Abstract Title:

[Apoptosis inhibition of capsaicin on myocardial ischemia-reperfusion injury in rats].

Abstract Source:

Sichuan Da Xue Xue Bao Yi Xue Ban. 2011 Mar ;42(2):218-21. PMID: 21500557

Abstract Author(s):

Su-lan Qin, Ru-rong Wang, Hong-wei Xu, Nan-fu Luo

Article Affiliation:

Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu 610041, China.


OBJECTIVE: To determine apoptosis inhibition effect of capsaicin on myocardial ischemia-reperfusion injury in rats and its underlying mechanisms.

METHODS: The rat model of myocardial ischemia-reperfusion injury was established by ligating the left anterior descending coronary artery for 45 min and then loosing the ligation (reperfusion) for 120 min. Twenty healthy male rats were randomly divided into sham group, control group (I/R), capsaicin group (CAP+I/R), capsazepine group (CAPZ+CAP+I/R), and S-3144 group (S-3144+CAP+I/R). All drugs were delivered bolusly into left ventricle (LV)via right carotid artery at 10 min and 5 min before ischemia. Rats in I/R group and sham group only received vehicle injection. Myocardial protection was assessed by measurements of heart rate (HR) and left ventricular developed pressure (LVDP). The pathologic changes of myocardial tissue in each group were observed under light microscopy. TUNEL-positive nuclei were tested by immunofluorescent method.

RESULTS: At 120 min after reperfusion, there were significant increases of HR and LVDP in CAP+I/R group when compared with control group, capsazepine group, and S-3144 group (P<0.05). The apoptotic index in the sham group was lower than that in the groups with ischemia/reperfusion injury (P<0.05). Among the groups with ischemia/reperfusion injury, CAP+I/R group had the lowest apoptotic index (P<0.05).

CONCLUSION: CAP could generate cardioprotection associated with cardiomyocyte apoptosis inhibition in vivo, likely by stimulating TRPV1 and further activating NK1 receptor.

Study Type : Animal Study

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