福建医科大学学报
福建醫科大學學報
복건의과대학학보
JOURNAL OF FUJIAN MEDICAL UNIVERSITY
2015年
1期
7-10
,共4页
趋化因子CXCL10%胰岛/细胞学%Toll样受体4%糖尿病
趨化因子CXCL10%胰島/細胞學%Toll樣受體4%糖尿病
추화인자CXCL10%이도/세포학%Toll양수체4%당뇨병
chemokine CXCL10%islets of Langerhans/cytology%Toll-like receptor 4%diabetes mellitus
目的探讨CXC趋化因子配体10（CXCL10）对βTC6细胞Toll样受体4（TLR4）表达及细胞凋亡的影响。方法体外培养βTC6细胞，0．1～10．0 ng／mL CXCL10分别干预βTC6细胞12，24，48 h后，应用Western‐blot检测TLR4表达情况，流式细胞术和DNA Ladder检测细胞凋亡情况。结果与对照组比较，CXCL10干预12 h ，10．0 ng／m L 干预组开始出现 T L R4蛋白的表达水平上调（0．840±0．049，P＜0．05）；干预24 h ，1．0和10．0 ng／m L 干预组T L R4的表达水平上调[分别为（0．851±0．052）和（0．893±0．030），P＜0．05]；干预48 h ，1．0和10．0 ng／m L干预组T L R4的表达进一步上调[分别为（0．876±0．046）和（0．923±0．027），P＜0．05]，且各干预浓度两两比较，差别均有统计学意义（P＜0．05）。CXCL10干预βTC6细胞24 h ，仅10．0 ng／mL干预组细胞出现DNA梯状条带；干预时间延长至48 h ，1．0和10．0 ng／mL 干预组均出现 DNA 梯状条带。流式细胞术显示， CXCL10诱导细胞凋亡呈浓度依赖性。结论长时间高浓度的CXCL10作用将导致 TLR4表达显著上调，并诱导β细胞凋亡。
目的探討CXC趨化因子配體10（CXCL10）對βTC6細胞Toll樣受體4（TLR4）錶達及細胞凋亡的影響。方法體外培養βTC6細胞，0．1～10．0 ng／mL CXCL10分彆榦預βTC6細胞12，24，48 h後，應用Western‐blot檢測TLR4錶達情況，流式細胞術和DNA Ladder檢測細胞凋亡情況。結果與對照組比較，CXCL10榦預12 h ，10．0 ng／m L 榦預組開始齣現 T L R4蛋白的錶達水平上調（0．840±0．049，P＜0．05）；榦預24 h ，1．0和10．0 ng／m L 榦預組T L R4的錶達水平上調[分彆為（0．851±0．052）和（0．893±0．030），P＜0．05]；榦預48 h ，1．0和10．0 ng／m L榦預組T L R4的錶達進一步上調[分彆為（0．876±0．046）和（0．923±0．027），P＜0．05]，且各榦預濃度兩兩比較，差彆均有統計學意義（P＜0．05）。CXCL10榦預βTC6細胞24 h ，僅10．0 ng／mL榦預組細胞齣現DNA梯狀條帶；榦預時間延長至48 h ，1．0和10．0 ng／mL 榦預組均齣現 DNA 梯狀條帶。流式細胞術顯示， CXCL10誘導細胞凋亡呈濃度依賴性。結論長時間高濃度的CXCL10作用將導緻 TLR4錶達顯著上調，併誘導β細胞凋亡。
목적탐토CXC추화인자배체10（CXCL10）대βTC6세포Toll양수체4（TLR4）표체급세포조망적영향。방법체외배양βTC6세포，0．1～10．0 ng／mL CXCL10분별간예βTC6세포12，24，48 h후，응용Western‐blot검측TLR4표체정황，류식세포술화DNA Ladder검측세포조망정황。결과여대조조비교，CXCL10간예12 h ，10．0 ng／m L 간예조개시출현 T L R4단백적표체수평상조（0．840±0．049，P＜0．05）；간예24 h ，1．0화10．0 ng／m L 간예조T L R4적표체수평상조[분별위（0．851±0．052）화（0．893±0．030），P＜0．05]；간예48 h ，1．0화10．0 ng／m L간예조T L R4적표체진일보상조[분별위（0．876±0．046）화（0．923±0．027），P＜0．05]，차각간예농도량량비교，차별균유통계학의의（P＜0．05）。CXCL10간예βTC6세포24 h ，부10．0 ng／mL간예조세포출현DNA제상조대；간예시간연장지48 h ，1．0화10．0 ng／mL 간예조균출현 DNA 제상조대。류식세포술현시， CXCL10유도세포조망정농도의뢰성。결론장시간고농도적CXCL10작용장도치 TLR4표체현저상조，병유도β세포조망。
Objective To investigate the changes of TLR4 expression and apoptosis in βcells in‐duced by CXCL10 . Methods Insulinoma cell line βTC6 cells were cultured in vitro , treating with CXCL10(0 .1 ,1 .0 ,10 .0 ng/mL) for 12 to 48 hours ,then the expression of TLR4 of theβTC6 cells and apoptosis were determined by Western‐blot ,DNA Ladder and flow cytometry . Results Compared with the control group ,theβTC6 cells intervened with CXCL10 for 12 hours at 10 .0 ng/mL showed an upregu‐lated TLR4 expression (0 .840 ± 0 .049 ,P<0 .05);when intervened for 24 hours ,the upregulated TLR4 expression was shown for the intervention with CXCL10 at 1 .0 and 10 .0 ng/mL (0 .851 ± 0 .052 and 0 .893 ± 0 .030 respectively , P< 0 .05);when intervened for 48 hours ,further upregulated expressions were shown for the intervention with CXCL10 at 1 .0 and 10 .0 ng/mL (0 .876 ± 0 .046 and 0 .923 ± 0 .027 respec‐tively ,P<0 .05) . Statistical analysis of each two CXCL10 intervention groups showed significant differ‐ences (P<0 .05) . When the βTC6 cells were intervened with CXCL10 for 12~24 hours ,DNA Ladder appeared at 10 .0 ng/mL ,w hile the DNA Ladder appeared at both 1 .0 and 10 .0 ng/mL if the intervention time period was extended to 48 hours . Conclusions CXCL 10 at high concentration and long intervention time could change the expression of TLR4 and induceβTC6 cells apoptosis .
