Effects and Mechanism of Jiedu Tongluo Formula on Myocardial Fibrosis in Rats
Objective:To explore the effect and mechanism of Jiedu tongluo formula on isoprenaline(ISO)-induced myocardial fi-brosis in rats based on oxidative stress and NF-κB.Methods:The male Wistar rats were randomly divided into normal control group,model group,captopril(5 mg/kg)positive control group,Jiedu tongluo formula low(1.8g/kg),medium(3.6 g/kg)and high(7.2 g/kg)dose groups.Except for the normal control group,the rat myocardial fibrosis model was established by subcutaneous injection of ISO(5 mg/kg/d)for 7 days.Intragastric administration was started on the second day after successful modeling and continued for 28 days.HE staining and Masson staining were used to observe the pathological changes of myocardial tissue and collagen fiber deposition.The ex-pression of ROS in myocardial tissue was observed by DHE staining.The level of HYP in myocardial tissue of rats was detected by alka-line water method.Serum LDH and CK-MB levels were detected by Elisa.The oxidative stress indexes in serum and myocardial tissue of rats were detected by the kit.The expressions of NF-κBP65,TGF-β,,CTGF mRNA and proteins,Smad2/3,Collagen Ⅰ,Collagen Ⅲ pro-teins in myocardial tissue of rats were detected by qPCR and Western Blot.Results:Compared with model group,the myocardial struc-ture disorder and collagen fiber deposition were improved in eaeh administration group.ROS in rat myocardium and the cardiac index,myocardial injury markers LDH,CK-MB levels were significantly decreased,the SOD,GSH levels in rat serum and myocardium were significantly increased,MDA level was significantly decreased.The expressions of NF-κBP65,TGF-β1,CTGF mRNA and proteins and Smad 2/3,Collagen Ⅰ,Collagen Ⅲ proteins were significantly decreased.Conclusion:Jiedu tongluo formula can effectively relieve myo-cardial structure disorder and interstitial collagen fibrotic deposition induced by ISO-induced myocardial fibrosis in rats,and its mecha-nism may be related to anti-oxidative stress and inhibition of NF-κB signaling pathway.
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