Protective effect of apigenin on Freund's complete adjuvant-induced arthritis in rats via inhibiting P2X7/NF-κB pathway

被引：96

作者：

Chang, Xiayun ^{[1
]}

He, He ^{[1
]}

Zhu, Lingpeng ^{[1
]}

Gao, Jin ^{[1
]}

Wei, Tingting ^{[1
]}

Ma, Zhanqian ^{[1
]}

Yan, Tianhua ^{[1
]}

机构：

[1] China Pharmaceut Univ, Dept Physiol & Pharmacol, Nanjing, Jiangsu, Peoples R China

来源：

CHEMICO-BIOLOGICAL INTERACTIONS | 2015年 / 236卷

关键词：

Apigenin; Arthritis; Inflammation; P2X7/NF-kappa B; COLLAGEN-INDUCED ARTHRITIS; RHEUMATOID-ARTHRITIS; P2X(7) RECEPTOR; TNF-ALPHA; PAIN; MECHANISMS; APOPTOSIS;

D O I：

10.1016/j.cbi.2015.04.021

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

To evaluate the effect of apigenin (AP) on arthritis in rats stimulated by Freund's complete adjuvant (FCA) was the main purpose of the investigation. Arthritis model was established by the administration of 0.1 ml FCA in the palmar surface. AP and diclofenac sodium (DS) were administered to explore and evidence the protective effects against adjuvant-induced arthritis (AA). Cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) were detected to assess the anti-inflammatory effect of AP. Besides, pathological conditions were examined in rat paws. Related-proteins of nuclear factor kappa B (NF-kappa B) signal pathway activated by P2X7 were investigated to determine the molecular mechanism of AP and their expressions were measured by western blot. The data showed that AP significantly suppressed the expressions of P2X7/NF-kappa B signal-related proteins and alleviated inflammatory reactions. Therefore, it was assumed that AP might be a potential therapeutic candidate to treat arthritis. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

引用

页码：41 / 46

页数：6

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