| Literature DB >> 35831547 |
Haofuzi Zhang1, Yuefan Yang1,2, Erwan Yang1, Zhicheng Tian1, Yutao Huang1, Zhuoyuan Zhang1,3, Mingdong Bao1, Dan Liao1, Junmiao Ge1, Chao Wang4, Xin Li5, Peng Luo6.
Abstract
Neuroinflammation is one of the most important pathological processes following brain ischemia. Pulsed electromagnetic fields (PEMFs) protect against brain ischemia, but their role in regulating neuroinflammation remains unclear. In the present study, we investigated the biological effects of PEMF exposure on brain ischemia-induced neuroinflammation through the astrocytic cholinergic anti-inflammatory pathway. PEMF exposure reduced the activation of astrocytes and neuroinflammation following brain ischemia by directly modulating astrocytic injury and inflammatory cytokine release. Inhibition of nicotinic acetylcholine receptor alpha 7 subunit (α7nAChR) by a specific antagonist reversed the regulatory effects of PEMF on astrocytes. Furthermore, negative regulation of signal transducer and activator of transcription 3 (STAT3) by α7nAChR was found to be an important downstream mechanism through which PEMF regulates astrocyte-related neuroinflammation. PEMF suppressed STAT3 phosphorylation and nuclear translocation by activating α7nAChR. These results demonstrate that PEMF exerts anti-inflammatory effects in the context of brain ischemia by modulating astrocytic α7nAChR/STAT3 signaling.Entities:
Keywords: Astrocytes; Brain ischemia; Neuroinflammation; Nicotinic acetylcholine receptor alpha 7 subunit; Pulsed electromagnetic field; Signal transducer and activator of transcription 3
Year: 2022 PMID： 35831547 DOI： 10.1007/s10571-022-01251-2
Source DB: PubMed Journal: Cell Mol Neurobiol ISSN： 0272-4340 Impact factor: 4.231