Objective: The purpose of this study was to explore the protective effects and potential mechanisms of aloin on lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods: Mice were pretreatment with aloin 1 h before LPS administration. The number of inflammatory cells and the levels of TNF-α and IL-1β was detected. The lung histopathological changes, wet/dry ratio, MPO activity, GSH, MDA, SOD, and the expression of NF-κB and NLRP3 inflammasome were measured.Results: The results showed that aloin significantly inhibited the number of total cells, neutrophils, and macrophages, as well as the levels of TNF-α and IL-1β in BALF induced by LPS. In addition, pretreatment with aloin also inhibited LPS-induced lung histopathological injuries, lung wet/dry ratio, MPO activity, and MDA content. The levels of GSH and SOD were decreased by LPS and treatment of aloin could increase the levels of GSH and SOD. To study the protective mechanisms of alion on LPS-induced ALI, the expression of SIRT1, NF-κB and NLRP3 inflammasome were tested. We found that aloin significantly inhibited the activation of NF-κB and NLRP3 inflammasome in ALI induced by LPS. Meanwhile, aloin was found to increase the expression of SIRT1 and inhibition of SIRT1 by EX-527 reversed the protective effects of aloin.Conclusions: These results suggest that aloin exerts its protective effects on LPS-induced ALI by activation SIRT1, which subsequently results in the suppression of NF-κB and NLRP3 inflammasome.

中文翻译：

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Aloin通过激活SIRT1抑制NLRP3 /NF-κB，从而抑制脂多糖诱导的急性肺损伤。

目的：本研究旨在探讨芦荟苷对脂多糖（LPS）诱导的急性肺损伤（ALI）的保护作用及其潜在机制。方法：在LPS给药前1小时，用芦荟苷预处理小鼠。检测炎症细胞的数目以及TNF-α和IL-1β的水平。测量肺组织病理学变化，干/湿比，MPO活性，GSH，MDA，SOD以及NF-κB和NLRP3炎性小体的表达。结果：结果表明，芦荟蛋白显着抑制总细胞，中性粒细胞和中性粒细胞的数量。 LPS诱导的BALF中巨噬细胞以及TNF-α和IL-1β的水平。此外，用芦荟素预处理还可以抑制LPS诱导的肺组织病理学损伤，肺干/湿比，MPO活性和MDA含量。脂多糖降低了谷胱甘肽和超氧化物歧化酶的水平，芦荟处理可以增加谷胱甘肽和谷胱甘肽的水平。为了研究alion对LPS诱导的ALI的保护机制，测试了SIRT1，NF-κB和NLRP3炎性小体的表达。我们发现芦荟蛋白显着抑制LPS诱导的ALI中NF-κB和NLRP3炎性小体的激活。同时，发现芦荟蛋白增加SIRT1的表达，EX-527对SIRT1的抑制作用逆转了芦荟蛋白的保护作用。结论：芦荟苷通过激活SIRT1对LPS诱导的ALI发挥保护作用，随后导致抑制NF-κB和NLRP3炎性体。测试了NF-κB和NLRP3炎性小体。我们发现芦荟蛋白显着抑制LPS诱导的ALI中NF-κB和NLRP3炎性小体的激活。同时，发现芦荟蛋白增加SIRT1的表达，EX-527对SIRT1的抑制作用逆转了芦荟蛋白的保护作用。结论：芦荟苷通过激活SIRT1对LPS诱导的ALI发挥保护作用，随后导致抑制NF-κB和NLRP3炎性体。测试了NF-κB和NLRP3炎性小体。我们发现芦荟蛋白显着抑制LPS诱导的ALI中NF-κB和NLRP3炎性小体的激活。同时，发现芦荟蛋白增加SIRT1的表达，EX-527对SIRT1的抑制作用逆转了芦荟蛋白的保护作用。结论：芦荟苷通过激活SIRT1对LPS诱导的ALI发挥保护作用，随后导致抑制NF-κB和NLRP3炎性体。