Amala Cancer Research Centre, Thrissur, Kerala, India.
Integr Cancer Ther. 2011 Jun;10(2):178-91. doi: 10.1177/1534735410384861. Epub 2010 Nov 8.
The effect of Vernonia cinerea Less. extract on the inhibition of lung metastasis induced by B16F-10 melanoma cells was studied in C57BL/6 mice. V cinerea extract significantly (P < .001) inhibited lung tumor formation (78.8%) and significantly increased the life span (72.5%). Moreover, lung collagen hydroxyproline, uronic acid, and hexosamine and also serum sialic acid, γ-glutamyltransferase (GGT), and vascular endothelial growth factor (VEGF) levels were found to be significantly (P < .001) lower in treated animals compared with untreated controls. Histopathological analysis of the lung tissues also correlated with these findings. V cinerea treatment significantly inhibited the invasion of B16F-10 melanoma cells across the collagen matrix of the Boyden chamber. V cinerea also inhibited the migration of B16F-10 melanoma cells across a polycarbonate filter in vitro. It downregulated the production and expression of proinflammatory cytokines such as TNF (tumor necrosis factor)-α, IL (interleukin)-1β, IL-6, and GM-CSF (granulocyte monocyte colony-stimulating factor). V cinerea extract administration could suppress or downregulate the expression of matrix metalloproteinase (MMP)-2, MMP-9, lysyl oxidase, prolyl hydroxylase, K-ras, extracellular signal-regulated kinase (ERK)-1, ERK-2, and VEGF and also upregulate the expression of nm-23, tissue inhibitor of metalloproteinase (TIMP-1), and TIMP-2 in the lung tissue of metastasis-induced animals. It also inhibited the protein expression of MMP-2 and MMP-9 in gelatin zymographic analysis of B16F-10 cells. These results indicate that V cinerea could inhibit the metastatic progression of B16F-10 melanoma cells in C57BL/6 mice by regulating MMPs, VEGF, prolyl hydroxylase, lysyl oxidase, ERK-1, ERK-2, TIMPs, nm23, and proinflammatory cytokine gene expression in metastatic lung tissue.
研究了 Vernonia cinerea Less. 提取物对 B16F-10 黑色素瘤细胞诱导的肺转移抑制作用，在 C57BL/6 小鼠中进行。V cinerea 提取物显著（P <.001）抑制肺肿瘤形成（78.8%）并显著延长寿命（72.5%）。此外，与未治疗的对照组相比，治疗动物的肺胶原羟脯氨酸、尿糖醛酸、己糖胺以及血清唾液酸、γ-谷氨酰转移酶（GGT）和血管内皮生长因子（VEGF）水平也显著（P <.001）降低。肺组织的组织病理学分析也与这些发现相关。V cinerea 处理显著抑制 B16F-10 黑色素瘤细胞穿过 Boyden 室胶原基质的侵袭。V cinerea 还抑制 B16F-10 黑色素瘤细胞在体外穿过聚碳酸酯滤器的迁移。它下调了促炎细胞因子如 TNF（肿瘤坏死因子）-α、IL（白细胞介素）-1β、IL-6 和 GM-CSF（粒细胞单核细胞集落刺激因子）的产生和表达。V cinerea 提取物给药可抑制或下调基质金属蛋白酶（MMP）-2、MMP-9、赖氨酰氧化酶、脯氨酰羟化酶、K-ras、细胞外信号调节激酶（ERK）-1、ERK-2 和 VEGF 的表达，并上调转移诱导动物肺组织中 nm-23、组织金属蛋白酶抑制剂（TIMP）-1 和 TIMP-2 的表达。它还抑制了 MMP-2 和 MMP-9 在 B16F-10 细胞明胶酶谱分析中的蛋白表达。这些结果表明，V cinerea 可通过调节 MMPs、VEGF、脯氨酰羟化酶、赖氨酰氧化酶、ERK-1、ERK-2、TIMP、nm23 和促炎细胞因子基因表达，抑制 C57BL/6 小鼠中 B16F-10 黑色素瘤细胞的转移进展。
