| Objective: The continuous development of myocardial fibrosis will eventually lead to heart failure,so it is necessary to intervene the process of myocardial fibrosis.Angiotensin Ⅱ(Ang 2)Ang Ⅱ can activate the downstream tyrosine kinase / signal transducer and transcription activator 3(jak/stat3)signaling pathway by activating the inflammatory factor IL-6,which can activate the signal pathway of jak/stat3,which can promote the process of myocardial fibrosis.Therefore,it can be used to regulate jak/stat3,a pathway promoting myocardial fibrosis,to intervene the process of myocardial fibrosis.Sandalwood,a Mongolian medicine,is a common prescription for cardiovascular disease.Previous studies have shown that it can improve ventricular remodeling.However,whether sandalwood can improve myocardial fibrosis by regulating jak/stat3,an important pathway to promote myocardial fibrosis,has not yet been clarified.In this study,we investigate whether Sanwei sandalwood can inhibit myocardial fibrosis in mice induced by Ang Ⅱ by regulating jak/stat3 pathway.Methods:Thirty C57 BL / 6J male mice were randomly divided into three groups:control group,model group and Mongolian medicine + model group.Establishment of myocardial fibrosis model in mice: the control group was subcutaneously implanted with a micro osmotic slow-release pump filled with normal saline,the model group was implanted with a micro osmotic slow-release pump filled with Ang Ⅱ solution,and the Mongolian medicine + model group was implanted with a micro osmotic slow-release pump filled with Ang Ⅱ solution;intervention measures: the control group,the model group and the Mongolian medicine + model group were respectively given water by gavage The mice in each group were intervened by three doses of Mongolian medicine sandalwood extract solution.The systolic blood pressure(SBP)and heart rate(HR)were measured by non-invasive blood pressure instrument before and after modeling.Interventricular septum end diastolic thickness(ivstd),left ventricular posterior wall thickness(lvpwtd),short axis shortening rate(FS),ejection fraction(EF),cardiac output(CO)and other indicators were detected by animal ultrasound.Two weeks later,the mice were killed,and the left ventricle was isolated to obtain serum.The morphological changes of myocardial tissue were observed by hematoxylin eosin staining(H & E).The level of IL-6 in serum was detected by ELISA.The levels of Col I and col in myocardial tissue were detected by Western blot The expression of STAT3 and p-STAT3 in JAK / STAT3 pathway.Results:(1)Before modeling,SBP,ivstd,lvpwtd,HR,EF,FS,Co of the three groups had no statistical difference(P > 0.05);after 2 weeks of modeling,SBP,ivstd,lvpwtd of the control group,model group and Mongolian medicine + model group had statistical difference(P < 0.05).LSD-t pairwise comparison,SBP,ivstd,lvpwtd,control group,model group,Mongolian medicine + model group were statistically significant(P < 0.05).Compared with the control group,SBP,ivstd and lvpwtd of the model group increased;compared with the model group,SBP,ivstd and lvpwtd of the Mongolian medicine + model group decreased.However,there were no significant differences in HR,EF,FS and co among the control group,model group and Mongolian medicine + model group(P > 0.05).(2)The results of H & E staining showed that the myocardial cells in the control group had less necrosis,orderly arrangement and normal intercellular space.Compared with the control group,myocardial cells in the model group showed necrosis,disordered arrangement,wide intercellular space and interstitial fibrosis.Compared with the model group,the myocardial cell necrosis,myocardial cell arrangement disorder and interstitial fibrosis in Mongolian medicine + model group were reduced to a certain extent.(3)The results of serum IL-6 level showed that: compared with the control group,the serum IL-6 level of the model group increased(P < 0.05);compared with the model group,the serum IL-6 level of the Mongolian medicine + model group decreased(P < 0.05).(4)Protein expression results showed that: compared with the control group,the protein expressions of Col I,col Ⅲ,STAT3 and p-STAT3 in the model group were increased(P < 0.01);compared with the model group,the protein expressions of Col I,col Ⅱ,STAT3 and p-STAT3 in the Mongolian medicine + model group were decreased(P < 0.05).Conclusion: 1.Ang Ⅱ can promote myocardial fibrosis by activating JAK / STAT3 signaling pathway;2.Mongolian medicine Sanwei sandalwood can improve Ang Ⅱ induced myocardial fibrosis in mice by inhibiting JAK / STAT3 signaling pathway. |
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