Epigallocatechingallate attenuates myocardial injury in a mouse model of heart failure through TGF‑β1/Smad3 signaling pathway

Figures

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  Figure 1.. The model of heart failure in mice was established and verified in all treatment groups. (A) The pathological alterations of myocardium were observed by hematoxylin and eosin staining (arrows represents widened myocardial cell gap and myocardial fiber rupture). (B) Alterations of LVIDs, LVIDd and EF in mice were observed by echocardiography in order to determine whether the model of heart failure was successfully established. (C) The peripheral blood of mice was collected, and serum was isolated, ELISA was used to detect BNP and NT-proBNP levels. *P<0.05 vs. the sham group; #P<0.05 vs. the HF group. HF, heart failure; LVIDs, left ventricular internal systolic diameter; LVIDd, left ventricular internal diastolic diameter; BNP, brain natriuretic peptide; NT-proBNP, N-terminal-proBNP; EGCG, epigallocatechingallate; LY group, LY364947 inhibitor and EGCG treatment group.

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  Figure 2.. The model of heart failure was established in mice and collagen remodeling-associated alterations were observed in different groups. (A) Masson staining was used to observe myocardial fibrosis. (B) Western blot assay was used to detect heart tissue collagen I and III protein expression. (C) Reverse transcription-quantitative polymerase chain reaction was used to detect mRNA expression of collagen I and III. *P<0.05 vs. the sham group; #P<0.05 vs. the HF group. HF, heart failure; EGCG, epigallocatechingallate; LY group, LY364947 inhibitor and EGCG treatment group.

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  Figure 3.. Peripheral blood of mice was collected and serum was isolated. ELISA was used to detect expression levels of oxidative stress-associated factors, including MDA, SOD and GSH-Px. *P<0.05 vs. the sham group; #P<0.05 vs. the HF group. HF, heart failure; EGCG, epigallocatechingallate; LY group, LY364947 inhibitor and EGCG treatment group; MDA, malondialdehyde; SOD, superoxide dismutase; GSH-Px, glutathione peroxidase.

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  Figure 4.. The peripheral blood of mice was collected and serum was isolated. ELISA was used to detect expression levels of inflammatory factors IL-1β, IL-6 and TNF-α. *P<0.05 vs. the sham group; #P<0.05 vs. the HF group. HF, heart failure; EGCG, epigallocatechingallate; LY group, LY364947 inhibitor and EGCG treatment group; IL, interleukin; TNF-α, tumor necrosis factor-α.

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  Figure 5.. The model of heart failure was established in mice. Heart tissue was collected and total protein was extracted. Western blot assay was used to detect Bax, Bcl2 and caspase-3 protein expression. *P<0.05 vs. the sham group; #P<0.05 vs. the HF group. HF, heart failure; EGCG, epigallocatechingallate; LY group, LY364947 inhibitor and EGCG treatment group; Bax, apoptosis regulator BAX; Bcl2, apoptosis regulator Bcl2.

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  Figure 6.. The model of heart failure was established in mice. (A) Heart tissue was collected and total protein was extracted. Western blot assay was used to detect expression of TGF-β1/Smad3 signaling pathway-associated proteins. Collected heart tissue was fixed in 10% formaldehyde for at least 48 h and sliced into sections. Immunofluorescence was used to detect (B) TGF-β1 expression. *P<0.05 vs. the sham group; #P<0.05 vs. the HF group. (C) Immunofluorescence was also used to detect p-Smad3 expression. HF, heart failure; EGCG, epigallocatechingallate; LY group, LY364947 inhibitor and EGCG treatment group.