荭草素通过激活PGC-1β发挥抗糖尿病心肌病作用

Orientin protect against diabetic cardiomyopathy via activating PGC-1β

目的探究外源补充荭草素(Orientin)对链脲佐菌素(STZ)诱导的糖尿病心肌损伤是否发挥保护作用及其分子机制。方法腹腔注射STZ构建C57BL/6J小鼠糖尿病模型(DCM组),DCM+orientin组小鼠除腹腔注射STZ外,每天通过口服灌胃方式外源补充荭草素,8周后超声心动图检测各组小鼠左心室心脏功能。HE染色观察左室心肌组织,用RT-qPCR法检测心肌氧化应激相关分子mRNA的表达。给予H9C2细胞高糖培养,外源给予荭草素观察其对心肌细胞炎症和氧化应激的影响。Western-blot检测各组PGC-1β信号通路的影响。结果8周后DCM组小鼠左室心肌较对照组显著肥厚,纤维化加重,心功能显著下降,氧化应激加重,而DCM+orientin组小鼠能够显著改善上述病变,且外源补充orientin能够显著升高心肌组织中PGC-1β的表达,且外源给予荭草素能够显著减轻高糖诱导的心肌细胞氧化应激损伤。结论荭草素能够通过激活PGC-1β在小鼠糖尿病心肌病模型中发挥抗氧化应激作用,从而减轻心肌损伤。

Objective To investigate whether exogenous supplementation of orientin had protective effects on streptozotocin(STZ)induced diabetic myocardial injury and its molecular mechanism.Methods C57 BL/6 J mouse model of diabetes mellitus(DCM group)was established by intraperitoneal injection of STZ.The mice in the DCM+orientin group were treated with oral administration of orientin by oral gavage every day except for intraperitoneal injection of STZ.Eight weeks later,echocardiography was used to detect left ventricular function of each group.Left ventricular myocardial tissue was observed by hematoxylin and eosin(HE)staining,and the expression of myocardial oxidative stress-related molecular mRNA was detected by RT-qPCR.H9 C2 cells were cultured in high glucose medium,and the effect of exogenously administered orientin on myocardial cell inflammation and oxidative stress was observed.Western-blot was used to detect the effects of PGC-1βsignaling pathways in each group.Results After 8 weeks,the left ventricular myocardium of the DCM group was significantly hypertrophic compared with the control group,the fibrosis was aggravated,the cardiac function was significantly decreased,and the oxidative stress was aggravated.The DCM+orientin group could significantly improve the lesions above.The exogenous supplement of orientin could significantly increase the expression of PGC-1βin myocardial tissue,and alleviate oxidative stress induced by high glucose.Conclusion Orientin can reduce myocardial damage by activating PGC-1βin a mouse model of diabetic cardiomyopathy.