文献类型：期刊文献

中文题名：GPR120介导NF-κB和MAPK调控LTA诱导的Mac-T细胞的保护作用

英文题名：GPR120 mediates mechanism of protective effect of NF-κB and MAPK in regulating LTA-induced Mac-T cells

作者：王斯琦[1];周佩瑶[1];牟泉宙[1];宛麟[1];李鑫丽[1];李杨[1];何兴丽[1];王昭元[1];王梓[1];高梓强[1];赵志辉[2];沈冰蕾[1]

机构：[1]黑龙江八一农垦大学动物科技学院,黑龙江大庆163319;[2]广东海洋大学农学院,广东湛江524088

年份：2024

卷号：44

期号：10

起止页码：2165

中文期刊名：中国兽医学报

外文期刊名：Chinese Journal of Veterinary Science

收录：北大核心2023、CSTPCD、、CSCD_E2023_2024、北大核心、CSCD

基金：国家自然科学基金资助项目(31200922,31472249);中国博士后科学基金资助项目(2018M631970);黑龙江省博士后启动基金资助项目(LBH-Z16166)。

语种：中文

中文关键词：GPR120;Mac-T细胞;NF-κB;MAPK

外文关键词：GPR120;Mac-T cells;NF-kB;MAPK

中文摘要：采用脂磷壁酸(lipophosphatidic acid,LTA)刺激Mac-T细胞,通过Western blot检测核因子κB(NF-κB)和促分裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)信号通路关键蛋白的表达水平和磷酸化水平,以及上游的关键作用因子TLR4和MyD88蛋白表达水平;EDU法检测细胞增殖水平;流式细胞术检测细胞凋亡情况。结果显示,激活G蛋白偶联受体120(G protein-coupled receptors 120,GPR120)能显著降低Mac-T细胞中LTA诱导NF-κB(P65和IκBα)(P<0.01)和MAPK(JNK、ERK、p38)(P<0.01)的磷酸化水平;抑制GPR120能够上调Mac-T细胞中LTA诱导NF-κB(P65和IκBα)(P<0.01)和MAPK(JNK、ERK、p38)(P<0.01)的磷酸化水平;激活GPR120可以极显著的缓解由LTA诱导的TLR4和MyD88的上调(P<0.01);抑制GPR120会显著加剧由LTA诱导的TLR4和MyD88的上调(P<0.05);LTA刺激会导致Mac-T细胞增殖水平呈减弱趋势,凋亡率显著增高,而激活GPR120基因可极显著增加细胞活性(P<0.01),促进细胞增殖,显著减少细胞凋亡(P<0.05)从而缓解了由LTA对Mac-T细胞的损伤;LTA刺激可使细胞凋亡率极显著增加(P<0.01),激活GPR120基因则可极显著(P<0.01)的逆转LTA所诱导的Mac-T细胞的凋亡率的提高;而抑制GPR120基因后可增强LTA对细胞凋亡的促进作用(P<0.05),表明激活GPR120基因可以减弱由LTA诱导的炎性Mac-T细胞导致的凋亡率增加。结果表明,GPR120可通过介导TLR4和MyD88表达抑制NF-κB/MAPK炎症通路活化调控炎症并能够促进细胞增殖。

外文摘要：Lipophosphatidic acid(LTA)was used to stimulate Mac-T cells,and the expression levels 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 activation 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 GPR120was able to upregulate LTA-induced NF-κB(p65and IκBα)in Mac-T cells(P<0.01)and MAPK(JNK,ERK,p38)phosphorylation levels(P<0.01);and activation of GPR120significantly alleviated LTA-induced upregulation of TLR4and MyD88(P<0.01);inhibition of GPR120significantly exacerbated LTA-induced upregulation of TLR4and MyD88(P<0.05);LTA stimulation led to a trend of diminished Mac-T cell proliferation and significantly increased apoptosis,whereas activation of the GPR120gene 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,activation of the GPR120gene significantly reversed the increase in the apoptosis rate of Mac-T cells induced by LTA(P<0.01),while inhibition of the GPR120gene enhanced the apoptosis-promoting effect of LTA(P<0.05),indicating that activation of the GPR120gene attenuated the increase of apoptosis rate caused by LTA-induced inflammatory Mac-T cells.The results suggest that GPR120can regulate inflammation by mediating TLR4and MyD88expression to inhibit NF-κB/MAPK inflammatory pathway activation and can promote cell proliferation.