基于PI3K/Akt/NF-kB信号通路探讨高尿酸血症合并非酒精性脂肪肝机制
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河南中医药大学

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Study on the Mechanism of Hyperuricemia combined with Nonalcoholic Fatty Liver based on PI3K/Akt/NF-kB
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1.Henan University of Chinese Medicine;2.Henan Provincial Hospital of Chinese Medicine

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    摘要:目的:基于PI3K/Akt/NF-kB信号通路研究高尿酸血症合并非酒精性脂肪肝(HUA-NAFLD)的发病机制。方法:64只SD大鼠,随机分为空白组、HUA组、NAFLD组、HUA-NAFLD组,每组16只,分别于8、12周末取材,对大鼠血清生化指标进行检测;苏木素-伊红法(HE)和油红O染色法观察肝脏组织病理变化和脂质沉积情况;蛋白免疫印迹法(WB)检测肝脏组织PI3K/Akt/NF-kB信号通路相关蛋白表达水平。结果:与其余3组比较,HUA-NAFLD组大鼠肝脏指数明显升高(P<0.05)。与空白组比较,HUA组UA、LDL水平升高,NAFLD组HDL水平降低,HUA-NAFLD组UA、CHOL、TG、LDL水平升高,HDL水平降低(P<0.05);与HUA组比较,NAFLD组UREA水平降低(P<0.05);与HUA-NAFLD组比较,HUA组CHOL、TG、LDL水平降低,NAFLD组UA、TG、LDL降低(P<0.05)。HE和油红O染色结果显示,与其余3组比较,HUA-NAFLD组大鼠肝细胞出现大量脂肪空泡,肝索结构模糊,病变更重。WB结果显示,与空白组比较,NAFLD组AKT、p65磷酸化水平显著升高,HUA-NAFLD组AKT、PI3K、p65、IKKβ磷酸化水平显著升高(P<0.05);与HUA-NAFLD组比较,HUA、NAFLD组AKT、p65磷酸化水平显著下降,HUA组IKKβ磷酸化水平显著下降(P<0.05);与HUA组比较,NAFLD组p65磷酸化水平显著升高(P<0.05)。结论:HUA-NAFLD组较单个疾病组生化指标更加异常,肝脏病变程度更重,PI3K/Akt/NF-KB信号通路可能在HUA、NAFLD以及HUA-NAFLD发病过程中发挥重要作用。

    Abstract:

    Abstract: Objective: To study the pathogenesis of hyperuricemia combined with nonalcoholic fatty liver disease (HUA-NAFLD) based on PI3K/Akt/NF-kB signaling pathway. Methods: 64 SD rats were randomly divided into blank group, HUA group, NAFLD group, and HUA-NAFLD group, 16 rats in each group. The samples were collected at the end of the 8th and 12th week, respectively. The serum biochemical indexes of the rats were detected; The pathological changes and lipid deposition in liver tissue were observed by hematoxylin-eosin staining (HE) and Oil Red O staining; the expression levels of PI3K/Akt/NF-kB signaling pathway-related proteins in liver tissue were detected by Western blot. Results: Compared with the other three groups, the liver index of the rats in the HUA-NAFLD group was significantly increased (P<0.05). Compared with the blank group, the levels of UA and LDL in the HUA group were increased, the levels of HDL in the NAFLD group were decreased, the levels of UA, CHOL, TG and LDL in the HUA-NAFLD group were increased, and the levels of HDL were decreased (P<0.05); Compared with the HUA-NAFLD group, the levels of CHOL, TG and LDL were decreased in the HUA group, and the levels of UA, TG and LDL in the NAFLD group were decreased (P<0.05). The results of HE and oil red O staining showed that compared with the other three groups, rat liver cells in the HUA-NAFLD group had a large number of fat vacuoles, blurred liver cord structure and more severe lesions. The WB results showed that compared with the blank group, the phosphorylation levels of AKT and p65 in the NAFLD group were significantly increased, and the phosphorylation levels of AKT, PI3K, p65 and IKKβ in the HUA-NAFLD group were significantly increased, and compared with the HUA-NAFLD group, the phosphorylation levels of AKT and p65 in the HUA-NAFLD group decreased significantly(P<0.05). The phosphorylation level of IKKβ decreased significantly in the HUA group, and compared with the HUA group, the phosphorylation level of p65 in the NAFLD group increased significantly (P<0.05). Conclusion: Compared with the single disease group, the HUA-NAFLD group has more abnormal biochemical indexes and more severe liver lesions. The PI3K/Akt/NF-KB signaling pathway may play an important role in the pathogenesis of HUA, NAFLD and HUA-NAFLD.

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  • 收稿日期:2023-03-13
  • 最后修改日期:2023-09-23
  • 录用日期:2023-11-03
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