Author + information
- Zheng Min and
- Jielin Pu
There is little evidence proving the molecular mechanism of WenxinKeli (WXKL). This study tried to explore the gene expression profile and pathology alteration of WXKL treated rabbits with myocardial infarction.
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 (817mg/kg/d), captopril (8mg/kg/d) 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.
WXKL could down-regulate genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (Cathepsin C and TTC5), neuro-humoral 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.
The present study showed that WXKL had played an important role in suppressing inflammation, inhibiting renin-angiotensin system, alleviating apoptosis and might be a promising Chinese medicine in treating patients with myocardial infarction.