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OA北大核心CHSSCDCSTPCD
Total flavones of Abelmoschus manihot Ameliorate Myocardial Ischemia-reperfusion Injury in Elderly Diabetic Rats via NF-κB Signaling Pathway
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.
Objective: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 in-dicators,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 re-duced myocardial infarction area,lowered levels of cardiac troponin T(cTnT),creatine kinase isoenzyme MB(CK-MB),lactate de-hydrogenase(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 ven-tricular 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 ar-ea,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.
王宏;刘丽;郭美珺;刘学永
河北燕达医院老年病科,廊坊,065201京东誉美中西医结合肾病医院肾内科,廊坊,065201
中医学
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
Total flavones of Abelmoschus manihotElderly diabetic ratsMyocardial ischemia-reperfusionMyocardial injuryCardiac functionOxidative stressApoptosisNuclear factor-κB signaling pathway
《世界中医药》 2024 (012)
1766-1771 / 6
河北省中医药管理局科研计划项目(2022289)
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