Wang Xiao-Ping, Wang Qiao-Xia, Lin Huan-Ping, Chang Na
Laboratory of Molecular Biology & Pathology, Shaanxi University of Chinese Medicine, Xianyang, PR China.
Food Funct. 2017 Sep 20;8(9):3319-3326. doi: 10.1039/c7fo00555e.
Curcumin, a derivative from the dried rhizome of curcuma longa, has been proven to possess anti-tumor effects. However, the detailed molecular mechanisms have not been fully elucidated. In this study, we aimed to explore the anti-tumor mechanisms of curcumin in treating gastric cancer. BALB/C mice grafted with a mouse gastric adenocarcinoma cell line (MFC) were used as the experimental model. Mice received different doses of curcumin after grafting. Tumor size was measured and tumor weight was determined after tumor inoculation. TUNEL assay and flow cytometric analysis were applied to evaluate the apoptosis of the cancer cells. Serum cytokines IFN-γ, TNF-α, granzyme B and perforin were detected by ELISA assay. The anti-tumor effect was determined using cytotoxic T-lymphocyte (CTL) assays and in vivo tumor prevention tests. The expression of DEC1, HIF-1α, STAT3 and VEGF in tumor tissues was examined by immunostaining and analyzed using an Image J analysis system. Compared with controls, tumor growth (size and weight) was significantly inhibited by curcumin treatment (P < 0.05). The apoptotic index in gastric cancer cells was significantly increased in the curcumin treatment group. Splenocyte cells from mice treated with curcumin exhibited higher cytolytic effects on MFC cancer cells than those from mice treated with saline (P < 0.01). The expression of DEC1, HIF-1α, STAT3 and VEGF in tumor tissues was down-regulated after curcumin treatment. Our results indicate that curcumin inhibits the proliferation of gastric carcinoma by inducing the apoptosis of tumor cells, activating immune cells to secrete a large amount of cytokines, and down-regulating the DEC1, HIF-1α, VEGF and STAT3 signal transduction pathways.
姜黄素是姜黄干燥根茎的衍生物，已被证明具有抗肿瘤作用。然而，其详细的分子机制尚未完全阐明。在本研究中，我们旨在探讨姜黄素治疗胃癌的抗肿瘤机制。将接种小鼠胃腺癌细胞系（MFC）的BALB/C小鼠作为实验模型。小鼠接种后接受不同剂量的姜黄素。接种肿瘤后测量肿瘤大小并测定肿瘤重量。采用TUNEL检测和流式细胞术分析评估癌细胞的凋亡情况。通过ELISA检测血清细胞因子IFN-γ、TNF-α、颗粒酶B和穿孔素。使用细胞毒性T淋巴细胞（CTL）检测和体内肿瘤预防试验确定抗肿瘤效果。通过免疫染色检测肿瘤组织中DEC1、HIF-1α、STAT3和VEGF的表达，并使用Image J分析系统进行分析。与对照组相比，姜黄素治疗显著抑制了肿瘤生长（大小和重量）（P < 0.05）。姜黄素治疗组胃癌细胞的凋亡指数显著增加。用姜黄素处理的小鼠的脾细胞对MFC癌细胞的细胞溶解作用高于用生理盐水处理的小鼠（P < 0.01）。姜黄素处理后，肿瘤组织中DEC1、HIF-1α、STAT3和VEGF的表达下调。我们的结果表明，姜黄素通过诱导肿瘤细胞凋亡、激活免疫细胞分泌大量细胞因子以及下调DEC1、HIF-1α、VEGF和STAT3信号转导通路来抑制胃癌的增殖。
