中华外科杂志
中華外科雜誌
중화외과잡지
CHINESE JOURNAL OF SURGERY
2010年
12期
919-923
,共5页
胆酸类%胆管肿瘤%细胞活力%白细胞介素6
膽痠類%膽管腫瘤%細胞活力%白細胞介素6
담산류%담관종류%세포활력%백세포개소6
Cholic acids%Bile duct neoplasms%Cell viability%Interleukin-6
目的 探讨不同胆汁酸对胆管癌细胞株QBC939中IL-6的表达和细胞活力的影响.方法 分别使用不同浓度的游离胆汁酸以及其对应的甘氨酸结合型胆汁酸作用于胆管癌细胞株QBC939,药物浓度分别为:胆酸(CA)800 μmol/L、脱氧胆酸(DCA)100 μmol/L、鹅脱氧胆酸(CDCA)100 μmol/L、甘氨胆酸(GCA)1200 μmol/L、甘氨脱氧月胆酸(GDCA)200 μmol/L以及甘氨鹅脱氧胆酸(GCDCA)300 μmol/L.以MTT法检测不同胆汁酸刺激24、48、72 h后胆管癌细胞活力的变化,并以ELISA法检测肿瘤细胞中IL-6表达的改变.结果 DCA、CDCA、GCDCA作用48 h后,肿瘤细胞活力比值(A处理组/A对照组)分别为0.61、0.58和1.26;作用72 h后,CA、DCA、CDCA、GCA、GDCA和GCDCA各组肿瘤细胞活力比值分别为0.48、0.50、0.42、1.29、1.30和1.41;与对照组相比,以上各组细胞活力变化均具有统计学意义(P＜0.05).对照组肿瘤细胞培养48和72 h后,IL-6表达量分别为(198±32)ng/L和(323±34)ng/L,CA、DCA、CDCA、GCA、GDCA和GCDCA作用48 h后IL-6的表达量分别为(106±33)ng/L、(88±29)ng/L、(116±54)ng/L、(413±21)ng/L、(587±32)ng/L和(366±30)ng/L,作用72 h后IL-6表达量分别为(123±66)ng/L、(45±21)ng/L、(74±45)ng/L、(792±13)ng/L、(1310±22)ng/L和(845±18)ng/L;与对照组相比,以上各组IL-6表达量变化均具有统计学意义(P＜0.05).结论 游离胆汁酸CA、DCA和CDCA能减少胆管癌细胞IL-6的表达,并抑制细胞活力;而结合胆汁酸GCA、GDCA和GCDCA能增加胆管癌细胞IL-6的表达,并促进细胞活力.胆汁酸能通过IL-6途径改变胆管癌细胞活力.
目的 探討不同膽汁痠對膽管癌細胞株QBC939中IL-6的錶達和細胞活力的影響.方法 分彆使用不同濃度的遊離膽汁痠以及其對應的甘氨痠結閤型膽汁痠作用于膽管癌細胞株QBC939,藥物濃度分彆為:膽痠(CA)800 μmol/L、脫氧膽痠(DCA)100 μmol/L、鵝脫氧膽痠(CDCA)100 μmol/L、甘氨膽痠(GCA)1200 μmol/L、甘氨脫氧月膽痠(GDCA)200 μmol/L以及甘氨鵝脫氧膽痠(GCDCA)300 μmol/L.以MTT法檢測不同膽汁痠刺激24、48、72 h後膽管癌細胞活力的變化,併以ELISA法檢測腫瘤細胞中IL-6錶達的改變.結果 DCA、CDCA、GCDCA作用48 h後,腫瘤細胞活力比值(A處理組/A對照組)分彆為0.61、0.58和1.26;作用72 h後,CA、DCA、CDCA、GCA、GDCA和GCDCA各組腫瘤細胞活力比值分彆為0.48、0.50、0.42、1.29、1.30和1.41;與對照組相比,以上各組細胞活力變化均具有統計學意義(P＜0.05).對照組腫瘤細胞培養48和72 h後,IL-6錶達量分彆為(198±32)ng/L和(323±34)ng/L,CA、DCA、CDCA、GCA、GDCA和GCDCA作用48 h後IL-6的錶達量分彆為(106±33)ng/L、(88±29)ng/L、(116±54)ng/L、(413±21)ng/L、(587±32)ng/L和(366±30)ng/L,作用72 h後IL-6錶達量分彆為(123±66)ng/L、(45±21)ng/L、(74±45)ng/L、(792±13)ng/L、(1310±22)ng/L和(845±18)ng/L;與對照組相比,以上各組IL-6錶達量變化均具有統計學意義(P＜0.05).結論 遊離膽汁痠CA、DCA和CDCA能減少膽管癌細胞IL-6的錶達,併抑製細胞活力;而結閤膽汁痠GCA、GDCA和GCDCA能增加膽管癌細胞IL-6的錶達,併促進細胞活力.膽汁痠能通過IL-6途徑改變膽管癌細胞活力.
