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Food Chem Toxicol. 2014 Jan;63:104-10. doi: 10.1016/j.fct.2013.10.045. Epub 2013 Nov 6.

Astilbin protects diabetic rat heart against ischemia-reperfusion injury via blockade of HMGB1-dependent NF-κB signaling pathway.

Author information

1
School of Pharmaceutical Sciences, Binzhou Medical University, Yantai 264003, PR China.
2
School of Pharmaceutical Sciences, Binzhou Medical University, Yantai 264003, PR China. Electronic address: jwl518@163.com.

Abstract

Astilbin, a flavonoid compound was isolated from the rhizome of Smilax china L. In this study, we investigated the anti-myocardial ischemia and reperfusion (I/R) injury effect of Astilbin on diabetic rats in vivo and elucidated the potential mechanism in vitro. The results showed that Astilbin significantly attenuated hypoxia-induced cell injury in a concentration-dependent manner. Treatment of H9c2 cells with Astilbin at 15 μM blocked nuclear factor kappaB (NF-κB) phosphorylation by blocking High-mobility group box protein 1 (HMGB1) expression. Treatment of diabetic rats with Astilbin by intravenous injection (i.v.) at a single dose of 50 mg/kg protected the rats from myocardial I/R injury as indicated by decreasing infarct volume, improving hemodynamics and reducing myocardial damage, and also lowered serum levels of pro-inflammatory factors, reduced HMGB1 and phosphorylated NF-κB expression in ischemic myocardial tissue from diabetic rats. Additionally, treatment of diabetic rats with Astilbin at dose of 50 mg/kg by i.v. for continuous 14 days attenuated cardiac remodeling in the model myocardial I/R injury. These protective effects suggested that Astilbin might be due to block of the myocardial inflammatory cascade via the HMGB1-dependent NF-κB signaling pathway.

KEYWORDS:

Astilbin; Diabetes mellitus; High mobility group box-1 protein; Myocardial ischemia and reperfusion; Nuclear factor kappaB

PMID:
24211745
DOI:
10.1016/j.fct.2013.10.045
[Indexed for MEDLINE]

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