实用药物与临床
實用藥物與臨床
실용약물여림상
PRACTICAL PHARMACY AND CLINICAL REMEDIES
2014年
10期
1243-1246
,共4页
凋亡%脂多糖%非酒精性脂肪肝炎%肿瘤坏死因子-α
凋亡%脂多糖%非酒精性脂肪肝炎%腫瘤壞死因子-α
조망%지다당%비주정성지방간염%종류배사인자-α
Apoptosis%Lipopolysaccharide%Non-alcoholic steatohepatitis%Tumour necrosis factor-α
目的：本研究旨在探讨脂多糖在非酒精性肝炎( NASH)模型中的作用。方法采用胆碱蛋氨酸缺乏(Methionine choline deficient,MCD)饮食诱导的小鼠 NASH 模型。18只雄性 C57BL/6小鼠分为3组, MCS+Saline组给予正常饮食+腹腔生理盐水,MCD+Saline组给予胆碱蛋氨酸缺乏饮食+腹腔注射生理盐水, MCD+LPS组给予胆碱蛋氨酸缺乏饮食+腹腔注射1 mg/kg脂多糖,共2周。在最后一次注射的6 h之后处死小鼠,取血清和肝组织。进行肝脏HE染色和Sirius Red染色,观察肝组织病理学变化。并测定血清中血清丙氨酸氨基转移酶( ALT)和肿瘤坏死因子-α( TNF-α)的含量。结果 MCD造成小鼠肝脏中大量脂肪滴的沉积和炎症细胞浸润,血清ALT升高,脂多糖注射进一步加重肝细胞凋亡,肝脏中TBARS进一步升高,血清TNF-α含量显著增加。结论在MCD所致非酒精性脂肪肝炎模型小鼠中,腹腔注射脂多糖引起血清中TNF-α升高,进一步加重细胞凋亡,因此,脂多糖在非酒精性脂肪肝炎的进程中具有重要作用,提示临床预防或治疗非酒精性脂肪肝炎需要关注患者肠道菌群失调症状。
目的：本研究旨在探討脂多糖在非酒精性肝炎( NASH)模型中的作用。方法採用膽堿蛋氨痠缺乏(Methionine choline deficient,MCD)飲食誘導的小鼠 NASH 模型。18隻雄性 C57BL/6小鼠分為3組, MCS+Saline組給予正常飲食+腹腔生理鹽水,MCD+Saline組給予膽堿蛋氨痠缺乏飲食+腹腔註射生理鹽水, MCD+LPS組給予膽堿蛋氨痠缺乏飲食+腹腔註射1 mg/kg脂多糖,共2週。在最後一次註射的6 h之後處死小鼠,取血清和肝組織。進行肝髒HE染色和Sirius Red染色,觀察肝組織病理學變化。併測定血清中血清丙氨痠氨基轉移酶( ALT)和腫瘤壞死因子-α( TNF-α)的含量。結果 MCD造成小鼠肝髒中大量脂肪滴的沉積和炎癥細胞浸潤,血清ALT升高,脂多糖註射進一步加重肝細胞凋亡,肝髒中TBARS進一步升高,血清TNF-α含量顯著增加。結論在MCD所緻非酒精性脂肪肝炎模型小鼠中,腹腔註射脂多糖引起血清中TNF-α升高,進一步加重細胞凋亡,因此,脂多糖在非酒精性脂肪肝炎的進程中具有重要作用,提示臨床預防或治療非酒精性脂肪肝炎需要關註患者腸道菌群失調癥狀。
목적：본연구지재탐토지다당재비주정성간염( NASH)모형중적작용。방법채용담감단안산결핍(Methionine choline deficient,MCD)음식유도적소서 NASH 모형。18지웅성 C57BL/6소서분위3조, MCS+Saline조급여정상음식+복강생리염수,MCD+Saline조급여담감단안산결핍음식+복강주사생리염수, MCD+LPS조급여담감단안산결핍음식+복강주사1 mg/kg지다당,공2주。재최후일차주사적6 h지후처사소서,취혈청화간조직。진행간장HE염색화Sirius Red염색,관찰간조직병이학변화。병측정혈청중혈청병안산안기전이매( ALT)화종류배사인자-α( TNF-α)적함량。결과 MCD조성소서간장중대량지방적적침적화염증세포침윤,혈청ALT승고,지다당주사진일보가중간세포조망,간장중TBARS진일보승고,혈청TNF-α함량현저증가。결론재MCD소치비주정성지방간염모형소서중,복강주사지다당인기혈청중TNF-α승고,진일보가중세포조망,인차,지다당재비주정성지방간염적진정중구유중요작용,제시림상예방혹치료비주정성지방간염수요관주환자장도균군실조증상。
Objective To investigate the effect of lipopolysaccharide on a non-alcoholic steatohepatitis ( NASH) model. Methods Male C57BL/6 mice were divided into 3 groups. MCS+Saline group was fed with methi-onine-choline-sufficient ( MCS) diet and intraperitoneally injected with saline;MCD+Saline group was fed with methi-onine-choline-deficient ( MCD) diet and intraperitoneally injected with saline;MCD+LPS group was fed with MCD diet and intraperitoneally injected with 1 mg/kg lipopolysaccharide ( LPS) twice weekly. Then mice were sacrificed 6 h after last injection. The changes on liver histology was assessed by HE and Sirius Red staining. ALT and TNF-αof ser-um were dectected. Results MCD diet could significantly increase the hepatic fat deposition and inflammatory cell in-filtration,and raise the serum ALT level of the MCD diet-fed mice. Apoptosis of hepatocytes and TBARS content of MCD mice were accelerated by LPS injection,and the TNF-α was increased. Conclusion LPS up-regulates TNF-αproduction of NASH mice induced by MCD. LPS may play a key role in the pathogenesis of NASH. The alteration of intestinal flora should be considered during the treatment and prevention of NASH.
