NF-κB) inhibitor BAY11-7082],and high-dose TFA+inhibitor(150 mg/kg TFA+10 mg/kg BAY11-7082) groups.The cardiac function indicators,myocardial infarction area,serum levels of indicators,apoptosis rate of myocardial cells,and expression of related proteins in the myocardial tissue were observed and compared.Results:Compared with the model group,the low-and high-dose TFA,inhibitor,and high-dose TFA+inhibitor groups showed reduced myocardial infarction area,lowered levels of cardiac troponin T(cTnT),creatine kinase isoenzyme MB(CK-MB),lactate dehydrogenase(LDH),and malondialdehyde(MDA),decreased positive rate of TdT-mediated dUDP nick end labeling(Tunel),and downregulated protein levels of phosphorylated NF-κB p65(P-NF-κB p65),cleaved cysteine aspartate proteinase-3(Cl-caspase-3) and B-cell lymphoma 2(Bcl-2)-associated X protein(Bax)(all P<0.05).Meanwhile,these groups showcased increased left ventricular ejection fraction(LVEF) and upregulated protein levels of nuclear factor κB inhibitory protein(IκBα) and Bcl-2(all P<0.05).Compared with the high-dose TFA group,the high-dose TFA+inhibitor group presented decreased myocardial infarction area,lowered levels of cTnT,CK-MB,LDH,and MDA,reduced Tunel positive cell rate,downregulated protein levels of p-NF-κB p65,Cl-caspase-3,and Bax(all P<0.05),increased LVEF,and upregulated protein levels of IκBα and Bcl-2(all P<0.05).Conclusion:TFA may inhibit myocardial apoptosis and oxidative stress and improve the cardiac function in elderly diabetic rats with myocardial ischemia-reperfusion by regulating the NF-κB signaling pathway. |
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