目的 探讨美洲大蠊提取物CII-3对卵巢癌SKOV3细胞的抗肿瘤作用及其潜在作用机制。方法 体外培养SKOV3细胞，分为对照组和CⅡ-3组，通过CCK-8法和细胞集落形成实验测定SKOV3细胞增殖能力；流式细胞术检测SKOV3细胞线粒体膜电位和细胞周期的改变；衰老相关-β-半乳糖苷酶（SA-β-Gal）染色法检测SKOV3细胞衰老阳性细胞率；荧光定量PCR检测SKOV3细胞端粒酶逆转录酶（TERT）和磷脂酰肌醇-3-激酶（PI3K）、蛋白激酶B（Akt）、叉头盒蛋白O4（FoxO4）mRNA表达情况；Western blotting检测p-PI3K、p-Akt、p-FoxO4蛋白表达情况。结果 与对照组比较，美洲大蠊提取物CⅡ-3可有效抑制SKOV3细胞增殖，细胞集落形成能力明显下降，细胞阻滞于G₀/G₁期，线粒体膜电位下降，SA-β-Gal细胞衰老阳性率增加，TERT活性降低，PI3K、Akt mRNA和p-PI3K、p-Akt蛋白表达上调，FoxO4 mRNA和p-FoxO4蛋白表达均下调。结论 美洲大蠊提取物CⅡ-3通过调控PI3K/Akt/FoxO4信号通路诱导SKOV3细胞衰老。

Objective To investigate the anti-tumour effects and potential mechanisms of the Periplaneta americana extract CⅡ-3 on ovarian cancer SKOV3 cells. Methods In vitro, SKOV3 cells were cultured and divided into control group and CⅡ-3 group, and the proliferative capacity of SKOV3 cells was determined by the Cell Counting Kit-8 (CCK-8) and the cell colony formation assay. Flow cytometry was used to detect the changes in the cell cycle and mitochondrial membrane potential of SKOV3 cells. Positive senescence-associated beta-galactosidase (SA-β-Gal) staining assay to detect senescence in SKOV3 cells. q-PCR was utilized to assess the modification of telomerase reverse transcriptase (TERT), and PI3K, Akt, FoxO4 mRNA in SKOV3 cells. Western blotting assays were conducted to determine the expression of p-PI3K, p-Akt, p-FoxO4 protein in cells. Results Compared with the control group, Periplaneta americana extract CII-3 exhibited a significant inhibitory effect on the proliferation of SKOV3 cells, accompanied by a notable reduction in colony-forming ability, an increase in the proportion of cells arrested in the G₀/G₁ phase. The mitochondrial membrane potential decreased, the positive rate of senescence of SA-β-Gal cells increased, the activity of TERT decreased, the expression of PI3K, Akt mRNA and p-PI3K, p-Akt protein expression were up-regulated, and both FoxO4 mRNA and p-FoxO4 protein expression were down-regulated. Conclusion Periplaneta americana extract CII-3 induced cellular senescence in SKOV3 cells by regulating the PI3K/Akt/FoxO4 signaling pathway.

R965

国家自然科学基金资助项目(81860038,81660731)