Fig. 2.

TRPV1 gene knockout partially abrogates paeoniflorin (PF)-mediated cardioprotection against MI. a TRPV1 knockout attenuated the decrease in myocardial infarct size by PF treatment, the black arrow indicates the infarction site. b TRPV1 knockout repressed the beneficial effects of PF on the release of myocardial enzymes in serum; c the activity of CGRP in serum measured at different time points before and after myocardial ischemia. d Heart function was assessed by fractional shortening {FS = [LV end-diastolic diameter (LVEDD) − LVend-systolic diameter (LVESD)] × 100/LVEDD} and ejection fraction [LVEF = (LVEDD² − LVESD²)/LVEDD²]. e Representative images of hematoxylin and eosin (H&E, 1–4) and Masson’s trichrome staining (5–8); (1 and 5) WTDM group (2 and 6) PF-WTDM group, (3 and 7) TRPV1^−/−DM group, (4 and 8) PF-TRPV1^−/−DM. PF-WTDM group: WTDM mice were pretreated with PF (140 mg/kg) before surgery, and TRPV1^−/−DM group: TRPV1 gene knockout mice with diabetes mellitus; PF-TRPV1^−/−DM, TRPV1 gene knockout DM mice were pretreated with PF (140 mg/kg) before surgery; n = 6 per group; *P < 0.01, PF-TRPV1^−/−WTDM vs. PF-WTDM-H; ^# P < 0.05, PF-TRPV1^−/−DM vs. TRPV1^−/−DM. (Mean ± SEM)