목적 탐토불동담즙산대담관암세포주QBC939중IL-6적표체화세포활력적영향.방법 분별사용불동농도적유리담즙산이급기대응적감안산결합형담즙산작용우담관암세포주QBC939,약물농도분별위:담산(CA)800 μmol/L、탈양담산(DCA)100 μmol/L、아탈양담산(CDCA)100 μmol/L、감안담산(GCA)1200 μmol/L、감안탈양월담산(GDCA)200 μmol/L이급감안아탈양담산(GCDCA)300 μmol/L.이MTT법검측불동담즙산자격24、48、72 h후담관암세포활력적변화,병이ELISA법검측종류세포중IL-6표체적개변.결과 DCA、CDCA、GCDCA작용48 h후,종류세포활력비치(A처리조/A대조조)분별위0.61、0.58화1.26;작용72 h후,CA、DCA、CDCA、GCA、GDCA화GCDCA각조종류세포활력비치분별위0.48、0.50、0.42、1.29、1.30화1.41;여대조조상비,이상각조세포활력변화균구유통계학의의(P＜0.05).대조조종류세포배양48화72 h후,IL-6표체량분별위(198±32)ng/L화(323±34)ng/L,CA、DCA、CDCA、GCA、GDCA화GCDCA작용48 h후IL-6적표체량분별위(106±33)ng/L、(88±29)ng/L、(116±54)ng/L、(413±21)ng/L、(587±32)ng/L화(366±30)ng/L,작용72 h후IL-6표체량분별위(123±66)ng/L、(45±21)ng/L、(74±45)ng/L、(792±13)ng/L、(1310±22)ng/L화(845±18)ng/L;여대조조상비,이상각조IL-6표체량변화균구유통계학의의(P＜0.05).결론 유리담즙산CA、DCA화CDCA능감소담관암세포IL-6적표체,병억제세포활력;이결합담즙산GCA、GDCA화GCDCA능증가담관암세포IL-6적표체,병촉진세포활력.담즙산능통과IL-6도경개변담관암세포활력.
Objective To research the effects of bile acids on the expression of interleukin-6 (IL-6)and the cell viability in QBC939 cell line. Methods Human cholangiocarcinoma cells were stimulated with 800 μmol/L bile acid (CA), 100 μmol/L deoxycholate (DCA), 100 μmol/L chenodeoxycholic acid (CDCA) ,1200 μmol/L gly acid (GCA) ,200 μmol/L glycodeoxycholic acid (GDCA) and 300 μmol/L gly chenodexycholic acid (GCDCA). MTT assay and ELISA were used to detect the cell viability and the expression of IL-6 at 24 h,48 h and 72 h. Results Treated by DCA, CDCA and GCDCA for 48 hours, the cell viability ratios changed to 0. 61,0. 58 and 1.26,which were significant differences between control group and treated groups. And after 72 hours, the viability ratios of group CA, group DCA, group CDCA, group GCA,group GDCA and group GCDCA turned into 0. 48,0. 50,0. 42,1.29,1.30 and 1.41. The differences of cell viability between bite acid-treated groups and control group were significant ( P ＜ 0. 05 ). The expression of IL-6 in control group at 48 h and 72 h was ( 198±32) ng/L and (323 ±34) ng/L,while treated by CA,DCA,CDCA,GCA,GDCA and GCDCA respectively for 48 hours,the expression of IL-6 altered to ( 106 ±33) ng/L,(88±29) ng/L,(116 ±54) ng/L,(413 ±21) ng/L,(587 ±32) ng/L and (366 ±30) ng/L.After 72 hours,the expression of IL-6 of each bile acid-treated groups as above was (123 ±66) ng/L, (45 ±21) ng/L,(74 ±45) ng/L,(792 ±13) ng/L,(1310 ±22) ng/L and (845 ±18) ng/L,respectively. The differences between each bile acid-treated group and control group were significant( P ＜0.05). Conclusions Free bile acids (CA, DCA and CDCA) can inhibit the expression of IL-6 and the cell viability, while glycineconjugates ( GCA, GDCA and GCDCA) can promote the expression of IL-6 and the cell viability. Bile acids can change tumor cell viability via IL-6 pathway.
