期刊
NEURAL REGENERATION RESEARCH
卷 15, 期 11, 页码 2154-2161出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.282271
关键词
apoptosis; calcium; caspase-1; NLRP3; mitochondrial impairment; oxidative stress; oxygen-glucose deprivation; PC12; shRNA; TRPM2
资金
- National Natural Science Foundation of China [81671532, 81771625]
- Jiangsu Provincial Key Medical Discipline of China [ZDXKA2016013]
- Jiangsu Provincial Medical Youth Talent of China [QNRC2016758]
- Jiangsu Province Women and Children Health Research Project of China [F201750]
- Public Health Technology Project of Suzhou City of China [SYS201765]
- Department of Pediatrics Clinical Center of Suzhou City of China [Szzx201504]
Transient receptor potential melastatin 2 (TRPM2) is an important ion channel that represents a potential target for treating injury caused by cerebral ischemia. However, it is unclear whether reducing TRPM2 expression can help repair cerebral injury, and if so what the mechanism underlying this process involves. This study investigated the protective effect of reducing TRPM2 expression on pheochromocytoma (PC12) cells injured by oxygen-glucose deprivation (OGD). PC12 cells were transfected with plasmid encoding TRPM2 shRNAS, then subjected to OGD by incubation in glucose-free medium under hypoxic conditions for 8 hours, after which the cells were allowed to reoxygenate for 24 hours. Apoptotic cells, mitochondrial membrane potentials, reactive oxygen species levels, and cellular calcium levels were detected using flow cytometry. The relative expression of C-X-C motif chemokine ligand 2 (CXCL2), NACHT, LRR, and PYD domain- containing protein 3 (NALP3), and caspase-1 were detected using fluorescence-based quantitative reverse transcription-polymerase chain reaction and western blotting. The rates of apoptosis, mitochondrial membrane potentials, reactive oxygen species levels, and cellular calcium levels in the TRPM2-shRNA + OGD group were lower than those observed in the OGD group. Taken together, these results suggest that TRPM2 knockdown reduces OGD-induced neuronal injury, potentially by inhibiting apoptosis and reducing oxidative stress levels, mitochondrial membrane potentials, intracellular calcium concentrations, and NLRP3 inflammasome activation.
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