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银杏双黄酮通过激活p38/NF-κB信号通路抑制HeLa细胞增殖。

Ginkgetin inhibits proliferation of HeLa cells via activation of p38/NF-κB pathway.

作者信息

Cheng Jianxia, Li Yun, Kong Jianping

机构信息

Department of Obstetrics and Gynecology, The First People's Hospital of Jiande, Jiande 311600, Zhejiang Province, China.

出版信息

Cell Mol Biol (Noisy-le-grand). 2019 Apr 30;65(4):79-82.

Abstract

Effect of ginkgetin on proliferation of human cervical cancer (HeLa) cells and the underlying mechanism   were investigated. Human cervical cancer (HeLa) cells were cultured at 37 °C in 10 % fetal bovine serum (FBS) supplemented RPMI 1640 medium in a humidified incubator containing 5 % CO2. Cell proliferation was determined using MTT assay, while real-time quantitative polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to determine the levels of expression of interleukin 1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin 8 (IL-8). The expressions of p38 mitogen-activated protein kinases (p38 MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF- κB) were determined using Western blotting. Treatment of HeLa cells with ginkgetin significantly and time- and dose-dependently inhibited their proliferation (p < 0.05). The invasion of the cells were also significantly and dose-dependently decreased, when compared with control cells (p < 0.05). The expressions of p-p38 and p-NF-κB were significantly and dose-dependently down-regulated, relative to control group (p < 0.05). However, the expressions of p38 and NF-κB in ginkgetin-treated cells were not significantly different from those of control group (p > 0.05). The results of qRT-PCR and ELISA showed that the levels of expression of TNF-α, IL-1β and IL-8 mRNAs were significantly and dose-dependently reduced in HeLa cells after 48 h of treatment with ginkgetin, when compared with the control group (p < 0.05). The anti-proliferative effect of ginkgetin on HeLa cells is exerted via a mechanism involving the p38/NF-κB pathway.

摘要

研究了银杏双黄酮对人宫颈癌(HeLa)细胞增殖的影响及其潜在机制。人宫颈癌(HeLa)细胞在含有5%二氧化碳的湿度培养箱中,于37℃在补充有10%胎牛血清(FBS)的RPMI 1640培养基中培养。使用MTT法测定细胞增殖,同时使用实时定量聚合酶链反应(qRT-PCR)和酶联免疫吸附测定(ELISA)来测定白细胞介素1β(IL-1β)、肿瘤坏死因子-α(TNF-α)和白细胞介素8(IL-8)的表达水平。使用蛋白质印迹法测定p38丝裂原活化蛋白激酶(p38 MAPK)和活化B细胞核因子κB(NF-κB)的表达。用银杏双黄酮处理HeLa细胞可显著且呈时间和剂量依赖性地抑制其增殖(p<0.05)。与对照细胞相比,细胞的侵袭也显著且呈剂量依赖性降低(p<0.05)。相对于对照组,p-p38和p-NF-κB的表达显著且呈剂量依赖性下调(p<0.05)。然而,银杏双黄酮处理组细胞中p38和NF-κB的表达与对照组无显著差异(p>0.05)。qRT-PCR和ELISA结果表明,与对照组相比,用银杏双黄酮处理48小时后,HeLa细胞中TNF-α、IL-1β和IL-8 mRNA的表达水平显著且呈剂量依赖性降低(p<0.05)。银杏双黄酮对HeLa细胞的抗增殖作用是通过涉及p38/NF-κB途径的机制发挥的。

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