GPR120 mediates mechanism of protective effect of NF-κB and MAPK in regula-ting LTA-induced Mac-T cells
10.16303/j.cnki.1005-4545.2024.10.12
- VernacularTitle:GPR120介导NF-κB和MAPK调控LTA诱导的Mac-T细胞的保护作用
- Author:
Siqi WANG
1
;
Peiyao ZHOU
;
Quanzhou MOU
;
Lin WAN
;
Xinli LI
;
Yang LI
;
Xingli HE
;
Zhaoyuan WANG
;
Zi WANG
;
Ziqiang GAO
;
Zhihui ZHAO
;
Binglei SHEN
Author Information
1. 黑龙江八一农垦大学动物科技学院,黑龙江大庆 163319
- Keywords:
GPR120;
Mac-T cells;
NF-κB;
MAPK
- From:
Chinese Journal of Veterinary Science
2024;44(10):2165-2171
- CountryChina
- Language:Chinese
-
Abstract:
Lipophosphatidic acid(LTA)was used to stimulate Mac-T cells,and the expression lev-els and phosphorylation levels of key proteins of nuclear factor-κB(NF-κB)and mitogen-activated protein kinase(MAPK)signaling pathway and the expression levels of upstream key action factors TLR4 and MyD88 proteins were detected by Western blot,and EDU assay was used to detect cell proliferation levels and flow cytometry was used to detect apoptosis.The results showed that acti-vation of GPR120 significantly decreased the phosphorylation levels of LTA-induced NF-κB(P65 and IκBα)(P＜0.01)and MAPK(JNK,ERK,p38)(P＜0.01)in Mac-T cells;inhibition of GPR120 was able to upregulate LTA-induced NF-κB(p65 and IκBα)in Mac-T cells(P＜0.01)and MAPK(JNK,ERK,p38)phosphorylation levels(P＜0.01);and activation of GPR120 significantly allevia-ted LTA-induced upregulation of TLR4 and MyD88(P＜0.01);inhibition of GPR120 significantly exacerbated LTA-induced upregulation of TLR4 and MyD88(P＜0.05);LTA stimulation led to a trend of diminished Mac-T cell proliferation and significantly increased apoptosis,whereas activa-tion of the GPR120 gene significantly increased cell activity(P＜0.01),promoted cell proliferation and significantly reduced apoptosis(P＜0.05)thereby alleviating the damage to Mac-T cells by LTA;LTA stimulation led to a highly significant increase in apoptosis(P＜0.01).In contrast,acti-vation of the GPR120 gene significantly reversed the increase in the apoptosis rate of Mac-T cells induced by LTA(P＜0.01),while inhibition of the GPR120 gene enhanced the apoptosis-promo-ting effect of LTA(P＜0.05),indicating that activation of the GPR120 gene attenuated the in-crease of apoptosis rate caused by LTA-induced inflammatory Mac-T cells.The results suggest that GPR120 can regulate inflammation by mediating TLR4 and MyD88 expression to inhibit NF-κB/MAPK inflammatory pathway activation and can promote cell proliferation.
