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lncRNA-uc007gqg.1在非酒精性脂肪肝中的表达规律
作者:袁静  朱雪萍 
单位:苏州大学附属儿童医院 新生儿科, 江苏 苏州 215025
关键词:非酒精性脂肪肝 内质网应激 lncRNA-uc007gqg.1 GRP94 Caspase-3 
分类号:R575.5
出版年·卷·期(页码):2019·38·第一期(6-13)
摘要:

目的:通过高脂饮食诱发肝脂肪变研究其与lncRNA-uc007gqg.1及GRP94、Caspase-3表达水平的相关性。方法:将80只8周龄新西兰雄性大耳白兔随机分为2组,对照组40只给予标准饮食,实验组40只给予高脂高胆固醇饮食喂养制非酒精性脂肪肝(NAFLD)模型。随机各取10只分别在造模第1、4、6、8 w检测两组兔的血生化指标;收集肝脏组织观察病理表现;分别以实时定量PCR和Westernblotting检测肝脏组织lncRNA-uc007gqg.1和GRP94、Caspase-3蛋白的表达水平。结果:与对照组相比,实验组ALT、AST、TC、LDL、HDL水平在造模4 w时出现明显增高;ALB、TB、CRP水平在造模6 w时明显增高;GGT、TG、ALT与AST比值水平在造模6、8 w时明显升高(P<0.01);肝细胞脂肪样变明显增加;肝组织lncRNA-uc007gqg.1基因表达水平和GRP94、Caspase-3蛋白表达量逐渐增加(P<0.05)。结论:肝组织lncRNA-uc007gqg.1表达水平升高与脂肪肝病变密切相关,可能参与NAFLD疾病进展,提示lncRNA-uc007gqg.1可能是防治该疾病的一个新靶点。

Objective:To investigate the relationship between high-fat diet-induced hepatic steatosis and the expression of GRP94, Caspase-3 and lncRNA-uc007gqg.1. Methods:Eighty 8-week-old New Zealand male white rabbits were randomly divided into control group (n=40) and experimental group (n=40). The blood biochemical indexes of 10 rabbits in each group were measured at the 1st, 4th, 6th and 8th week of the model, respectively. The pathological features of liver tissue were collected and the expression levels of lncRNA-uc007gqg.1 and GRP94,Caspase-3 protein in liver tissue were detected by real-time quantitative PCR and Westernblotting, respectively. Results:Compared with the control group, the levels of ALT,AST,TC,LDL,HDL and ALB,TB and CRP in the experimental group were significantly higher than those in the control group at the 4th weeks and 6th weeks, respectively. GGT,TG and the ratio of ALT to AST increased significantly at 6 weeks, and increased significantly at 8 weeks (P<0.01). The expression of lncRNA-uc007gqg.1 and GRP94,Caspase-3 protein increased gradually in liver tissue (all P<0.05). Conclusion:Uc007gqg.1 may be involved in the progression of NAFLD, suggests that uc007gqg. may be a new target for the prevention and treatment of NAFLD.

参考文献:

[1] YOUNOSSI Z,ANSTEE Q M,MARIETTI M,et al.Global burden of nafld and nash:trends,predictions,risk factors and prevention[J].Nat Rev Gastroenterol Hepatol,2018,15(1):11-20.
[2] YOUNOSSI Z M,STEPANOVA M,RAFIQ N,et al.Nonalcoholic steatofibrosis independently predicts mortality in nonalcoholic fatty liver disease[J].Hepatol Commun,2017,1(5):421-428.
[3] RUFINATSCHA K,RESS C,FOLIE S,et al.Metabolic effects of reduced growth hormone action in fatty liver disease[J].Hepatol Int,2018,12(5):474-481.
[4] ZHU X P,XIAO Z H,XU Y M,et al.Differential impacts of soybean and fish oils on hepatocyte lipid droplet accumulation and endoplasmic reticulum stress in primary rabbit hepatocytes[J].Gastroenterol Res Pract,2016,2016(6):9717014.
[5] YOUNOSSI Z M,BLISSETT D,BLISSETT R,et al.The economic and clinical burden of nonalcoholic fatty liver disease in the united states and europe[J].Hepatology,2016,64(5):1577-1586.
[6] LEBEAUPIN C,VALLÉE D,HAZARI Y,et al. Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease[J].J Hepatol,2018,69(4):927-947.
[7] CHEN T,ZHU H,WANG Y,et al.Apoptosis of bone marrow mesenchymal stromal/stem cells via the mapk and endoplasmic reticulum stress signaling pathways[J].Am J Transl Res,2018,10(8):2555-2566.
[8] ALBHAISI S,ISSA D,ALKHOURI N,et al.Non-alcoholic fatty liver disease:a pandemic disease with multisystem burden.Hepatobiliary Surg Nutr,2018,7(5):389-391.
[9] JOO I,LEE J M,YOON J H,et al.Nonalcoholic fatty liver disease:intravoxel incoherent motion diffusion-weighted mr imaging-an experimental study in a rabbit model[J].Radiology,2014,270(1):131-40.
[10] 中华医学会肝脏病学分会脂肪肝和酒精性肝病学组.非酒精性脂肪性肝病诊断标准[J].中华肝脏病杂志,2003,11(2):71.
[11] RAO R V,NIAZI K,MOLLAHAN P,et al.Coupling endoplasmic reticulum stress to the cell-death program:a novel hsp90-independent role for the small chaperone protein p23[J].Cell Death Differ,2007,14(6):1172-1180.
[12] KOBAYASHI M,SUZUKI M,OHNO T,et al.Detection of differentially expressed candidate genes for a fatty liver qtl on mouse chromosome 12[J].BMC Genet,2016,17(1):1-10.
[13] WANG C Y,JÉGU T,CHU H P,et al.Smchd1 merges chromosome compartments and assists formation of super-structures on the inactive x[J].Cell,2018,174(2):406-421.
[14] PARAFATI M,KIRBY R J,KHORASANIZADEH S,et al.A nonalcoholic fatty liver disease model in human induced pluripotent stem cell-derived hepatocytes,created by endoplasmic reticulum stress-induced steatosis[J].Dis Model Mech,2018,11(9):dmm033530.
[15] PARAFATI M,RHO H S,KIM A,et al.Fxr inhibits endoplasmic reticulum stress-induced nlrp3 inflammasome in hepatocytes and ameliorates liver injury[J].Cell Rep,2018,24(11):2985-2999.
[16] WANG D,LAO L,PANG X,et al.Asiatic acid from potentilla chinensis alleviates non-alcoholic fatty liver by regulating endoplasmic reticulum stress and lipid metabolism[J].Int Immunopharmacol,2018,65:256-267.
[17] LIU C,FU Q,MU R,et al.Dexmedetomidine alleviates cerebral ischemia-reperfusion injury by inhibiting endoplasmic reticulum stress dependent apoptosis through the perk-chop-caspase-11 pathway[J].Brain Res,2018,1701:246-254.

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