Visfatin is involved in the body's inflammation and immune response. Inflammation could promote, while visfatin may directly or indirectly mitigate the effects of apoptosis and autophagy. Whether visfatin lessens the detrimental effects of lipopolysaccharide (LPS)-induced mouse acute lung injury (ALI) is poorly understood yet. Therefore, in the current study, the regulation mechanism of visfatin on apoptosis and autophagy was explored in Kunming mice by replicating LPS-induced inflammatory ALI model. Based on the mouse model of ALI, HE staining, TUNEL, transmission electron microscopy, immunohistochemical staining, real-time fluorescence quantitative PCR and western blot were used and the results showed that the alveolar septum was thinner than that of the LPS group, slight lung interstitial and alveolar exudation appeared, and a small number of inflammatory cell infiltration was found in the visfatin intervention group, indicating reduced tissue damage in lungs. After visfatin treatment, the expression of pro-apoptotic genes Bax, Bik, and p53 decreased and the expression of anti-apoptotic genes Bcl-2 and Bcl-xl increased, and expression of autophagy factors LC3 and Beclin1 decreased, indicating that visfatin inhibits apoptosis and reduces autophagy. The expression of PI3K and p-AKT was upregulated in the visfatin intervention group, the expression of AKT was downregulated, and the PI3K/AKT signaling pathway was activated. Hence, visfatin could activate the PI3K/AKT signaling pathway, reduce the apoptotic rate in alveolar epithelial cells and the level of autophagy in ALI by regulating the expression of autophagy factors, ultimately causing a protective effect on lung tissue.

中文翻译：

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Visfatin在减轻小鼠急性肺损伤期间通过PI3K / AKT信号通路引起的脂多糖诱导的细胞凋亡和自噬中起重要作用。

Visfatin参与人体的炎症和免疫反应。炎症可以促进炎症，而visfatin可以直接或间接减轻细胞凋亡和自噬的影响。visfatin是否减轻了脂多糖（LPS）诱导的小鼠急性肺损伤（ALI）的有害作用，对此知之甚少。因此，在目前的研究中，通过复制LPS诱导的炎症性ALI模型，探讨了visfatin对细胞凋亡和自噬的调控机制。根据ALI小鼠模型，HE染色，TUNEL，透射电镜，免疫组织化学染色，实时荧光定量PCR和western blot结果显示，肺泡隔薄于LPS组，肺轻出现间隙和肺泡渗出，visfatin干预组发现少量炎性细胞浸润，表明肺部组织损伤减少。visfatin处理后，促凋亡基因Bax，Bik和p53的表达降低，抗凋亡基因Bcl-2和Bcl-xl的表达增加，自噬因子LC3和Beclin1的表达降低，表明visfatin抑制凋亡并减少自噬。visfatin干预组PI3K和p-AKT的表达上调，AKT的表达下调，PI3K / AKT信号通路被激活。因此，visfatin可以通过调节自噬因子的表达来激活PI3K / AKT信号通路，降低肺泡上皮细胞的凋亡率和ALI中的自噬水平，