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. 2021 Sep 7;24(5):778. doi: 10.3892/mmr.2021.12418

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Copyright: © Pan et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 1. — LBP counteracts I/R-induced heart malfunction, histopathological abnormalities and inflammation in rats. (A) A diagram of the establishment of the I/R model and LBP treatment. (B) LVEDs, (C) LVEDd, (D) EF and (E) FS in I/R- and LBP-treated rats were determined via transthoracic echocardiography. (F) Representative images of heart sections of I/R-injured rats treated with LBP were analyzed via Evan's blue and 2,3,5-triphenyl-tetrazolium chloride double-staining. The percentages of (G) AAR/LV and (H) INF/AAR were estimated. AAR/LV reflects the extent of myocardial ischemia, while NF/AAR reflects the level of dead myocardium. (I) The histopathological changes in the heart of I/R-injured rats treated with LBP was examined via H&E staining (scale bar, 200 µm; magnification, ×100). The levels of (J) LDH, (K) CK, (L) cTnT, (M) IL-1β, (N) IL-6 and (O) TNF-α in I/R-injured rats treated with LBP were measured using ELISAs. **P<0.01, ***P<0.001 vs. Sham; ^{^}P<0.05, ^{^^}P<0.01, ^{^^^}P<0.001 vs. LBP; ^##P<0.01, ^###P<0.001 vs. I/R. Sham, rats received sham operation; I/R, ischemia/reperfusion; LBP, Lycium barbarum polysaccharide; LVEDs, left ventricular end-systolic diameter; LVEDd, left ventricular end-diastolic diameter; EF, ejection fraction; FS, fractional shortening; LDH, lactate dehydrogenase; CK, creatine kinase; AAR, area at risk; INF, infarcted area; LV, left ventricle.