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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Format: | Article |
Language: | zho |
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Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College.
2023-10-01
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Series: | Jichu yixue yu linchuang |
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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. |
first_indexed | 2024-03-08T15:53:48Z |
format | Article |
id | doaj.art-98b7ed2672a24bcebdf429a307420971 |
institution | Directory Open Access Journal |
issn | 1001-6325 |
language | zho |
last_indexed | 2024-03-08T15:53:48Z |
publishDate | 2023-10-01 |
publisher | Institute of Basic Medical Sciences and Peking Union Medical College Hospital, Chinese Academy of Medical Sciences / Peking Union Medical College. |
record_format | Article |
series | Jichu yixue yu linchuang |
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 |