马齿Poly多糖通过诱导TLR4 /NF-κB信号传导对HeLa细胞的抗肿瘤活性。,Nutrition and Cancer

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马齿Poly多糖通过诱导TLR4 /NF-κB信号传导对HeLa细胞的抗肿瘤活性。
Nutrition and Cancer ( IF 2.0 ) Pub Date : 2016-12-03 , DOI: 10.1080/01635581.2017.1248294
Rui Zhao ₁ , Tao Zhang ₂ , Baoling Ma ₃ , Xing Li ₄

Affiliation

Abstarct我们以前已经表明，马齿Port马齿藻多糖（POL-P3b）具有在体外和体内抑制宫颈癌细胞生长的能力。在这项研究中，我们探索了收费样受体4（TLR4）信号转导与POL-P3b的抗肿瘤机制之间的关系。Western blotting被用于检测TLR4的表达和下游信号通路。使用酶联免疫吸附测定（ELISA）试剂盒定量测定炎症介质的水平。通过WST-8分析和Hoechst 33342 /碘化丙啶（PI）分析确定POL-P3b对HeLa细胞增殖和凋亡的影响。我们的结果表明，脂多糖（LPS）与肿瘤细胞上的TLR4结合可以增强HeLa细胞的增殖并增加TLR4和下游分子的表达。用POL-P3b处理HeLa细胞可以降低HeLa细胞的增殖，并以浓度依赖的方式上调Bax水平和下调Bcl-2水平。此外，POL-P3b抑制HeLa细胞中TLR4，MyD88，TRAF6，激活蛋白1（AP-1）和核因子-κB（NF-κB）亚基P65的蛋白表达水平。此外，POL-P3b还减少了细胞因子/趋化因子的产生。综上所述，目前的工作通过下调TLR4下游信号通路并诱导细胞凋亡，提示了POL-P3b的抗肿瘤机制。我们的结果可能提供直接证据，表明POL-P3b应该被认为是用于肿瘤治疗的有效营养补充剂。此外，POL-P3b抑制HeLa细胞中TLR4，MyD88，TRAF6，激活蛋白1（AP-1）和核因子-κB（NF-κB）亚基P65的蛋白表达水平。此外，POL-P3b还减少了细胞因子/趋化因子的产生。综上所述，目前的工作通过下调TLR4下游信号通路并诱导细胞凋亡，提示了POL-P3b的抗肿瘤机制。我们的结果可能提供直接证据，表明POL-P3b应该被认为是用于肿瘤治疗的有效营养补充剂。此外，POL-P3b抑制HeLa细胞中TLR4，MyD88，TRAF6，激活蛋白1（AP-1）和核因子-κB（NF-κB）亚基P65的蛋白表达水平。此外，POL-P3b还减少了细胞因子/趋化因子的产生。综上所述，目前的工作通过下调TLR4下游信号通路并诱导细胞凋亡，提示了POL-P3b的抗肿瘤机制。我们的结果可能提供直接证据，表明POL-P3b应该被认为是用于肿瘤治疗的有效营养补充剂。目前的工作通过下调TLR4下游信号通路并诱导细胞凋亡来提示POL-P3b的抗肿瘤机制。我们的结果可能提供直接的证据，表明POL-P3b应该被认为是用于肿瘤治疗的有效营养补充剂。目前的工作通过下调TLR4下游信号通路并诱导细胞凋亡来提示POL-P3b的抗肿瘤机制。我们的结果可能提供直接证据，表明POL-P3b应该被认为是用于肿瘤治疗的有效营养补充剂。

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Antitumor Activity of Portulaca Oleracea L. Polysaccharide on HeLa Cells Through Inducing TLR4/NF-κB Signaling.

Abstarct We have previously shown that Portulaca oleracea L. polysaccharide (POL-P3b) possesses the ability to inhibit cervical cancer cell growth in vitro and in vivo. In this study, we explored how toll-like receptor 4 (TLR4) signaling correlated with the antitumor mechanism of POL-P3b. Western blotting was utilized to detect the expression of TLR4 and the downstream signaling pathway. The level of inflammatory mediator was quantified using enzyme-linked immunosorbent assay (ELISA) kits. The effects of POL-P3b on the proliferation and apoptosis in HeLa cells were determined by WST-8 assay and Hoechst 33342/propidium iodide (PI) assay. Our results demonstrated that lipopolysaccharide (LPS) binding to TLR4 on tumor cells could enhance HeLa cell proliferation and increase the expression of TLR4 and the downstream molecules. Treating HeLa cells with POL-P3b could decrease the proliferation of HeLa cells, and upregulate Bax level and downregulate Bcl-2 level in a concentration-dependent manner. In addition, POL-P3b inhibited the protein expression levels of TLR4, MyD88, TRAF6, Activator Protein-1 (AP-1) and nuclear factor-κB (NF-κB) subunit P65 in HeLa cells. Furthermore, POL-P3b also reduced the production of cytokine/chemokine. Taken together, the present work suggested the antitumor mechanism of POL-P3b by downregulating TLR4 downstream signaling pathway and inducing cell apoptosis. Our results may provide direct evidence to suggest that POL-P3b should be considered as a potent nutrient supplement for oncotherapy.

更新日期：2019-11-01

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