Table 1.
Echocardiographic study.
Table 2.
Morphological data.
Figure 1.
HE-stained pathological images of left ventricular tissue.
a: Cardiomyocytes in the control group were orderly arranged, and the nuclei were lightly stained and located in the center of muscle fibers. b: Thickening and lengthening of myocardial fibers could be observed in the smoking group, wherein the nuclei were darkly stained, showing local tissue fibrosis and inflammatory cell infiltration. c: Cardiomyocyte hypertrophy, cellular degeneration and inflammatory cell infiltration were significantly improved in the trimetazidine group by contrast with those in the smoking group.
Table 3.
Assessment of oxidative stress.
Figure 2.
Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining.
The apoptotic rate in the smoking group (b) was significantly higher than in the control group (a), while this rate in the trimetazidine group (c) was significantly lower than in the smoking group.
Figure 3.
The apoptotic rate of cardiomyocytes in the smoking group increased significantly compared with that in the control group, while the apoptotic rate in the trimetazidine group declined remarkably in comparison with that in the smoking group.
*P<0.05, vs. control group; **P<0.05, vs. smoking group.
Figure 4.
The gene expression of inflammatory markers were deteced by quantitative real-time PCR.
The mRNA expression of IL-1β, IL-6, and TNF-α were up-regulated in the smoking group compared to the control group, while the expression of these markers were down-regulated in the trimetazidine group compared to the smoking group. *P<0.05, vs. control group; **P<0.05, vs. smoking group.
Table 4.
Serum levels of inflammatory cytokines.