Peroxiredoxin 1/2 protects brain against H₂O₂‐induced apoptosis after subarachnoid hemorrhage

Abstract

Recent studies suggest that peroxiredoxin1/2 (Prx1/2) may be involved in the pathophysiology of post‐ischemic inflammatory responses in the brain. In this study, we assessed the distribution and function of Prx1/2 in mice after experimental subarachnoid hemorrhage (SAH). We investigated the distribution of Prx1/2 in the brains of mice both in vivo and in vitro using immunofluorescence staining. The expression of Prx1/2 after SAH was determined by Western blot. Adenanthin was used to inhibit Prx1/2 function, and Prx1/2 overexpression was achieved by injecting adeno‐associated virus. Oxidative stress and neuronal apoptosis were assessed both in vivo and in vitro. The neurologic function, inflammatory response, and related cellular signals were analyzed. The results showed that Prx1 was mainly expressed in astrocytes, and Prx2 was abundant in neurons. The expression of Prx1/2 was elevated after SAH, and their expression levels peaked before proinflammatory cytokines. Inhibiting Prx1/2 promoted neuronal apoptosis by increasing the hydrogen peroxide (H2O2) levels via the apoptosis signal‐regulating kinase 1/p38 pathway. By contrast, overexpression of Prx1/2 attenuated oxidative stress and neuronal apoptosis after SAH. Thus, early expression of Prx1/2 may protect the brain from oxidative damage after SAH and may provide a novel target for treating SAH.—Lu, Y., Zhang, X.‐S., Zhou, X.‐M., Gao, Y.‐Y., Chen, C.‐L., Liu, J.‐P., Ye, Z.‐N., Zhang, Z.‐H., Wu, L.‐Y., Li, W., Hang, C.‐H. Peroxiredoxin 1/2 protects brain against H2O2‐induced apoptosis after subarachnoid hemorrhage. FASEB J. 33, 3051–3062 (2019). http://www.fasebj.org

Inhibition of AIM2 inflammasome activation alleviates GSDMD-induced pyroptosis in early brain injury after subarachnoid haemorrhage

“…Immunofluorescence staining was performed as previously described 11 . Briefly, frozen brain sections (7 μm) and cultured cells on coverslips were fixed in ice-cold acetone and 4% paraformaldehyde, respectively.…”

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

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Prdx1 Reduces Intracerebral Hemorrhage-Induced Brain Injury via Targeting Inflammation- and Apoptosis-Related mRNA Stability

“…Although Prdx1, an RBP (Baltz et al, 2012;Castello et al, 2012;Kim et al, 2012;Kwon et al, 2013;Sebestyén et al, 2016), has been shown to be elevated after ICH (Nakaso et al, 2000), its roles in brain injury after ICH are still largely unknown. Prdx1 is a member of the peroxiredoxin family (Wood et al, 2003) and has been shown to be involved in regulating many pathological processes, such as redox reactions (Yamaguchi et al, 1993), inflammatory responses, apoptosis (Liu et al, 2014(Liu et al, , 2018Min et al, 2018;Lu et al, 2019), and tumorigenesis (Hoshino et al, 2005;Cao et al, 2009). These findings suggest that Prdx1 may also play important roles in regulating the above-mentioned pathological processes to influence the brain injury caused by ICH.…”