洛沙坦通过调控JAK2/STAT3通路对卵巢癌动物模型的抑瘤作用及机制研究  

The anti-tumor effect and mechanism of losartan on ovarian cancer animal models by regulating JAK2/STAT3 pathway

作　　者：王娜[1] 李毅[1] 王永 WANG Na;LI Yi;WANG Yong(Department of Pathology,Zibo Women&Children Hospital,Zibo Shandong 255000,China)

机构地区：[1]山东省淄博市妇幼保健院病理科,255000

出　　处：《中国妇产科临床杂志》2021年第5期471-473,共3页Chinese Journal of Clinical Obstetrics and Gynecology

摘　　要：目的探究洛沙坦通过调控JAK2/STAT3通路对卵巢癌动物模型的抑瘤作用及机制。方法将30只卵巢癌小鼠模型分为对照组、洛沙坦低剂量组(30 mg/kg)和洛沙坦高剂量组(60 mg/kg)(n=10)。检测Ki67、Cyclin D1、Bcl-2和Bax蛋白表达量分析卵巢癌细胞增殖和凋亡水平,检测CD34和血管内皮生长因子(vascular endothelial growth factor, VEGF)分析微血管密度和血管生成能力。并分析各组JAK2和STAT3 mRNA及蛋白水平。结果三组的各项指标比较差异均有统计学意义(P <0.05)。洛沙坦低剂量组的肿瘤体积、质量、Ki67、Cyclin D1和Bcl-2蛋白水平、微血管密度、VEGF水平、JAK2和STAT3 mRNA及蛋白水平均显著低于对照组,Bax蛋白水平显著高于对照组(P <0.05)。洛沙坦高剂量组的肿瘤体积、质量、Ki67、Cyclin D1和Bcl-2蛋白水平、微血管密度、VEGF水平、JAK2和STAT3m RNA及蛋白水平显著低于洛沙坦低剂量组和对照组(P <0.05),Bax蛋白水平显著高于洛沙坦低剂量组和对照组(P <0.05)。结论洛沙坦可能通过抑制JAK2/STAT3通路抑制卵巢癌细胞的增殖和血管生成能力,并诱导凋亡。Objective To explore the anti-tumor effect and mechanism of Losartan on ovarian cancer animal models by regulating the JAK2/STAT3 pathway. Methods Thirty mouse models of ovarian cancer were divided into control group, losartan low-dose group(30 mg/kg) and losartan high-dose group(60 mg/kg)(N = 10). The protein expressions of Ki67, CyclinD1, Bcl-2 and Bax were detected to analyze the proliferation and apoptosis of ovarian cancer cells. CD34 and Vascular Endothelial Growth Factor(VEGF) were detected to analyze the microvessel density and angiogenesis. The mRNA and protein levels of JAK2 and STAT3 in each group were analyzed. Results The indicators of the three groups were significantly different(P < 0.05). Tumor volume, mass, Ki67, CyclinD1 and Bcl-2 protein levels, microvessel density, VEGF levels, JAK2 and STAT3 mRNA in the low-dose losartan group were all significantly lower than the control group, while Bax was significantly higher than the control group(P < 0.05). Tumor volume, mass, Ki67, CyclinD1 and Bcl-2 protein levels, microvessel density, VEGF levels, JAK2 and STAT3 mRNA in the high-dose losartan group and protein levels were significantly lower than the low-dose Losartan group and the control group, and the Bax was significantly higher than the low-dose Losartan group and the control group(P < 0.05). Conclusion Losartan may inhibit the proliferation and angiogenesis of ovarian cancer cells by inhibiting the JAK2/STAT3 pathway, and induce apoptosis.

关 键 词：卵巢癌 洛沙坦 凋亡 血管生成 JAK2/STAT3 

分 类 号：R965[医药卫生—药理学]