Da-wu Zhang1, Lei Zhang, Jian-gang Liu. 1. Department of Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091.
Abstract
OBJECTIVE: To investigate effect of Xiongshao Capsule (XSC) combined with ischemic postconditioning (IPoC) on tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) contents as well as inflammatory cell infiltration (ICI) in myocardium of rat with ischemic reperfusion (I/R) injury. METHODS: Seventy-five Sprague-Dawley rats were equally randomized into 5 groups, the sham-operated group (A), the I/R group (B), the IPoC group (C), the fosinopril sodium plus IPoC group (D), and the XSC plus IPoC group (E). Excepting rats in Group A, all animals received I/R injury through a 30-min occlusion of left anterior descending artery followed by 1-h reperfusion. Additionally, IPoC (3 cycles of 10 s reperfusion/10 s of ischemia) was applied on rats in Group C before 1 h of reperfusion; while rats in Groups D and E were pretreated for 14 days with 0.9 mg/kg fosinopril sodium and 0.135 g/kg XSC respectively via gastrogavage, and the I/R injury with IPoC applied 2 h after the final gavage. Serum creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels were detected by colorimetric method, myocardial infarction size was measured by nitro blue tetrazolium chloride (NBT) staining, MCP-1 and TNF-alpha contents in myocardial tissue were examined by enzyme-linked immunosorbent assay (ELISA), and ICI was detected by HE staining. RESULTS: Compared with Group B, myocardial enzymes and infarction size were significantly decreased (P<0.01), contents of MCP-1, TNF-alpha and ICI in myocardial tissue were significantly decreased (P<0.05, P<0.01) in Group C. Compared with Group C, further reduced infarction size and release of myocardial enzyme CK-MB (P<0.01) were seen in Group E, and contents of MCP-1 and TNF-alpha as well as ICI in myocardial tissue in Group E were also significantly lower (P<0.05, P<0.01). CONCLUSION: XSC could enhance the protective effect of IPoC on rat with myocardial I/R injury, and the mechanism may be related to its inhibition on MCP-1 and TNF-alpha expressions as well as ICI suppression.
OBJECTIVE: To investigate effect of Xiongshao Capsule (XSC) combined with ischemic postconditioning (IPoC) on tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) contents as well as inflammatory cell infiltration (ICI) in myocardium of rat with ischemic reperfusion (I/R) injury. METHODS: Seventy-five Sprague-Dawley rats were equally randomized into 5 groups, the sham-operated group (A), the I/R group (B), the IPoC group (C), the fosinopril sodium plus IPoC group (D), and the XSC plus IPoC group (E). Excepting rats in Group A, all animals received I/R injury through a 30-min occlusion of left anterior descending artery followed by 1-h reperfusion. Additionally, IPoC (3 cycles of 10 s reperfusion/10 s of ischemia) was applied on rats in Group C before 1 h of reperfusion; while rats in Groups D and E were pretreated for 14 days with 0.9 mg/kg fosinopril sodium and 0.135 g/kg XSC respectively via gastrogavage, and the I/R injury with IPoC applied 2 h after the final gavage. Serum creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels were detected by colorimetric method, myocardial infarction size was measured by nitro blue tetrazolium chloride (NBT) staining, MCP-1 and TNF-alpha contents in myocardial tissue were examined by enzyme-linked immunosorbent assay (ELISA), and ICI was detected by HE staining. RESULTS: Compared with Group B, myocardial enzymes and infarction size were significantly decreased (P<0.01), contents of MCP-1, TNF-alpha and ICI in myocardial tissue were significantly decreased (P<0.05, P<0.01) in Group C. Compared with Group C, further reduced infarction size and release of myocardial enzyme CK-MB (P<0.01) were seen in Group E, and contents of MCP-1 and TNF-alpha as well as ICI in myocardial tissue in Group E were also significantly lower (P<0.05, P<0.01). CONCLUSION:XSC could enhance the protective effect of IPoC on rat with myocardial I/R injury, and the mechanism may be related to its inhibition on MCP-1 and TNF-alpha expressions as well as ICI suppression.