现代消化及介入诊疗
現代消化及介入診療
현대소화급개입진료
Modern Digestion & Intervention
2015年
4期
339-342
,共4页
殷汉华%何雅军%邓延梅%潘立武%刘序友%韩馥缦%叶国荣%吕霞%舒建昌
慇漢華%何雅軍%鄧延梅%潘立武%劉序友%韓馥縵%葉國榮%呂霞%舒建昌
은한화%하아군%산연매%반립무%류서우%한복만%협국영%려하%서건창
MyD88%姜黄素%肝星状细胞
MyD88%薑黃素%肝星狀細胞
MyD88%강황소%간성상세포
MyD88%Curcumin%Hepatic stellate cells
目的:观察姜黄素干预前后肝星状细胞(HSC)中髓样分化因子88(MyD88)蛋白的变化水平,以探讨姜黄素抗肝纤维化的相关机制。方法构建pCMV-Myc-MyD88重组质粒,将人肾上皮细胞293T细胞及HSC-T6细胞分别设为空白对照组、MyD88过表达组、姜黄素+MyD88过表达组,其中MyD88过表达组给予转染pCMV-Myc-MyD88重组质粒72 h,姜黄素+MyD88过表达组在转染48 h后加入姜黄素继续作用24 h。采用Western blot法检测MyD88蛋白表达。结果①转染pCMV-myc-MyD88重组质粒48 h后,MyD88在293T细胞及HSC中表达均明显增高(P<0.05),且经姜黄素处理后两类细胞中表达量明显降低(P<0.05)。②姜黄素处理后MyD88表达量较MyD88质粒转染组明显降低(P<0.05)。结论姜黄素可能通过抑制肝星状细胞MyD88蛋白表达,阻断MyD88依赖性信号通路的转导而发挥抗肝纤维化的作用。
目的:觀察薑黃素榦預前後肝星狀細胞(HSC)中髓樣分化因子88(MyD88)蛋白的變化水平,以探討薑黃素抗肝纖維化的相關機製。方法構建pCMV-Myc-MyD88重組質粒,將人腎上皮細胞293T細胞及HSC-T6細胞分彆設為空白對照組、MyD88過錶達組、薑黃素+MyD88過錶達組,其中MyD88過錶達組給予轉染pCMV-Myc-MyD88重組質粒72 h,薑黃素+MyD88過錶達組在轉染48 h後加入薑黃素繼續作用24 h。採用Western blot法檢測MyD88蛋白錶達。結果①轉染pCMV-myc-MyD88重組質粒48 h後,MyD88在293T細胞及HSC中錶達均明顯增高(P<0.05),且經薑黃素處理後兩類細胞中錶達量明顯降低(P<0.05)。②薑黃素處理後MyD88錶達量較MyD88質粒轉染組明顯降低(P<0.05)。結論薑黃素可能通過抑製肝星狀細胞MyD88蛋白錶達,阻斷MyD88依賴性信號通路的轉導而髮揮抗肝纖維化的作用。
목적:관찰강황소간예전후간성상세포(HSC)중수양분화인자88(MyD88)단백적변화수평,이탐토강황소항간섬유화적상관궤제。방법구건pCMV-Myc-MyD88중조질립,장인신상피세포293T세포급HSC-T6세포분별설위공백대조조、MyD88과표체조、강황소+MyD88과표체조,기중MyD88과표체조급여전염pCMV-Myc-MyD88중조질립72 h,강황소+MyD88과표체조재전염48 h후가입강황소계속작용24 h。채용Western blot법검측MyD88단백표체。결과①전염pCMV-myc-MyD88중조질립48 h후,MyD88재293T세포급HSC중표체균명현증고(P<0.05),차경강황소처리후량류세포중표체량명현강저(P<0.05)。②강황소처리후MyD88표체량교MyD88질립전염조명현강저(P<0.05)。결론강황소가능통과억제간성상세포MyD88단백표체,조단MyD88의뢰성신호통로적전도이발휘항간섬유화적작용。
Objective To observe the expression difference of myeloid differentiation factor 88(MyD88) protein in hepatic stellate cell (HSC) treated with curcumin, and to investigate the related mechanism of the an-ti-fibrotic effect of curcumin. Methods 293T cell and HSC cell were individually divided into control group, vector of MyD88 plasmid group,and curcumin+vectors of MyD88 plasmid group. The expression of MyD88 was detected by Western blot. Results ①After transfection of pCMV-Myc-MyD88, the expression of MyD88 was significantly increased (P<0.05), while the expression of MyD88 in curcumin+vectors of MyD88 plas-mid group was significantly decreased than vectors of MyD88 plasmid group (P<0.05). ②After transfection of pCMV-Myc-MyD88 HSC, the expression of MyD88 was significantly increased (P<0.05). The expression of MyD88 in curcumin+vectors of MyD88 plasmid group was significantly decreased compared with vectors of MyD88 plasmid group(P<0.05). Conclusions Curcumin might prevent liver fibrosis by inhabiting the ex-pression of MyD88 protein and blocking MyD88-dependent signaling pathway.