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Stattic alleviates acute hepatic damage induced by LPS/d-galactosamine in mice
Innate Immunity ( IF 3.2 ) Pub Date : 2021-02-12 , DOI: 10.1177/1753425920988330
Sijia Li 1 , Kai Hu 1 , Longjiang Li 1 , Yi Shen 1 , Jiayi Huang 1 , Li Tang 1 , Li Zhang 1 , Ruyue Shao 2, 3 , Han Lu 4 , Yongqiang Yang 1
Affiliation  

Increasing evidence indicates that signal transducer and activator of transcription 3 (STAT3), a vital transcription factor, plays crucial roles in the regulation of inflammation. STAT3 has become a novel therapeutic target for intervention in inflammation-related disorders. However, it remains unclear whether STAT3 plays a part in acute hepatic damage. To investigate the effects of STAT3 here, LPS/d-GalN-induced hepatic damage was induced in mice, the STAT3 inhibitor Stattic was administered, and the degree of liver injury, inflammation, and hepatocyte apoptosis were investigated. The results showed that Stattic mitigated the hepatic morphologic abnormalities and decreased the level of aminotransferase in LPS/D-GalN-insulted mice. The results also indicated that Stattic decreased the levels of TNF-α and IL-6, prevented the activation of the caspase cascade, suppressed cleavage of PARP, and decreased the quantity of TUNEL-positive cells. These results suggest that Stattic provided protective benefits in LPS/d-GalN-induced hepatic damage, and the protective effects might be associated with its anti-inflammatory and anti-apoptotic effects. Therefore, STAT3 might become a novel target for intervening in inflammation-based and apoptosis-based hepatic disorders.



中文翻译:

Stattic 可减轻 LPS/d-半乳糖胺对小鼠的急性肝损伤

越来越多的证据表明,信号转导和转录激活因子 3 (STAT3) 是一种重要的转录因子,在炎症调节中起着至关重要的作用。STAT3 已成为干预炎症相关疾病的新治疗靶点。然而,目前尚不清楚 STAT3 是否在急性肝损伤中起作用。为了研究 STAT3 在这里的作用,在小鼠中诱导 LPS/ d -GalN 诱导的肝损伤,给予 STAT3 抑制剂 Stattic,并研究肝损伤程度、炎症和肝细胞凋亡。结果表明,Stattic 减轻了肝脏形态学异常并降低了 LPS/ D中的转氨酶水平-GalN 侮辱的小鼠。结果还表明,Stattic 降低了 TNF-α 和 IL-6 的水平,阻止了 caspase 级联的激活,抑制了 PARP 的切割,并减少了 TUNEL 阳性细胞的数量。这些结果表明,Stattic 在 LPS/ d -GalN 诱导的肝损伤中提供了保护作用,并且保护作用可能与其抗炎和抗凋亡作用有关。因此,STAT3 可能成为干预基于炎症和基于细胞凋亡的肝脏疾病的新靶点。

更新日期:2021-02-12
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