Dihydromyricetin protects against lipopolysaccharide‑induced cardiomyocyte injury through the toll‑like receptor‑4/nuclear factor‑κB pathway

Zhou,Meng‑Qiao; Shao,Ling; Wu,Jing; Peng,Na; Jin,Lu‑Ping; Wei,Guo‑Zhen; Cheng,Wei; Deng,Chang‑Jin

doi:10.3892/mmr.2017.7742

Dihydromyricetin protects against lipopolysaccharide‑induced cardiomyocyte injury through the toll‑like receptor‑4/nuclear factor‑κB pathway

Authors:
- Meng‑Qiao Zhou
- Ling Shao
- Jing Wu
- Na Peng
- Lu‑Ping Jin
- Guo‑Zhen Wei
- Wei Cheng
- Chang‑Jin Deng
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Affiliations: Department of Cardiology, The First People's Hospital of Jingmen, Jingmen, Hubei 448000, P.R. China
Published online on: October 9, 2017 https://doi.org/10.3892/mmr.2017.7742
Pages: 8983-8988

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Abstract

Dihydromyricetin (DHM) is a bioactive flavonoid compound extracted from the stems and leaves of Ampelopsis grossedentata. Previous studies have indicated that DHM has antioxidation and antitumor capabilities, while the effect of DHM on lipopolysaccharide (LPS)‑induced cardiomyocyte injury has not been clarified. Therefore, the aim of the present study was to investigate the effect of DHM on LPS‑induced cardiomyocyte injury. In the present study, cardiomyocytes were randomized to the control (PBS), LPS and DHM + LPS groups. The LPS group was treated with 10 µg/ml LPS for 12 h and the DHM + LPS group was treated with 100 or 25 µM DHM 12 h prior to treatment with LPS. The protective effect of DHM on LPS‑induced cardiomyocytes injury was evaluated by Cell Counting kit‑8 assay, TUNEL staining, reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The results demonstrated that LPS treatment led to cardiomyocyte apoptosis, and these effects were significantly attenuated by DHM. Furthermore, LPS treatment downregulated the expression of B‑cell lymphoma 2 apoptosis regulator (Bcl‑2) and induced increased expression of Bcl‑2‑associated X apoptosis regulator (Bax). Additionally, DHM treatment reversed LPS‑induced changes in Bcl‑2 expression and Bax expression in cardiomyocytes, and rescued cells from apoptosis. In addition, increased mRNA expression levels of tumor necrosis factor‑α and interleukin‑6 induced by LPS were attenuated following treatment with DHM. Further investigation demonstrated that DHM suppressed the activation of toll‑like receptor‑4 (TLR4), which is involved in regulating the downstream signaling pathway of nuclear factor‑κB (NF‑κB). DHM attenuated LPS‑induced cardiomyocyte injury, the potential mechanism responsible for this effect may involve inhibition of TLR4 activation and subsequent regulation of the associated downstream signaling pathway of NF‑κB. The current study indicates that DHM may protect cardiomyocytes against LPS‑induced injury by inhibition of the TLR4/NF‑κB signaling pathway. The results of the present study may provide support for the development DHM as a strategy for the treatment of heart failure in septic shock.

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