目的探讨异常黑胆质成熟剂总酚与顺铂、多西他赛联合应用对Hela细胞生长的影响。方法体外培养Hela细胞,分别用顺铂、多西他赛、总酚、顺铂+总酚、多西他赛+总酚处理Hela细胞,并设对照组。肼法检测细胞增殖抑制情况,流式细胞术检测细胞凋亡率和Bcl-2表达,半定量RT-PCR法检测生存素表达。结果总酚、顺铂和多西他赛对Hela有明显的抑制及促凋亡作用,早期凋亡率分别为(12.80±0.70)%、(18.87±3.79)%和(15.87±3.81)%(P〈O.05)。应用总酚、顺铂和多西他赛处理Hela细胞后,BcF2表达分别降低(63.63±3.84)%、(49.20±4.08)%和(51.40±6.35)%,生存素表达分别降低(0.636±0.040)%、(o.431±0.048)%和(0.577±0.040)%;联合使用时更明显(P〈O.01)。结论异常黑胆质成熟剂总酚与顺铂、多西他赛联合可能通过降低Bcl_2和生存素表达促进Hela细胞凋亡。
Objective To investigate the underlying mechanism for inducing Hela cells apoptosis with total phenolics from abnormal savda munziq (TP) combined with chemotherapeutic agents. Methods Hda cells were treated with TP combined with cisplatin or docetaxe1. The inhibiting effects were tested by MTT assay, and flow cytometry was used to examine cell apoptosis rate and Bcl-2,semi-quantitative PCR was used to detect survivin expression. Results The early inhibiting rates of TP,cisplatin and docetaxel were (12. 80±0. 70)%, (18. 87± 3. 79)% and (15: 87±3.81)%, respectively. After treated with TP, cisplatin or docetaxel for 48 hours, Bcl-2 expression rate was reduced by (63.63±3. 84)%, (49. 20±4. 08)% or (51.40±6.35)% and survivin expression was reduced by (0. 636±0. 040)%, (0. 431±0. 048)% or (0. 577±0. 040) % (P〈0. 05). The decreases were even more when combined use of TP with cisplatin or docetaxel(P〈0. 01). Conclusion The total phenolics from abnormal savda munziq combined with cisplatin or docetaxel can induce Hela cells aDootosis via decreasimz the expressions of Bcl-2 and survivin.