A20-Binding Inhibitor of NF- κ B 1 Ameliorates Neuroinflammation and Mediates Antineuroinflammatory Effect of Electroacupuncture in Cerebral Ischemia/Reperfusion Rats

Xueling Zhou; Wenhao Lu; You Wang; Jiani Li; Yong Luo

doi:10.1155/2020/6980398

A20-Binding Inhibitor of NF- κ B 1 Ameliorates Neuroinflammation and Mediates Antineuroinflammatory Effect of Electroacupuncture in Cerebral Ischemia/Reperfusion Rats

Evid Based Complement Alternat Med. 2020 Oct 13:2020:6980398. doi: 10.1155/2020/6980398. eCollection 2020.

Authors

Xueling Zhou^{1

2}, Wenhao Lu^{1

2}, You Wang³, Jiani Li³, Yong Luo¹

Affiliations

¹ Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
² Laboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
³ Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.

Abstract

A20-binding inhibitor of NF-κB 1 (ABIN1) is an inhibitor of NF-κB and exerts anti-inflammatory effect. Electroacupuncture (EA) is considered as a neuroprotective strategy by inhibiting neuroinflammatory damage after cerebral ischemia. This study was performed to explore the role of ABIN1 and investigate whether the ABIN1 is involved in the mechanism of EA in cerebral ischemia/reperfusion (I/R) rats. Male Sprague-Dawley (SD) rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and received EA after reperfusion once a day. Lentivirus-mediated ABIN1 gene knockdown was used to detect the role of ABIN1 in neuroinflammation after I/R. ABIN1 expression, proinflammatory cytokine levels, microglial activation, neurological function, infarct volumes, and NF-κB activation were assessed. ABIN1 expression was elevated in the peri-infarct cortex and was further upregulated by EA. ABIN1 knockdown increased the levels of proinflammatory cytokines and activation of microglia, worsened neurological deficits, and enlarged the infarct volume. Moreover, ABIN1 was blocked to partially reverse the neuroprotective effect of EA, and this treatment weakened the ability of EA to suppress NF-κB activity. Based on these findings, ABIN1 is a potential suppressor of neuroinflammation and ABIN1 mediates the antineuroinflammatory effect of EA in cerebral I/R rats.