NLRP3参与肝细胞癌(HCC)的发展。雌二醇对肝癌细胞增殖有抑制作用。然而,艾氏醇在HCC中的潜在机制尚不清楚。本研究旨在探讨艾替多醇对肝癌的作用及其机制。在这项研究中,与烯醇(0μM)组相比,灯盏细辛显著抑制HepG2细胞(灯盏细辛为25、50和100μM)和Huh-7细胞(灯盏细辛为50和100μM)的活力,入侵,管形成,转移相关基因MMP3、MMP16和血管生成调节因子VEGFA在体外表达,IC50为45.63μM和78.26μM,分别。此外,灯盏醇显著抑制NLRP3表达,并降低NLRP3炎性体相关蛋白的蛋白水平,衔接蛋白ASC,HepG2细胞(25、50和100μM的厄尼多醇)和Huh-7细胞(50和100μM的厄尼多醇)中的caspase-1,白介素(IL)-18和IL-1β,分别。同时,与对照组相比,NLRP3过表达逆转100μM麦片醇对肝癌细胞侵袭的抗转移作用,管形成,和转移相关基因MMP3,MMP16和血管生成调节因子VEGFA的表达,而NLRP3敲低增强100μM麦片对肝癌细胞的抗转移作用。在体内,与对照组相比,厄尼替醇显著降低了肿瘤的生长,肝损伤,抑制NLRP3炎性体的激活,和改善肝功能,而过表达NLRP3则中和了艾替地醇的抗肿瘤作用并降低了肝功能。因此,二烯醚抑制HCC细胞活力,运动性,体外和体内通过NLRP3炎性体失活的血管生成和肿瘤生长。
NLRP3 involves in the development of hepatocellular carcinoma (HCC).
Eriodictyol has shown its inhibitory effect on HCC cell proliferation. However, the underlying mechanism of
eriodictyol in HCC is still unclear. This study aimed to explore the effect of and mechanism of
eriodictyol on HCC. In this study, compared with
eriodictyol (0 μM) group,
eriodictyol significantly suppressed HepG2 cells (
eriodictyol of 25, 50 and 100 μM) and Huh-7 cells (
eriodictyol of 50 and 100 μM) viability, invasion, tube formation, metastasis-related genes MMP3, MMP16 and angiogenesis regulator VEGFA expressions with IC50 of 45.63 μM and 78.26 μM in vitro, respectively. Besides, eriodictyol significantly repressed NLRP3 expression, and reduced the protein levels of NLRP3 inflammasome-related proteins, adapter protein ASC, caspase-1, interleukin (IL)-18, and IL-1β in HepG2 (eriodictyol of 25, 50 and 100 μM) and Huh-7 cells (eriodictyol of 50 and 100 μM), respectively. Meanwhile, compared with control group, NLRP3 overexpression reversed the anti-metastatic effects of 100 μM eriodictyol on HCC cells invasion, tube formation, and metastasis-related genes MMP3, MMP16 and angiogenesis regulator VEGFA expressions, whereas NLRP3 knockdown enhanced the anti-metastatic effects of 100 μM eriodictyol on HCC cells. In vivo, compared with control group, eriodictyol significantly reduced the tumor growth, liver damage, inhibited the activation of NLRP3 inflammasome, and improved liver function, whereas NLRP3 overexpressing neutralized the anti-tumor effects of eriodictyol and degraded liver function. Hence, eriodictyol inhibited HCC cell viability, motility, angiogenesis and tumor growth via NLRP3 inflammasome inactivation both in vitro and in vivo.