Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia
Objective To investigate the role and mechanism of mitochondrial oxidative stress in lead (Pb)-induced microglial inflammation. Methods BV2 microglia cells were divided into 4 groups and treated with 0 μmol/L (control group), 1 μmol/L, 5 μmol/L and 10 μmol/L lead acetate, respectively. The mRNA expr...
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| Format: | Article |
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Editorial Office of Journal of Guangxi Medical University
2024-07-01
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| Series: | Guangxi Yike Daxue xuebao |
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| Online Access: | https://journal.gxmu.edu.cn/article/doi/10.16190/j.cnki.45-1211/r.2024.07.001 |
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| author | ZHOU Qin LI Lifan HUANG Dingbang CHEN Kaiju ZHANG Xiaoshun CHEN Lixuan LI Hecheng MENG Xiaojing |
| author_facet | ZHOU Qin LI Lifan HUANG Dingbang CHEN Kaiju ZHANG Xiaoshun CHEN Lixuan LI Hecheng MENG Xiaojing |
| author_sort | ZHOU Qin |
| collection | DOAJ |
| description | Objective To investigate the role and mechanism of mitochondrial oxidative stress in lead (Pb)-induced microglial inflammation. Methods BV2 microglia cells were divided into 4 groups and treated with 0 μmol/L (control group), 1 μmol/L, 5 μmol/L and 10 μmol/L lead acetate, respectively. The mRNA expression levels of interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF-α) in microglia were detected by reverse transcription-quantitative PCR (RT-qPCR). The activation state of microglia and the expression of mitochondrial reactive oxygen species (mtROS) were observed by immunofluorescence, and the mitochondrial membrane potential was detected by JC-1. C57BL/6 mice were divided into control group, Pb exposure group (Pb group) (100 ppm), MitoTEMPO treatment group (MitoTEMPO group) (5 mg/kg), MitoTEMPO combined with Pb treatment group (MitoTEMPO+Pb group), and the levels of serum and cerebral cortex inflammatory factors IL-1β and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA). The levels of NLRP3, Caspase-1 and IL-1β in the hippocampus of mice were determined by western blotting. Results Pb could activate BV2 microglia cells. Compared with the control group, the levels of IL-6, IL-8 and TNF-α mRNA in the Pb group were increased in a dosedependent manner, mtROS was increased, and mitochondrial membrane potential was decreased. MitoTEMPO could inhibit the activation of microglia in hippocampus of mice, decrease the levels of IL-1β and TNF-α in serum and cerebral cortex, and increase the levels of NLRP3, Caspase-1 and IL-1β proteins in hippocampus (all P＜0.05). Conclusion Pb induces mitochondrial oxidative stress, which can activate microglia. The mechanism may be related to NLRP3 inflammasome activation. |
| format | Article |
| id | doaj-art-b131e6e1ce0345cca62ded35fdcdc83e |
| institution | DOAJ |
| issn | 1005-930X |
| language | zho |
| publishDate | 2024-07-01 |
| publisher | Editorial Office of Journal of Guangxi Medical University |
| record_format | Article |
| series | Guangxi Yike Daxue xuebao |
| spelling | doaj-art-b131e6e1ce0345cca62ded35fdcdc83e2025-08-20T02:57:28ZzhoEditorial Office of Journal of Guangxi Medical UniversityGuangxi Yike Daxue xuebao1005-930X2024-07-0141794595110.16190/j.cnki.45-1211/r.2024.07.00120240701Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microgliaZHOU Qin0LI Lifan1HUANG Dingbang2CHEN Kaiju3ZHANG Xiaoshun4CHEN Lixuan5LI Hecheng6MENG Xiaojing7Department of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaDepartment of Occupational Health and Occupational Medicine, School of Public Health, Southern Medical University, Guangzhou 510515, ChinaObjective To investigate the role and mechanism of mitochondrial oxidative stress in lead (Pb)-induced microglial inflammation. Methods BV2 microglia cells were divided into 4 groups and treated with 0 μmol/L (control group), 1 μmol/L, 5 μmol/L and 10 μmol/L lead acetate, respectively. The mRNA expression levels of interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF-α) in microglia were detected by reverse transcription-quantitative PCR (RT-qPCR). The activation state of microglia and the expression of mitochondrial reactive oxygen species (mtROS) were observed by immunofluorescence, and the mitochondrial membrane potential was detected by JC-1. C57BL/6 mice were divided into control group, Pb exposure group (Pb group) (100 ppm), MitoTEMPO treatment group (MitoTEMPO group) (5 mg/kg), MitoTEMPO combined with Pb treatment group (MitoTEMPO+Pb group), and the levels of serum and cerebral cortex inflammatory factors IL-1β and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA). The levels of NLRP3, Caspase-1 and IL-1β in the hippocampus of mice were determined by western blotting. Results Pb could activate BV2 microglia cells. Compared with the control group, the levels of IL-6, IL-8 and TNF-α mRNA in the Pb group were increased in a dosedependent manner, mtROS was increased, and mitochondrial membrane potential was decreased. MitoTEMPO could inhibit the activation of microglia in hippocampus of mice, decrease the levels of IL-1β and TNF-α in serum and cerebral cortex, and increase the levels of NLRP3, Caspase-1 and IL-1β proteins in hippocampus (all P＜0.05). Conclusion Pb induces mitochondrial oxidative stress, which can activate microglia. The mechanism may be related to NLRP3 inflammasome activation.https://journal.gxmu.edu.cn/article/doi/10.16190/j.cnki.45-1211/r.2024.07.001pbmicrogliamitochondrial oxidative stressinflammatory reactionnlrp3 inflammasome |
| spellingShingle | ZHOU Qin LI Lifan HUANG Dingbang CHEN Kaiju ZHANG Xiaoshun CHEN Lixuan LI Hecheng MENG Xiaojing Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia Guangxi Yike Daxue xuebao pb microglia mitochondrial oxidative stress inflammatory reaction nlrp3 inflammasome |
| title | Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia |
| title_full | Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia |
| title_fullStr | Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia |
| title_full_unstemmed | Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia |
| title_short | Effect of mitochondrial oxidative stress on lead-exposed inflammatory activation of microglia |
| title_sort | effect of mitochondrial oxidative stress on lead exposed inflammatory activation of microglia |
| topic | pb microglia mitochondrial oxidative stress inflammatory reaction nlrp3 inflammasome |
| url | https://journal.gxmu.edu.cn/article/doi/10.16190/j.cnki.45-1211/r.2024.07.001 |
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