Dihydromyricetin protects against lipopolysaccharideinduced cardiomyocyte injury through the tolllike receptor4/nuclear factorκB pathway.
Mol Med Rep
; 16(6): 8983-8988, 2017 Dec.
Article
en En
| MEDLINE
| ID: mdl-29039483
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 LPSinduced 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 LPSinduced cardiomyocytes injury was evaluated by Cell Counting kit8 assay, TUNEL staining, reverse transcriptionquantitative 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 Bcell lymphoma 2 apoptosis regulator (Bcl2) and induced increased expression of Bcl2associated X apoptosis regulator (Bax). Additionally, DHM treatment reversed LPSinduced changes in Bcl2 expression and Bax expression in cardiomyocytes, and rescued cells from apoptosis. In addition, increased mRNA expression levels of tumor necrosis factorα and interleukin6 induced by LPS were attenuated following treatment with DHM. Further investigation demonstrated that DHM suppressed the activation of tolllike receptor4 (TLR4), which is involved in regulating the downstream signaling pathway of nuclear factorκB (NFκB). DHM attenuated LPSinduced 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 NFκB. The current study indicates that DHM may protect cardiomyocytes against LPSinduced injury by inhibition of the TLR4/NFκB 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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Cardiotónicos
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Transducción de Señal
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FN-kappa B
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Miocitos Cardíacos
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Flavonoles
Límite:
Animals
Idioma:
En
Revista:
Mol Med Rep
Año:
2017
Tipo del documento:
Article