He Sheng, Bao Haiying, Wei Ying, Liu Ying, Liu Jie
Engineering Research Center of Chinese Ministry of Education for Edible and Medicinal Fungi, Jilin Agricultural University, Changchun 130118, Jilin, China.
Yanbian Xinglin Biotechnology Limited Company, Yanbian 133000, Jilin, China.
Sheng Wu Gong Cheng Xue Bao. 2022 Mar 25;38(3):1025-1038. doi: 10.13345/j.cjb.210185.
In order to explore the antitumor effect and mechanism of different extracts of cultivated fruit body on H tumor bearing mice, 150 ICR mice were randomly divided into blank group, model group, CTX group, . water extract group, ethanol extract group, petroleum ether extract group and crude polysaccharide group. H liver cancer cells were used to establish a solid tumor model and the mice were sacrificed on the 10th day after administration. The spleen and thymus organ index and tumor inhibition rate were calculated, the serum levels of TNF-α, INF-γ, VEGF, and hematoxylin-eosin were detected, and the immunohistochemical staining method was used to observe the pathological changes of tumor tissues, while Western blotting was used to detect the expression of tumor-related proteins. The high-dose petroleum ether extract group showed the best tumor inhibition rate (73.21%), increased serum levels of TNF-α, IFN-γ, and VEGF, as well as significantly promoted tumor necrosis and ablation. The immunohistochemistry of the water extract group showed negative regulation, indicating an insignificant tumor suppression. Western blotting showed the apoptosis genes , and pathway genes and were all highly expressed in each administration group compared with the model group, and their expression levels gradually decreased with increasing doses. In summary, the petroleum ether extract of . fruit body showed a significant anti-tumor effect which is presumably mediated through the mitochondrial pathway. The metabolism of drug in the body induces activation of Caspase-3 and Caspase-9 apoptotic proteins by Bax, Bcl-2, and TNF, which further caused nuclear chromatin or DNA to condense or degrade, and subsequently destroy the normal proliferation of tumor cells, thereby inducing their apoptosis and inhibiting tumor growth.
为探讨人工栽培子实体不同提取物对荷H瘤小鼠的抗肿瘤作用及机制,将150只ICR小鼠随机分为空白组、模型组、环磷酰胺(CTX)组、水提取物组、乙醇提取物组、石油醚提取物组和粗多糖组。采用H肝癌细胞建立实体瘤模型,给药10天后处死小鼠。计算脾脏和胸腺脏器指数及肿瘤抑制率,检测血清中肿瘤坏死因子-α(TNF-α)、干扰素-γ(INF-γ)、血管内皮生长因子(VEGF)水平及苏木精-伊红染色,采用免疫组化染色法观察肿瘤组织病理变化,同时采用蛋白质免疫印迹法检测肿瘤相关蛋白表达。高剂量石油醚提取物组肿瘤抑制率最佳(73.21%),血清TNF-α、IFN-γ和VEGF水平升高,且显著促进肿瘤坏死和消融。水提取物组免疫组化显示为负调控,表明肿瘤抑制作用不显著。蛋白质免疫印迹法显示,与模型组相比,各给药组凋亡基因及通路基因均高表达,且其表达水平随剂量增加逐渐降低。综上所述,人工栽培子实体的石油醚提取物具有显著的抗肿瘤作用,其机制可能是通过线粒体途径介导。药物在体内的代谢通过Bax、Bcl-2和TNF诱导半胱天冬酶-3(Caspase-3)和半胱天冬酶-9(Caspase-9)凋亡蛋白活化,进而导致核染色质或DNA浓缩或降解,随后破坏肿瘤细胞的正常增殖,从而诱导其凋亡并抑制肿瘤生长。