IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2

Objective To explore the regulatory mechanism of microglia apoptosis in neuroinflammation. Methods LPS was used to establish mouse microglia cell line BV2 cells as a neuroinflammatory microglia model, IL-6 antagonist siltuximab was applied to treat LPS-induced BV2 cells. CCK-8 was used to...

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Main Author: ZHENG Jianbin, WU Shaohua, HUANG Yujing
Format: Article
Language:zho
Published: Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. 2023-10-01
Series:Jichu yixue yu linchuang
Subjects:
Online Access:http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2023-43-10-1562.pdf
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author ZHENG Jianbin, WU Shaohua, HUANG Yujing
author_facet ZHENG Jianbin, WU Shaohua, HUANG Yujing
author_sort ZHENG Jianbin, WU Shaohua, HUANG Yujing
collection DOAJ
description Objective To explore the regulatory mechanism of microglia apoptosis in neuroinflammation. Methods LPS was used to establish mouse microglia cell line BV2 cells as a neuroinflammatory microglia model, IL-6 antagonist siltuximab was applied to treat LPS-induced BV2 cells. CCK-8 was used to detect the proliferation of cells. Cell apoptosis was detected by flow cytometry. ELISA kit was used to detect the content of pro-inflammatory related factors IL-6 and TNF-α. The expression of M1 polarization markers IL-1β, IFN-γ and M2 polarization markers CD206, Arg-1 in BV2 cell was detected by qRT-PCR. The expression of JAK-STAT3 signaling pathway key proteins and necroptosis related proteins RIP1 and RIP3 was detected by Western blot. Results After LPS induction, the proliferation of BV2 cells decreased, apoptosis increased, and the contents of inflammatory factors IL-6 and TNF-α increased (P<0.01). The expression of M1 polarization markers IL-1β and IFN-γ increased, and the expression of M2 polarization markers CD206 and Arg-1 decreased(P<0.01). The phosphorylation of JAK-STAT3 key protein increased, and the relative protein expression of RIP1 and RIP3 (P<0.01). After treatment with IL-6 antagonist siltuximab, phosphorylation of JAK-STAT3 key proteins decreased, and RIP1 and RIP3 protein decreased (P<0.01). Conclusions IL-6 may activate JAK-STAT3 signaling pathway to promote necroptosis of mouse microglia in neuroinflammation.
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spelling doaj.art-98b7ed2672a24bcebdf429a3074209712024-01-09T03:15:35ZzhoInstitute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.Jichu yixue yu linchuang1001-63252023-10-0143101562156610.16352/j.issn.1001-6325.2023.10.1562IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2ZHENG Jianbin, WU Shaohua, HUANG Yujing0Department of Anesthesiology, Ningde Municipal Hospital of Ningde Normal University, Ningde 352100, ChinaObjective To explore the regulatory mechanism of microglia apoptosis in neuroinflammation. Methods LPS was used to establish mouse microglia cell line BV2 cells as a neuroinflammatory microglia model, IL-6 antagonist siltuximab was applied to treat LPS-induced BV2 cells. CCK-8 was used to detect the proliferation of cells. Cell apoptosis was detected by flow cytometry. ELISA kit was used to detect the content of pro-inflammatory related factors IL-6 and TNF-α. The expression of M1 polarization markers IL-1β, IFN-γ and M2 polarization markers CD206, Arg-1 in BV2 cell was detected by qRT-PCR. The expression of JAK-STAT3 signaling pathway key proteins and necroptosis related proteins RIP1 and RIP3 was detected by Western blot. Results After LPS induction, the proliferation of BV2 cells decreased, apoptosis increased, and the contents of inflammatory factors IL-6 and TNF-α increased (P<0.01). The expression of M1 polarization markers IL-1β and IFN-γ increased, and the expression of M2 polarization markers CD206 and Arg-1 decreased(P<0.01). The phosphorylation of JAK-STAT3 key protein increased, and the relative protein expression of RIP1 and RIP3 (P<0.01). After treatment with IL-6 antagonist siltuximab, phosphorylation of JAK-STAT3 key proteins decreased, and RIP1 and RIP3 protein decreased (P<0.01). Conclusions IL-6 may activate JAK-STAT3 signaling pathway to promote necroptosis of mouse microglia in neuroinflammation.http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2023-43-10-1562.pdfneuroinflammation|necroptosis|microglia|lipopolysaccharide|siltuximab
spellingShingle ZHENG Jianbin, WU Shaohua, HUANG Yujing
IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2
Jichu yixue yu linchuang
neuroinflammation|necroptosis|microglia|lipopolysaccharide|siltuximab
title IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2
title_full IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2
title_fullStr IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2
title_full_unstemmed IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2
title_short IL-6 promotes necrotic apoptosis of mouse microglia cell line BV2
title_sort il 6 promotes necrotic apoptosis of mouse microglia cell line bv2
topic neuroinflammation|necroptosis|microglia|lipopolysaccharide|siltuximab
url http://journal11.magtechjournal.com/Jwk_jcyxylc/fileup/1001-6325/PDF/1001-6325-2023-43-10-1562.pdf
work_keys_str_mv AT zhengjianbinwushaohuahuangyujing il6promotesnecroticapoptosisofmousemicrogliacelllinebv2