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. Author manuscript; available in PMC: 2021 Oct 29.
Published in final edited form as: Basic Res Cardiol. 2015 Apr 25;110(3):31. doi: 10.1007/s00395-015-0486-5

Fig. 4.

Fig. 4

Cardiac-specific STAT3 deficiency abolishes infarct-limiting effect of rapamycin (RAPA) against ischemia/reperfusion (I/R) injury in diabetic mice. a STAT3-deficient (MCM TG:STAT3flox/flox) and WT (MCM NTG:STAT3flox/flox) male mice (8–10 weeks) were fed high fat diet (HFD) for 16 weeks, after which they received tamoxifen (20 mg/kg/day i.p.) for 10 days. Representative immunoblots of STAT3 and GAPDH in hearts of HFD-fed and tamoxifen treated STAT3-deficient and WT mice. Densitometric analysis representing fold change in STAT3/GAPDH ratio. b Myocardial infarct sizes of WT and STAT3-deficient mice following global I/R as well as infusion of rapamycin (RAPA, 100 nM) or DMSO (solvent of rapamycin) at reperfusion. c Product of heart rate and ventricular developed force (% of pre-ischemic baseline). d Coronary flow rate (% of pre-ischemic coronary flow)