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作 者:向波[1] 李世琪[2] 颜娅[1] XIANG Bo;LI Shi-qi;YAN Ya(Department of Anesthesiology,Chongqing Maternal and Child Health Hospital,Chongqing 401147,China;Department of Anesthesiology,The Second Affiliated Hospital of Chongqing Medical University,Chongqing 400010,China)
机构地区:[1]重庆市妇幼保健院麻醉科,重庆401147 [2]重庆医科大学附属第二医院麻醉科,重庆400010
出 处:《中国临床药理学杂志》2022年第7期667-670,共4页The Chinese Journal of Clinical Pharmacology
基 金:重庆市卫生健康委基金资助项目(2021FY106)。
摘 要:目的观察丙泊酚对卵巢癌细胞侵袭、转移的影响,并探讨相关机制。方法取对数期OVCAR3细胞,随机分为溶剂对照组(0.1%二甲亚砜),低、中、高3个剂量实验组(5,10,20μg·mL^(-1)丙泊酚),联合组[0.5μmol·L^(-1)信号转导及转录激活子3(STAT3)激活剂(colivelin)+20μg·mL^(-1)丙泊酚],培养24 h。用Transwell实验检测细胞侵袭能力;划痕实验检测细胞迁移能力。结果溶剂对照组、高剂量实验组和联合组的穿膜细胞数/视野分别为(125.40±15.87),(42.20±4.17)和(64.40±7.83)个;这3组的细胞迁移率分别为(72.59±8.36)%,(17.03±2.57)%和(35.07±6.52)%。溶剂对照组与高剂量实验组比较,高剂量实验组与联合组比较,差异均有统计学意义(均P<0.05)。结论丙泊酚可抑制卵巢癌细胞侵袭、迁移及血管生成,推测与抑制JAK2/STAT3通路有关。Objective To observe the effect of propofol on the invasion and metastasis of ovarian cancer cells,and to explore related mechanisms.Methods The log phase OVCAR3 cells was taken and randomly divided into solvent control group(0.1%dimethyl sulfoxide),experimental-L,M,H groups(5,10,20μg·mL^(-1)propofol),combined group[0.5μmol·L^(-1)signal transducer and activator of transcription 3(STAT3)activator colivelin,20μg·mL^(-1)propofol]cultured for 24 h.The cell invasion ability was detected by Transwell test.The cell migration ability was detected by Scratch test.Results The number of penetrating cells/field in solvent control group,experimental-H group,combined group were(125.40±15.87),(42.20±4.17)and(64.40±7.83).The cell migration rates in these three groups were(72.59±8.36)%,(17.03±2.57)%and(35.07±6.52)%.The above indicators,the differences between the control group and the experimental-H group,the experimental-H group and the combined group were statistically significant(P<0.05).Conclusion Propofol can inhibit the invasion,migration and angiogenesis of ovarian cancer cells in a dose-dependent manner.It is speculated that its mechanism of action is related to the inhibition of JAK2/STAT3 pathway.
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