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Iranian Journal of Basic Medical Sciences، جلد ۲۶، شماره ۱۱، صفحات ۱۳۰۵-۱۳۱۲
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عنوان انگلیسی Peroxiredoxin 1 alleviates oxygen-glucose deprivation/ reoxygenation injury in N2a cells via suppressing the JNK/caspase-3 pathway
چکیده انگلیسی مقاله 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.
کلیدواژه‌های انگلیسی مقاله Caspase-3, Cell Hypoxia, c-Jun N-terminal kinase, Mice, Neuroblastoma, Peroxiredoxin 1, Reperfusion injury
نویسندگان مقاله | Yang Yuan
Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong, China


| Hongchen Tan
Malvern College Qingdao, Qingdao, Shandong, China


| Huailong Chen
Department of Anesthesiology, Qingdao Eight People’s Hospital, Qingdao, Shandong, China


| Jiawen Zhang
Department of Anesthesiology, Qingdao Clinical College Affiliated to Nanjing Medical University, Qingdao, Shandong, China


| Fei Shi
Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong, China


| Mingshan Wang
Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong, China


| Gaofeng Zhang
Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong, China


| Haipeng Wang
Department of Anesthesiology, Weifang No.2 People’s Hospital, Weifang, Shandong, China


| Rui Dong
Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, Shandong, China
نشانی اینترنتی https://ijbms.mums.ac.ir/article_22706.html
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