Baicalein Inhibits HMGB1 Release and MMP-2/-9 Expression in Lipopolysaccharide-Induced Cardiac Hypertrophy

doi:10.1142/S0192415X14500505

CNU IR > Pharmacy and Science > Dept. of Pharmacy > Periodical Articles > Item 310902800/28518

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/28518

Title:	Baicalein Inhibits HMGB1 Release and MMP-2/-9 Expression in Lipopolysaccharide-Induced Cardiac Hypertrophy
Authors:	Chen, Huai-Min Liou, Shu-Fen Hsu, Jong-Hau Chen, Tsan-Ju Cheng, Tsung-Lin Chiu, Chaw-Chi Yeh, Jwu-Lai
Contributors:	藥學系
Keywords:	Baicalein Lipopolysaccharide Cardiac Hypertrophy Reactive Oxygen Species Matrix Metalloproteinases High Mobility Group Box 1
Date:	2014
Issue Date:	2015-05-06 21:19:10 (UTC+8)
Publisher:	World Scientific Publ Co Pte Ltd
Abstract:	Myocardial dysfunction, a common complication after sepsis, significantly contributes to the death of patients with septic shock. In the search for potentially effective drugs to decrease mortality from sepsis, we investigated the cardioprotective effects of baicalein, a flavonoid present in the root of Scutellaria baicalensis, on lipopolysaccharide (LPS)-induced pro-inflammatory cytokine production and matrix metalloproteinase-2 and -9 (MMP-2/-9) expression. We found that baicalein significantly attenuated LPS-induced cardiac hypertrophy and counteracted reactive oxygen species (ROS) generation in neonatal rat cardiomyocytes. In addition, pretreatment with baicalein inhibited LPS-induced early (e. g., tumor necrosis factor-alpha (TNF-alpha) and interleukin-6) and late (e.g., high mobility group box 1 (HMGB1) pro-inflammatory cytokine release, inducible nitric oxide synthase (iNOS) expression and NO production. Finally, baicalein also significantly down-regulated the expression of MMP-2/-9 and attenuated HMGB1 translocation from the nucleus to the cytoplasm. These results suggest that baicalein can protect cardiomyocytes from LPS-induced cardiac injury via the inhibition of ROS and inflammatory cytokine production. These cardioprotective effects are possibly mediated through the inhibition of the HMGB1 and MMP-2/-9 signaling pathways.
Relation:	American Journal of Chinese Medicine, v.42 n.4, pp.785-797
Appears in Collections:	[Dept. of Pharmacy] Periodical Articles

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