Objective:To explore the effect of clerodendrum bungei steud flavonoids (CBSF)on mice with Lewis lung cancer and its correlation to the expression of p53,bcl-2,and bax.Methods:To select 50 C57BL/6 male mice,after modelling,choose 40 with Lewis lung cancer and randomly divided them into four groups:model group,DDP group,CBSF high dose group,CBSF low dose group (with 10 in each),and 10 healthy mice into blank group.Drug administration:model group:intraperitoneal injection of physi-ological saline 0.01 mL/g for 14 days;DDP group:intraperitoneal injection of DDP 0.4 mg/kg for 5 days;CBSF high dose group:intraperitoneal injection of CBSF 0.6 g/kg for 14 days;CBSF low dose group:intraperitoneal injection of CBSF 0.3 g/kg for 14 days.Execute all mice after the medication,then weight up the tumors and calculate the tumor inhibition rate.Besides,using real-time PCR method to detect the expression of p53,bcl-2 and bax.Results:1)The effect on tumor weight(x ±s).The tumor weight of four groups are as follow:model group (4.70 ±1.29)g,DDP group (2.24 ±0.68)g,CBSF high dose group (3.26 ±1.06)g, CBSF low dose group (3.99 ±1.31)g.The tumor weight of DDP group and CBSF high dose group are lighter than that of the model group (P <0.05).Besides,there is no significant difference between these two groups (P >0.05).2)The tumor inhibition rate (IR).The IR of DDP group is 53.4%,CBSF high dose group is 30.6%,and CBSF high dose group is 15.1%.3)The effect on gene expression.Both CBSF groups can up-regulate the expression of p53 mRNA and bax mRNA (P <0.05 or P <0.01);DDP group can down-regulate the expression of bcl-2 mRNA (P <0.05)and up-regulate the expression of bax mRNA (P <0.01). Conclusion:Clerodendrum bungei flavonoids can improve the living quality of Lewis lung cancer mice and inhibit growth of tumor. Its antineoplastic mechanisms might be up-regulation of the expression of p53 mRNA and bax mRNA and induce apotosis of tumor.%目的：探讨臭牡丹总黄酮对 Lewis 肺癌小鼠的抑瘤作用及其与 p53、bcl-2、bax 基因表达的相关性。方法：取近交系雄性 C57BL／6小鼠50只，造模，将造模成功的 Lewis 肺癌小鼠40只随机分成模型组，顺铂组，臭牡丹总黄酮高、低剂量组；另取10只无瘤小鼠作为空白对照组。腹腔注射给药，模型组给予生理盐水0.01 mL／g，连续14 d；顺铂组给予顺铂0.4 mg／kg 连续5 d；臭牡丹高、低剂量组分别予臭牡丹总黄酮提取物0.6 g／kg、0.3 g／（kg·d），连续14 d。给药结束后次日处死小鼠，称取瘤重，计算肿瘤抑制率，采用 Real-time PCR 法检测 p53、bcl-2及 bax mRNA 的表达水平。结果：1）对瘤重影响：4组瘤重结果如下（珋x ±s）：模型组（4.70＋1.29）g、顺铂组（2.24＋0.68）g、总黄酮高剂量组（3.26±1.06）g、总黄酮低剂量组（3.99±1.31）g；其中顺铂组、总黄酮高剂量组瘤重低于模型组（P ＜0.05），并且该2组瘤重无统计学意义（P ＞0.05）。2）肿瘤抑制率：顺铂组：53.4％；臭牡丹总黄酮高剂量组：30.6％，臭牡丹总黄酮低剂量组：15.1％。3）对基因表达影响：臭牡丹总黄酮高、低剂量组皆能上调 p53和 bax mRNA 表达（高剂量组 P ＜0.01，低剂量组 P ＜0.05）；顺铂组能下调bcl-2（P ＜0.05）及上调 bax mRNA 表达（P ＜0.01）。结论：臭牡丹总黄酮能够改善 Lewis 肺癌小鼠生存状况，能有效抑制肿瘤生长；并且其抑制肿瘤生长的分子机制可能与上调 p53和 bax mRNA 的表达以诱导肿瘤细胞凋亡有关。
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