中国实用医刊
中國實用醫刊
중국실용의간
CENTRAL PLAINS MEDICAL JOURNAL
2009年
12期
27-29
,共3页
张军峰%陈伟%李宏伟%赵丽萍%王雪剑%张献朝
張軍峰%陳偉%李宏偉%趙麗萍%王雪劍%張獻朝
장군봉%진위%리굉위%조려평%왕설검%장헌조
肾小管上皮细胞%白细胞介素-18%转分化%α-平滑肌肌动蛋白%SB203580
腎小管上皮細胞%白細胞介素-18%轉分化%α-平滑肌肌動蛋白%SB203580
신소관상피세포%백세포개소-18%전분화%α-평활기기동단백%SB203580
Renal tubular epithelial cells%Interleukin - 18%Transdifferentiation%α - smooth muscle actin%SB203580
目的 探讨白细胞介素-18(IL-18)诱导体外培养的人近端肾小管上皮细胞转分化的细胞内信号的转导机制.方法 应用细胞培养技术培养HK-2细胞.予不同浓度的p38MAPK通路特异性阻断剂SB203580预孵育细胞30 min后,再加入IL-18共同培养.应用RT-PCR方法检测α-SMA mRNA的表达水平,EEISA方法测定细胞胞浆中α-SMA的表达水平.结果 SB203580可呈剂量依赖性地抑制IL-18诱导的HK-2细胞α-SMA基因和蛋白的表达.结论 阻断p38MAPK信号通路可明显抑制IL-18诱导的HK-2细胞转分化作用;p38MAPK通路可能是调控IL-18诱导的HK-2细胞转分化的主要信号通路之一.
目的 探討白細胞介素-18(IL-18)誘導體外培養的人近耑腎小管上皮細胞轉分化的細胞內信號的轉導機製.方法 應用細胞培養技術培養HK-2細胞.予不同濃度的p38MAPK通路特異性阻斷劑SB203580預孵育細胞30 min後,再加入IL-18共同培養.應用RT-PCR方法檢測α-SMA mRNA的錶達水平,EEISA方法測定細胞胞漿中α-SMA的錶達水平.結果 SB203580可呈劑量依賴性地抑製IL-18誘導的HK-2細胞α-SMA基因和蛋白的錶達.結論 阻斷p38MAPK信號通路可明顯抑製IL-18誘導的HK-2細胞轉分化作用;p38MAPK通路可能是調控IL-18誘導的HK-2細胞轉分化的主要信號通路之一.
목적 탐토백세포개소-18(IL-18)유도체외배양적인근단신소관상피세포전분화적세포내신호적전도궤제.방법 응용세포배양기술배양HK-2세포.여불동농도적p38MAPK통로특이성조단제SB203580예부육세포30 min후,재가입IL-18공동배양.응용RT-PCR방법검측α-SMA mRNA적표체수평,EEISA방법측정세포포장중α-SMA적표체수평.결과 SB203580가정제량의뢰성지억제IL-18유도적HK-2세포α-SMA기인화단백적표체.결론 조단p38MAPK신호통로가명현억제IL-18유도적HK-2세포전분화작용;p38MAPK통로가능시조공IL-18유도적HK-2세포전분화적주요신호통로지일.
Objective To explore the intracellular signal transduction mechanism of transdiffer-entiation induced by IL - 18 in HK -2 cells. Methods Human proximal tubular epithelial cell lines (HK -2 cells) were cultured in vitro. After preincubated with SB203580 for 30 minutes, cells were ex-posed to IL- 18 for 24, 48 and 72 hours respectively. The expression level of α- SMA mRNA in cul-tured HK- 2 cells were assessed by quantitative reverse transcription polymerase chain reaction (RT-PCR). The expression level of α - SMA were measured by enzyme linked immunosorbent assay (ELISA). Results IL - 18 - induced expression of α - SMA mRNA and protein were inhibited obvious-ly by a dose - dependent manner when HK - 2 cells were incubated with SB203580. Conclusions IL -18- induced transdifferentiation of RTECs is suppressed obviously by blocking p38MAPK; IL- 18 -in-duced transdifferentiation of RTECs is probably mediated, at least in part, through the activation of p38MAPK and signaling pathways.