mRNA expression profile analysis of WenxinKeli-treated rabbits with myocardial infarction

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AIM: There is little evidence proving the molecular mechanism of Wenxin Keli( WXKL). This study tried to explore the gene expression profile and pathology alteration of WXKL-treated rabbits with myocardial infarction. METHOD: Twenty male adult rabbits were randomly divided into 4 groups: sham,model,WXKL and captopril groups. Model,WXKL and captopril groups underwent the ligation of the left anterior descending coronary artery,while sham group went through an identical procedure without ligation. WXKL(817 mg·kg~(-1)·d~(-1)),captopril(8 mg·kg~(-1)·d~(-1)) and distilled water(model and sham) were administered orally to the rabbits.4 weeks later,hearts were taken out for expression chip and pathological staining( HE,Masson and TUNEL) after echocardiography.RESULT: WXKL could down-regulate genes associated with inflammation( CX3CR1,MRC1,and FPR1),apoptosis( cathepsin C and TTC5) and neuro-hormonal system( ACE and EDN1),and up-regulate angiogenesis promoting gene like RSPO3,which explained why WXKL group represented with better cardiac function,less histopathological injury and slighter apoptosis. CONCLUSION:WXKL plays an important role in suppressing inflammation,inhibiting renin-angiotensin system and alleviating apoptosis,and might be a promising Chinese medicine in treating patients with myocardial infarction. AIM: There is little evidence proving the molecular mechanism of Wenxin Keli (WXKL). This study tried to explore the gene expression profile and pathology alteration of WXKL-treated rabbits with myocardial infarction. METHOD: Twenty male adult rabbits were randomly divided into 4 groups : sham, model, WXKL and captopril groups. Model, WXKL and captopril groups underwent the ligation of the left anterior descending coronary artery, while sham group went through an identical procedure without ligation. WXKL (817 mg · kg -1 captopril (8 mg · kg -1 · d -1) and distilled water (model and sham) were orally to the rabbits.4 weeks later, hearts were taken out for expression chip and pathological staining (HE, Masson and TUNEL) after echocardiography. RESULT: WXKL could down-regulate genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (cathepsin C and TTC5) and neuro-hormonal system and EDN1), and up-regulate angiogenesis promoting genes like RSPO3, which explain ed why WXKL group represented with better cardiac function, less histopathological injury and slighter apoptosis. CONCLUSION: WXKL plays an important role in suppressing inflammation, inhibiting renin-angiotensin system and alleviating apoptosis, and possibly be a promising Chinese medicine in treating patients with myocardial infarction .
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