Gao Jian-Zhi, DU Jing-Li, Wang Yong-Ling, Li Jia, Wei Li-Xin, Guo Ming-Zhou
Department of Pathology, General Hospital of the People's Liberation Army, Beijing 100853, P.R. China ; Basic Medical College of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Department of Gastroenterology and Hepatology, General Hospital of the People's Liberation Army, Beijing 100853, P.R. China ; Department of Gastroenterology, Armed Police Corps Hospital of Qinghai, Xining, Qinghai 810006, P.R. China.
Oncol Lett. 2015 Jan;9(1):295-299. doi: 10.3892/ol.2014.2694. Epub 2014 Nov 10.
The aim of the present study was to explore the effects of curcumin in combination with bevacizumab on the vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR)/K-ras pathway in hepatocellular carcinoma. A total of 30 Sprague Dawley (SD) rats were randomly divided into five groups: Control, model, curcumin, VEGF blocker, and curcumin + VEGF blocker groups. The mRNA levels of VEGF and VEGFR in all groups were subsequently measured by quantitative reverse transcriptase-polymerase chain reaction and the protein expression of K-ras was detected by western blot analysis. Compared with the control group, the mRNA levels of VEGF and VEGFR were revealed to be significantly increased in the model, curcumin and VEGF blocker groups. The VEGF mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were all decreased when compared with the model group. In addition, the VEGF mRNA levels in the curcumin + VEGF blocker group were significantly lower compared with the curcumin group (P<0.05). The VEGF mRNA levels in the curcumin, VEGF blocker and curcumin + VEGF blocker groups were decreased when compared with the model group (P=0.0001). No significant differences in VEGF mRNA levels were identified between the VEGF blocker and curcumin groups (P=0.863), whereas the VEGF mRNA levels in the curcumin + VEGF blocker group were significantly lower than that of the curcumin group (P=0.025). Curcumin and the VEGF blocker are each capable of inhibiting hepatocellular carcinoma progression by regulating the VEGF/VEGFR/K-ras pathway. The combination of the two compounds has a synergistic effect on the inhibition of the effects of the VEGF signaling pathways in hepatocellular carcinoma progression.
本研究的目的是探讨姜黄素联合贝伐单抗对肝细胞癌血管内皮生长因子(VEGF)/VEGF受体(VEGFR)/K-ras通路的影响。总共30只Sprague Dawley(SD)大鼠被随机分为五组:对照组、模型组、姜黄素组、VEGF阻断剂组和姜黄素+VEGF阻断剂组。随后通过定量逆转录-聚合酶链反应测量所有组中VEGF和VEGFR的mRNA水平,并通过蛋白质印迹分析检测K-ras的蛋白表达。与对照组相比,模型组、姜黄素组和VEGF阻断剂组中VEGF和VEGFR的mRNA水平显著升高。与模型组相比,姜黄素组、VEGF阻断剂组和姜黄素+VEGF阻断剂组的VEGF mRNA水平均降低。此外,姜黄素+VEGF阻断剂组的VEGF mRNA水平显著低于姜黄素组(P<0.05)。与模型组相比,姜黄素组、VEGF阻断剂组和姜黄素+VEGF阻断剂组的VEGF mRNA水平降低(P=0.0001)。VEGF阻断剂组和姜黄素组之间的VEGF mRNA水平无显著差异(P=0.863),而姜黄素+VEGF阻断剂组的VEGF mRNA水平显著低于姜黄素组(P=0.025)。姜黄素和VEGF阻断剂均可通过调节VEGF/VEGFR/K-ras通路抑制肝细胞癌进展。这两种化合物的组合对抑制肝细胞癌进展中VEGF信号通路的作用具有协同效应。