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Lei Chen,Kui-Po Yan,Xin-Can Liu,Wei Wang,Chao Li,Ming Li,Chun-Guang Qiu 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.1
This study investigated the interaction amongvalsartan (VAL), TGF-b pathways, and long non-codingRNA (lncRNA) cardiac hypertrophy-related factor (CHRF)in doxorubicin (DOX)-induced heart failure (HF), andexplored their roles in DOX-induced HF progression. HFmice models in vivo were constructed by DOX induction. The expression of CHRF and TGF-b1 in hearts wasdetected, along with cardiac function, caspase-3 activity,and cell apoptosis. Primary myocardial cells were pretreatedwith VAL, followed by DOX induction in vitro forfunctional studies, including the detection of cell apoptosiswith terminal deoxynucleotidyl transferase dUTP nick-endlabeling and the expression of proteins associated withTGF-b1 pathways. HF models were established in vivo andin vitro. Expression of CHRF and TGF-b1 was up-regulated,and cell apoptosis and caspase-3 activity wereincreased in the hearts and cells of the HF models. VALsupplementation alleviated the cardiac dysfunction andinjury in the HF process. Moreover, overexpressed CHRFup-regulated TGF-b1, promoted myocardial cell apoptosis,and reversed VAL’s cardiac protective effect, while interferenceof CHRF (si-CHRF) did the opposite. Down-regulationof CHRF reversed the increased expression of TGFb1and the downstream proteins induced by pcDNA-TGFb1in HL-1 cells, while overexpression of CHRF reversedthe VAL’s cardiac protective effect in vivo. In conclusion,VAL regulates TGF-b pathways through lncRNA CHRF toimprove DOX-induced HF.