سامانه مدیریت نشریات علمی دانشگاه علوم پزشکی مشهد

Yuan, Yang, Tan, Hongchen, Chen, Huailong, Zhang, Jiawen, Shi, Fei, Wang, Mingshan, Zhang, Gaofeng, Wang, Haipeng, Dong, Rui. (1402). Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway. , 26(11), 1305-1312. doi: 10.22038/ijbms.2023.71390.15528
Yang Yuan; Hongchen Tan; Huailong Chen; Jiawen Zhang; Fei Shi; Mingshan Wang; Gaofeng Zhang; Haipeng Wang; Rui Dong. "Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway". , 26, 11, 1402, 1305-1312. doi: 10.22038/ijbms.2023.71390.15528
Yuan, Yang, Tan, Hongchen, Chen, Huailong, Zhang, Jiawen, Shi, Fei, Wang, Mingshan, Zhang, Gaofeng, Wang, Haipeng, Dong, Rui. (1402). 'Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway', , 26(11), pp. 1305-1312. doi: 10.22038/ijbms.2023.71390.15528
Yuan, Yang, Tan, Hongchen, Chen, Huailong, Zhang, Jiawen, Shi, Fei, Wang, Mingshan, Zhang, Gaofeng, Wang, Haipeng, Dong, Rui. Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway. , 1402; 26(11): 1305-1312. doi: 10.22038/ijbms.2023.71390.15528

Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway

Iranian Journal of Basic Medical Sciences
مقاله 7، دوره 26، شماره 11، بهمن 2023، صفحه 1305-1312    اصل مقاله (495.69 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2023.71390.15528
نویسندگان
Yang Yuan1؛ Hongchen Tan2؛ Huailong Chen3؛ Jiawen Zhang4؛ Fei Shi1؛ Mingshan Wang1؛ Gaofeng Zhang* 1؛ Haipeng Wang* 5؛ Rui Dong1
1Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong, China
2Malvern College Qingdao, Qingdao, Shandong, China
3Department of Anesthesiology, Qingdao Eight People’s Hospital, Qingdao, Shandong, China
4Department of Anesthesiology, Qingdao Clinical College Affiliated to Nanjing Medical University, Qingdao, Shandong, China
5Department of Anesthesiology, Weifang No.2 People’s Hospital, Weifang, Shandong, China
چکیده
Objective(s): Cerebral ischemia/reperfusion (I/R) injury inevitably aggravates the initial cerebral tissue damage following a stroke. Peroxiredoxin 1 (Prdx1) is a representative protein of the endogenous antioxidant enzyme family that regulates several reactive oxygen species (ROS)-dependent signaling pathways, whereas the JNK/caspase-3 proapoptotic pathway has a prominent role during cerebral I/R injury. This study aimed to examine the potential mechanism of Prdx1 in Neuro 2A (N2a) cells following oxygen–glucose deprivation and reoxygenation (OGD/R) injury. 
Materials and Methods: N2a cells were exposed to OGD/R to simulate cerebral I/R injury. Prdx1 siRNA transfection and the JNK inhibitor (SP600125) were used to interfere with their relative expressions. CCK-8 assay, flow cytometry, and lactate dehydrogenase (LDH) assay were employed to determine the viability and apoptosis of N2a cells. The intracellular ROS content was assessed using ROS Assay Kit. Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analyses were conducted to detect the expression levels of Prdx1, JNK, phosphorylated JNK (p-JNK), and cleaved caspase-3. 
Results: Firstly, Prdx1, p-JNK, and cleaved caspase-3 expression were significantly induced in OGD/R-exposed N2a cells. Secondly, the knockdown of Prdx1 inhibited cell viability and increased apoptosis rate, expression of p-JNK, and cleaved caspase-3 expression. Thirdly, SP600125 inhibited the JNK/caspase-3 signaling pathway and mitigated cell injury following OGD/R. Finally, SP600125 partially reversed Prdx1 down-regulation-mediated cleaved caspase-3 activation and OGD/R damage in N2a cells. 
Conclusion: Prdx1 alleviates the injury to N2a cells induced by OGD/R via suppressing JNK/caspase-3 pathway, showing promise as a potential therapeutic for cerebral I/R injury.
کلیدواژه‌ها
Caspase-3؛ Cell Hypoxia؛ c-Jun N-terminal kinase؛ Mice؛ Neuroblastoma؛ Peroxiredoxin 1؛ Reperfusion Injury
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