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首页> 外文期刊>Drug Design, Development and Therapy >Ghrelin reduces liver impairment in a model of concanavalin A-induced acute hepatitis in mice
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Ghrelin reduces liver impairment in a model of concanavalin A-induced acute hepatitis in mice

机译：Ghrelin在伴刀豆球蛋白A诱发的小鼠急性肝炎模型中减少肝脏损伤

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Background and aims: Ghrelin is a 28-amino-acid gut hormone that was first discovered as a potent growth hormone secretagogue. Recently, it has been shown to exert a strong anti-inflammatory effect. The purpose of the study reported here was to explore the effect and mechanism of ghrelin on concanavalin (Con) A-induced acute hepatitis.Methods: Balb/C mice were divided into four groups: normal control (NC) (mice injected with vehicle [saline]); Con A (25 mg/kg); Con A + 10 μg/kg ghrelin; and Con A + 50 μg/kg ghrelin (1?hour before Con A injection). Pro-inflammatory cytokine levels were detected. Protein levels of phosphoinositide 3-kinase (PI3K); phosphorylated Akt (p-Akt); caspase 3, 8, and 9; and microtubule-associated protein 1 light chain 3 (LC3) were also detected. Perifosine (25 mM) (an Akt inhibitor) was used to investigate whether the protective effect of ghrelin was interrupted by an Akt inhibitor. Protein levels of p-AKT; Bcl-2; Bax; and caspase 3, 8, and 9 were also detected.Results: Aspartate aminotransferase, alanine aminotransferase, and pathological damage were significantly ameliorated by ghrelin pretreatment in Con A-induced hepatitis. Inflammatory cytokines were significantly reduced by ghrelin pretreatment. Bcl-2; Bax; and caspase 3, 8, and 9 expression were also clearly affected by ghrelin pretreatment, compared with the Con A-treated group. However, the Akt kinase inhibitor reversed the decrease of Bax and caspase 3, 8, 9, and reduced the protein level of p-Akt and Bcl-2. Ghrelin activated the PI3K/Akt/Bcl-2 pathway and inhibited activation of autophagy.Conclusion: Our results demonstrate that ghrelin attenuates Con A-induced acute immune hepatitis by activating the PI3K/Akt pathway and inhibiting the process of autophagy, which might be related to inhibition of inflammatory cytokine release, and prevention of hepatocyte apoptosis. These effects could be interrupted by an Akt kinase inhibitor.
机译：背景和目的：Ghrelin是一种28个氨基酸的肠道激素，最初被发现是一种有效的生长激素促分泌素。近来，已经显示出其具有很强的抗炎作用。本文报道的研究目的是探讨ghrelin对伴刀豆球蛋白（Con）A诱导的急性肝炎的作用和机制。方法：Balb / C小鼠分为四组：正常对照组（NC）（注射媒介物的小鼠[盐水]）; Con A（25 mg / kg）; Con A + 10μg/ kg ghrelin;和Con A + 50μg/ kg ghrelin（Con A注射前1小时）。检测到促炎细胞因子水平。磷酸肌醇3-激酶（PI3K）的蛋白质水平;磷酸化的Akt（p-Akt）;半胱天冬酶3、8和9;并检测到微管相关蛋白1轻链3（LC3）。使用Perifosine（25 mM）（一种Akt抑制剂）来研究生长素释放肽的保护作用是否被Akt抑制剂打断。 p-AKT的蛋白质水平; Bcl-2;巴克斯结果：ghrelin预处理可显着改善Con A诱发的肝炎患者的天冬氨酸转氨酶，丙氨酸转氨酶和病理损伤。 ghrelin预处理可显着减少炎症细胞因子。 Bcl-2;巴克斯与Con A处理组相比，ghrelin预处理也明显影响caspase 3和caspase 3、8和9的表达。但是，Akt激酶抑制剂可逆转Bax和caspase 3、8、9的下降，并降低p-Akt和Bcl-2的蛋白质水平。 Ghrelin激活了PI3K / Akt / Bcl-2途径并抑制了自噬的激活。抑制炎性细胞因子的释放，并防止肝细胞凋亡。这些作用可以被Akt激酶抑制剂打断。

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