Subarachnoid hemorrhage (SAH) is a subtype of stroke with high mortality and morbidity due to the lack of effective therapy. Atorvastatin has been reported to alleviate early brain injury (EBI) following subarachnoid hemorrhage (SAH) via reducing reactive oxygen species, antiapoptosis, regulated autophagy, and neuroinflammation. Which was the related to the pyroptosis? Pyroptosis can be defined as a highly specific inflammatory programmed cell death, distinct from classical apoptosis and necrosis. However, the precise role of pyroptosis in atorvastatin‐mediated neuroprotection following SAH has not been confirmed. The present study aimed to investigate the neuroprotection and potential molecular mechanisms of atorvastatin in the SAH‐induced EBI via regulating neural pyroptosis using the filament perforation model of SAH in male C57BL/6 mice, and the hemin‐induced neuron damage model in HT‐22. Atorvastatin or vehicle was administrated 2 h after SAH and hemin‐induced neuron damage. The mortality, neurological score, brain water content, and neuronal death were evaluated. The results show that the atorvastatin treatment markedly increased survival rate, neurological score, greater survival of neurons, downregulated the protein expression of NLRP1, cleaved caspase‐1, interleukin‐1β (IL‐1β), and IL‐18, which indicated that atorvastatin‐inhibited pyroptosis and neuroinflammation, ameliorated neuron death in vivo/vitro subjected to SAH. Taken together, this study demonstrates that atorvastatin improved the neurological outcome in rats and reduced the neuron death by against neural pyroptosis and neuroinflammation.

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Nuclear factor of activated T cells 45 kDa (NF45), is a transcription factor that interacts with NF90 to regulate gene expression. It has been proved to be associated with tumor proliferation in various human malignancies. However, the role of NF45 in glioma is poorly understood. The aim of our study was to examine the relationship between NF45 expression and pathological grade in glioma and the impact of NF45 on the proliferation of glioma cells. Expression levels of NF45 are significantly elevated in high-grade human tissue samples compared with low-grade human glioma tissues samples (P < 0.0001) in Western blot analysis. The result of immunohistochemical also revealed that the expression of NF45 was overexpressed in 121 resected gliomas of different pathologic grades and associated with Ki-67. To investigate the role of NF45 in glioma carcinogenesis, we reduced the expression of NF45 by small interfering RNAs, and results showed suppression of cell proliferation, arrest of the cell cycle, and reduction in clone in vitro. Importantly, we show that SiNF45 can induce the expression of p21 and reduce the expression of proliferating cell nuclear antigen (PCNA) and cyclin E. These findings indicate that NF45 plays an important role in the growth regulation of glioma cells, suggesting that NF45 maybe a molecular marker for pathology and a novel therapeutic target for malignant glioma.

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