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姜黄素通过抑制 P2X7 受体的激活来纠正小胶质细胞中的钙失调。

Curcumin amends Ca dysregulation in microglia by suppressing the activation of P2X7 receptor.

机构信息

Department of Integrated Chinese and Western Medicine, The First Affiliated Hospital of Xinxiang Medical University, No. 88 Jiankang Road, Weihui, Xinxiang, 453100, Henan, China.

出版信息

Mol Cell Biochem. 2020 Feb;465(1-2):65-73. doi: 10.1007/s11010-019-03668-8. Epub 2020 Jan 1.

DOI:10.1007/s11010-019-03668-8
PMID:31894530
Abstract

Curcumin (Cur) is widely used as an anti-inflammation agent and has anti-depression potential. Neuroinflammation mediated by Ca channel activation is closely associated with the progression of post-stroke depression (PSD). In the current study, the role of P2X7 receptor (P2X7R) in the anti-PSD function of Cur was explored. Rats were subjected to middle cerebral artery occlusion (MCAO) surgery and chronic mild stress administration to induce PSD symptoms and then treated with Cur. The behaviors of rats were assessed with sucrose preference and forced swim tests. The accumulation of Ca and the systemic inflammatory response in rats were detected. To determine the role of P2X7R in the anti-PSD function of curcumin, the PSD mice were further administrated with P2X7R agonist and antagonist. The administration of Cur attenuated behavior disorders associated with PSD. Moreover, the Ca accumulation and the inflammatory response associated with PSD were also blocked by Cur. Cur also inhibited the activation of Ca channel. The induced activity of P2X7R blocked the function of Cur by maintaining the symptoms of PSD in Cur-treated rats. Collectively, the anti-PSD function of Cur was dependent on the inhibition of P2X7R, which then deactivated Ca channel-mediated inflammatory response associated with PSD progression.

摘要

姜黄素(Cur)被广泛用作抗炎剂,具有抗抑郁作用。钙通道激活介导的神经炎症与卒中后抑郁(PSD)的进展密切相关。在本研究中,探讨了 P2X7 受体(P2X7R)在姜黄素抗 PSD 功能中的作用。大鼠接受大脑中动脉闭塞(MCAO)手术和慢性轻度应激处理,以诱导 PSD 症状,然后用姜黄素治疗。通过蔗糖偏好和强迫游泳试验评估大鼠的行为。检测大鼠 Ca 积累和全身炎症反应。为了确定 P2X7R 在姜黄素抗 PSD 功能中的作用,进一步用 P2X7R 激动剂和拮抗剂处理 PSD 小鼠。姜黄素的给药减轻了与 PSD 相关的行为障碍。此外,姜黄素还阻断了与 PSD 相关的 Ca 积累和炎症反应。姜黄素还抑制钙通道的激活。P2X7R 的诱导活性通过维持姜黄素治疗大鼠的 PSD 症状来阻断姜黄素的功能。总之,姜黄素的抗 PSD 功能依赖于抑制 P2X7R,从而使钙通道介导的与 PSD 进展相关的炎症反应失活。

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