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目的研究血清溶血卵磷脂(LPC)水平在非酒精性脂肪性肝病(NAFLD)进展中的变化及机制。方法雄性C57/BL6小鼠60只,分为高脂模型组(HFD)和正常对照组,分别给予高脂纯化饲料和低脂纯化饲料。高效液相色谱-蒸发光散射检测法(HPLC-ELSD)于饲养第4、8、12、16、20周分批测定两组小鼠血清中几种LPC的含量变化。Milliplex多因子检测法测定血清白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平。重组白细胞介素-6(IL-6)体外干预小鼠肝原代细胞,实时荧光定量PCR测溶血卵磷脂酰基转移酶1-4(LPCAT1-4)的基因表达。结果高脂模型组血清LPC16∶0、LPC18∶0和LPC18∶1水平从16周开始出现明显降低,第20周LPC16∶0和LPC18∶1的水平均显著低于正常对照组。高脂模型组血清IL-6水平在第16周和20周显著高于正常对照组;TNF-α水平在第16周显著高于正常对照组。此外,IL-6可诱导LPCAT1-4基因表达升高。结论在NAFLD进展中血清溶血卵磷脂(LPC)水平下降,可能与肝脏内激活的炎症信号通路有关。
Objective To investigate the changes and mechanisms of serum lysophosphatidylcholine (LPC) in the progression of non-alcoholic fatty liver disease (NAFLD). Methods Sixty male C57 / BL6 mice were divided into high fat model group (HFD) and normal control group, and were given high fat diet and low fat diet respectively. HPLC-ELSD was used to determine the changes of the contents of several LPCs in two groups of mice at 4, 8, 12, 16 and 20 weeks. The levels of serum IL-6 and TNF-α were measured by Milliplex multifactorial test. Recombinant interleukin-6 (IL-6) was used to interfere mouse primary hepatocytes in vitro, and the gene expression of lysolecithin acyltransferase 1-4 (LPCAT1-4) was detected by real-time fluorescence quantitative PCR. Results Serum levels of LPC16: 0, LPC18: 0 and LPC18: 1 in the model group were significantly decreased from the 16th week. The levels of LPC16: 0 and LPC18: 1 in the model group were significantly lower than those in the normal control group at the 20th week. Serum IL-6 levels in high-fat model group were significantly higher than those in normal control group at the 16th week and the 20th week, and TNF-α levels were significantly higher in the 16th week than that in the normal control group. In addition, IL-6 induces an increase in LPCAT1-4 gene expression. Conclusions The decrease of serum L-LPS in the progression of NAFLD may be related to the activation of inflammatory signal pathway in the liver.