Paeoniflorin protects PC12 cells from oxygen-glucose deprivation/reoxygenation-induced injury via activating JAK2/STAT3 signaling
Affiliations: Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China
- Published online on: March 29, 2021 https://doi.org/10.3892/etm.2021.10004
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Ischemic stroke is the most common type of stroke, and it has become a major health issue as it is characterized by high mortality and morbidity rates. Paeoniflorin (PF) is a natural compound and the main active ingredient of Radix Paeoniae. The aim of the present study was to investigate the role of PF in oxygen‑glucose deprivation/reoxygenation (OGD/R)‑induced injury of PC12 cells and its association with the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway. An in vitro model of OGD/R injury was established in PC12 cells. Subsequently, Cell Counting Kit‑8 assay and ELISA were used to evaluate cell viability and the secretion of inflammatory factors, respectively, in PC12 cells subjected to OGD/R and treated with PF. The levels of oxidative stress indicators and inflammatory factors were measured using corresponding commercial kits. In addition, the apoptosis rate of PC12 cells subjected to OGD/R and treated with PF was determined by flow cytometry, and the expression of apoptosis‑related proteins was analyzed by western blotting. Additionally, the expression levels of JAK2/STAT3 pathway‑related proteins were also evaluated. The cell viability, levels of oxidative stress, inflammation and apoptosis were also measured in OGD/R‑induced PC12 cell injury models following co‑treatment of cells with PF and FLLL32, a specific inhibitor of JAK2/STAT3 signaling. Cell viability was reduced, while oxidative stress and inflammation were increased after OGD/R‑induced injury. However, the treatment of cells with PF significantly enhanced cell viability, and alleviated oxidative stress, inflammation and apoptosis of OGD/R‑treated PC12 cells. Furthermore, PF activated the JAK2/STAT3 signaling pathway. Following FLLL32 intervention, the effects of PF on oxidative stress, inflammation and apoptosis of OGD/R‑treated PC12 cells were reversed. In conclusion, the findings of the present study suggested that PF may protect PC12 cells from OGD/R‑induced injury via activating the JAK2/STAT3 signaling pathway, thus providing novel insight into the mechanism through which PF may alleviate ischemic stroke and indicating a potential strategy for ischemic stroke treatment.