Protective effect of apigenin on Freund's complete adjuvant-induced arthritis in rats via inhibiting P2X7/NF-κB pathway. (5th July 2015)

• Record Type: Journal Article
• Authors: Chang, Xiayun; He, He; Zhu, Lingpeng; Gao, Jin; Wei, Tingting; Ma, Zhanqian; Yan, Tianhua
• Is Part Of: Chemico-biological interactions. Volume 236(2015)
• Page Start: 41
• Page End: 46
• Publication Date: 2015-07-05
• Subjects: Apigenin -- Arthritis -- Inflammation -- P2X7/NF-κB; Biochemistry -- Periodicals; Toxicological chemistry -- Periodicals; Biochemistry -- Periodicals; Biologie moléculaire -- Périodiques; Biochimie -- Périodiques; Toxicologie biochimique -- Périodiques; 572
• DOI: 10.1016/j.cbi.2015.04.021
• Languages: English
• ISSNs: 0009-2797

Abstract

Highlights: Apigenin reduced inflammation in AA. Apigenin inhibited P2X7 in AA. Apigenin inhibited NF-κB in AA. Abstract: 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-α), interleukin-1 beta (IL-1β) 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-κB) 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-κB signal-related proteins and alleviated inflammatory reactions. Therefore, it was assumed that AP might be a potential therapeutic candidate to treat arthritis.