雷公藤红素联合顺铂对舌鳞状细胞癌Tca8113细胞作用机制的研究

Effect of Combination of Tripterine and Cisplatin on Oral Squamous Cell Carcinoma Tca8113 Cells

目的探讨雷公藤红素联合顺铂对舌鳞状细胞癌Tca8113细胞作用机制。方法将Tca8113细胞分为对照组(0μmol/L顺铂和0μg/m L雷公藤红素)、顺铂组(15μmol/L顺铂)、雷公藤红素组(50μg/m L雷公藤红素)以及联合组(15μmol/L顺铂和50μg/m L雷公藤红素),MTT法检测细胞活力,酶联免疫吸附法测定血管内皮生长因子(VEGF)、血管内皮生长因子-C(VEGF-C)、抗凋亡蛋白(Bcl-2)、凋亡蛋白(Bax)水平。结果顺铂组、雷公藤红素组以及联合组Tca8113细胞存活率分别为:(0.61±0.12)%、(0.59±0.12)%、(0.27±0.11)%,顺铂组、雷公藤红素组Tca8113细胞存活率低于对照组的(1.00±0.00)%,差异有统计学意义(P<0.05),联合组Tca8113细胞存活率低于对照组、顺铂组与雷公藤红素组,差异有统计学意义(P均<0.05),雷公藤红素组Tca8113细胞存活率低于顺铂组,但差异无统计学意义(P>0.05);顺铂组、雷公藤红素组Tca8113细胞VEGF、VEGF-C、Bcl-2水平低于对照组[VEGF:(39.14±1.78)μmol/L、(41.11±1.45)μmol/L比(61.45±2.73)μmol/L,P<0.05;VEGF-C:(43.11±1.37)μmol/L、(43.13±1.65)μmol/L比(61.33±2.16)μmol/L,P<0.05;Bcl-2:(52.47±0.98)μmol/L、(53.47±1.03)μmol/L比(78.47±1.33)μmol/L,P<0.05],Bax水平高于对照组[(45.14±0.89)μmol/L、(44.14±1.12)μmol/L比(43.14±1.36)μmol/L,P<0.05)];联合组VEGF、VEGFC、Bcl-2水平显著低于对照组、顺铂组与雷公藤红素组[VEGF:(23.1±2.13)μmol/L分别与(61.45±2.73)μmol/L、(39.14±1.78)μmol/L和(41.11±1.45)μmol/L比较,P<0.05;VEGF-C:(21.45±1.47)μmol/L分别与(61.33±2.16)μmol/L、(43.11±1.37)μmol/L和(43.13±1.65)μmol/L比较,P<0.05;Bcl-2:(36.47±1.25)μmol/L分别与(78.47±1.33)μmol/L、(52.47±0.98)μmol/L和(53.47±1.03)μmol/L比较,P<0.05];Bax水平高于对照组、顺铂组与雷公藤红素组(79.14±1.45)μmol/L分别与(43.14±1.36)μmol/L、(45.14±0.89)μmol/L和(44.14±1.12)μmol/L比较,P<0.05];雷公藤红素组VEGF、VEGF-C、Bcl-2、Bax水平与顺铂组相近,差异无统计学意义(P>0.05)。结论雷公藤红素联合顺铂对舌鳞状细胞癌Tca8113细胞作用优于顺铂和雷公藤红素单独作用,作用机制可能与其抑制VEGF、VEGFC、Bcl-2表达,促进Bax表达相关。

Objective To investigate the effect of combination of tripterine and cisplatin on oral squamous cell carcinoma. Methods Tca8113 cells were divided into four groups： control group （0μmol/L eisplatin and 0μg/mL tripterine ）, eisplatin group （ 15 μmol/L cisplatin）, triptefine group （ 50μg/mL tripterine ） and combined group （ 15 μmol/L eisplatin and 50p, g/mL tripterine）. MTr assay was used to assess cell activity, then ELISA assay was used to detect the protein level of vascular endothelial growth factor（VEGF）, VEGF-C, Bel-2 and Bax. Results The survival rates of cisplatin group, tripterine group and combination group bility of Tea8113 cells in cisplatin group, tripterine group and control group （1.00±0.00, P〈0.05）; the viability in combined were 0.61±0.12, 0.59±0.12, and 0.27±0.11; the viacombined group was significantly lower than that of group was lower than those in cisplatin group and tripterine group, with a statistical difference （P〈0.05）; no significant difference was found between tripterine group and cisplatin group （P〉0.05）. VEGF, VEGF-C and Bcl-2 protein levels on Tca8113 cells in cisplatin group （39.14±1.78μmol/L, 43.11±1.37μmol/L, 52.47±0.98μ mo1/L）, tripterine group （41.11±1.45μmol/L, 43.13±1.65μmol/L, 53.47±1.03p, mol/L）, and combined group （23.1±2.13μ mol/L, 21.45±1.47μmol/L, 36.47±1.25μmol/L） were lower than those in control group （61.45±2.73μmol/L, 61.33±2.16μmol/L, 78.47±1.33μmol/L）, but the Bax level in cisplatin group（45.14±0.89μmol/L）, tripterine group（44.14±1.12μmol/L）, and combined group（79.14±1.45） was higher than that in control group（43.14±1.36μ mol/L）, with significant differeuces（P〈0.05）; significant differences were noted between combined group and cisplatin and tripterine groups; but the levels of VEGF, VEGF-C, Bcl-2 and Bax were similar between cisplatin group and tripterine group （P〉0.05）. Conclusion The combination of tripterine and cisplatin has better curative effects on oral squamous cell carcinoma Tea8113 cells than using these two separately. The underlying mechanism of action may inhibit the expression of VEGF, VEGF-C and Bcl-2, meanwhile promote Bax,