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首页> 外文期刊>Journal of biochemical and molecular toxicology >Crocin treatment promotes the oxidative stress and apoptosis in human thyroid cancer cells FTC-133 through the inhibition of STAT/JAK signaling pathway
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Crocin treatment promotes the oxidative stress and apoptosis in human thyroid cancer cells FTC-133 through the inhibition of STAT/JAK signaling pathway

机译：Crocin治疗通过抑制统计/ jak信号通路，促进人甲状腺癌细胞FTC-133中的氧化应激和凋亡

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摘要

Thyroid cancer is the most frequent endocrine malignancy, which accounts for nearly 1% of all the cancer worldwide. Crocin has a diverse biological function, such as anti-cancer, anti-inflammatory and antioxidant functions, specifically in the respiratory related diseases. Using in vitro techniques, this work was intended to illuminate the anti-cancer effect of crocin in follicular thyroid carcinoma (FTC) (FT 133 cells), and the potential molecular mechanism convoluted. The outcome of the present work showed that crocin was able to prevent the proliferation and triggering the apoptosis in a dose-dependent mode, of FTC-133 cells by methyl thiazolyldiphenyl-tetrazolium bromide and staining assay (acridine orange/propi-duim iodide [PI], 4',6-diamidino-2-phenylindole, and PI dye). Crocin did not show toxicity to the normal thyroid (PCCL3) cells. Crocin-induced reactive oxygen species, mitochondrial membrane potential activity, caspase-8 and -9, lipid per-oxidation (thiobarbituric acid reactive substances) activity while suppressing antioxidant activity (superoxide dismutase, catalase, and glutathione) in FTC-133 cells. In addition, crocin was also participated in a halting of the proteins related to cell cycle, cyclin D1, and pro-apoptotic proteins; Bax and caspase-3 expression, together with the elevation of anti-apoptotic factor Bcl-2. Further, crocin have a dual inhibition of two major pathways, nuclear factor-κB, extracellular signal-regulated kinase, and janus kinase-signal transducer and activator of transcription signaling pathways. In conclusion, crocin can inhibit follicular thyroid carcinoma proliferation and promote cell apoptosis.
机译：甲状腺癌是最常见的内分泌恶性肿瘤，约占全球所有癌症的1%。藏红花苷具有多种生物学功能，如抗癌、抗炎和抗氧化功能，特别是在呼吸相关疾病中。利用体外技术，本研究旨在阐明西红花苷对滤泡性甲状腺癌（FTC）（FT133细胞）的抗癌作用，以及潜在的分子机制。本研究的结果表明，通过甲基噻唑基二苯基四唑溴化铵和染色试验（吖啶橙/碘化丙二亚胺[PI]，4'，6-二氨基-2-苯基吲哚和PI染料），西红花苷能够以剂量依赖的方式阻止FTC-133细胞的增殖并触发其凋亡。藏红花素对正常甲状腺（PCCL3）细胞没有毒性。藏红花素在抑制FTC-133细胞抗氧化活性（超氧化物歧化酶、过氧化氢酶和谷胱甘肽）的同时，诱导活性氧物种、线粒体膜电位活性、半胱氨酸蛋白酶-8和-9、每氧化脂质（硫代巴比妥酸反应物质）活性。此外，藏红花苷还参与了与细胞周期、细胞周期蛋白D1和促凋亡蛋白相关的蛋白质的终止；Bax和caspase-3的表达，以及抗凋亡因子Bcl-2的升高。此外，藏红花苷对两条主要途径具有双重抑制作用，即核因子-κB、细胞外信号调节激酶和janus激酶信号转导和转录激活信号通路。综上所述，番红花苷能抑制甲状腺滤泡癌的增殖，促进细胞凋亡。

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