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Biomed Pharmacother. 2018 Jan;97:1673-1679. doi: 10.1016/j.biopha.2017.12.024. Epub 2017 Dec 8.

Baicalin alleviates atherosclerosis by relieving oxidative stress and inflammatory responses via inactivating the NF-κB and p38 MAPK signaling pathways.

Author information

1
Department of Cardiology, The First Affiliated Hospital of Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, 710061, China.
2
Department of Cardiology, Han Zhong Central Hospital, Hanzhong City, Shaanxi Province, 723000, China.
3
Department of Cardiology, The First Affiliated Hospital of Xi'an Jiao Tong University, Xi'an City, Shaanxi Province, 710061, China. Electronic address: baixiaojunxa@163.com.

Abstract

Atherosclerosis (AS) is a chronic progressive disease related to inflammatory reaction. Baicalin is a flavonoid isolated from Scutellaria baicalensis georgi (Huang-qin) and exerts anti-inflammation effects in various diseases. Here, we investigated the protective effects of baicalin treatment and the potential mechanism in AS progression on AS mouse model. After ApoE-/- mice with high-lipid diets had received 12 weeks' of baicalin treatment at different concentrations, plasma lipids levels and atherosclerotic plaque areas in aorta were measured and there exhibited a prominent improvement in the baicalin treated mice compared with mice in AS model group. The expression of lipolysis related proteins (PPARα, CPT-1) was increased while the expression of adipogenesis related proteins (SREBP-1c, ACS) was decreased by baicalin treatment, indicating the anti-adipogenic effect of baicalin. Moreover, baicalin up-regulated the activities of antioxidant enzymes (SOD, CAT and GSH-Px) and down-regulated the activity of oxidative parameter MDA compared with AS model group, indicating the anti-oxidant effect of baicalin. The increased levels of pro-inflammatory cytokines (IL-6, TNF-α, sVE-cadherin) induced by AS were also decreased by baicalin treatment, indicating that baicalin acted as an anti-inflammation regulator in AS. In addition, we further explored the potential mechanism of baicalin treatment on AS, and found that baicalin treatment attenuated the high phosphorylation levels of JNK, p65, p-38 and ERK1/2 induced by AS, indicating that baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways in AS. In conclusion, baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways, thereby achieved its anti-adipogenic effect, anti-oxidant effect and anti-inflammation effect in a dose-dependent manner in AS.

KEYWORDS:

Atherosclerosis; Baicalin; Inflammation; NF-κB; Oxidative stress; p38 MAPK

PMID:
29793330
DOI:
10.1016/j.biopha.2017.12.024
[Indexed for MEDLINE]

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