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??OBJECTIVE To study the inhibitory effect of Ke-ai-xin pill on tumor growth and angiogenesis of transplanted colon cancer cell line HCT116 in nude mice. METHODS To establish the transplant tumor model in nude mice for HCT116. All tumor-bearing nude mice were randomly divided into control group (normal saline), positive group (bevacizumab,5 mg??kg^-1, intraperitioneally), and low-, medium-, high-dose Ke-ai-xin pill-treated groups(200, 400 and 800 mg??kg^{- 1}, intragastrically). The tumor xenografts were harvested and measured for their weights. Immunohistochemistry was used to detecte microvessel density (MVD)and vascular endothelial growth factor(VEGF)expression. RESULTS Ke-ai-xin pill inhibited tumor growth in nude mice in varying degrees. After the administration of each treatment group, TV, RTV, and T/C decreased significantly(P<0.05). SABC assay showed that MVD of Ke-ai-xin pill treatment group was sparse, MVD value decreased from (59.62??18.83) to (55.56??12.63),(46.72??11.57) and (41.35??10.27), Ke-ai-xin pill treatment group can significantly reduce the positive expression of VEGF. the positive expression rate reduced from(78.46??16.53)% to (58.64??14.19)%, (49.27??13.29)% and (43.68??11.71)%. CONCLUSION Ke-ai-xin pill can inhibit tumor growth of transplanted colon cancer cell line HCT116 in nude mice in varying degrees, reduce MVD value and the expression of VEGF in tumor tissue, so its antitumor activity may be related to inhibiting angiogenesis.     

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??OBJECTIVE To investigate the antitumor effect and molecular mechanism of ginsenoside Rg1 pyrolysis products (HPPRg1) on H₂₂ tumor bearing mice. METHODS To establish tumor model of transplanting H₂₂ tumor-bearing mice and observe the anti-tumor effects of HPPRg1, H₂₂ tumor-bearing mice were randomly divided into groups of control, model, cyclophosphamide (CTX, 30 mg??kg^-1), low dosage of HPPRg1 (HPPRg1-L, 10 mg??kg^-1), middle dosage of HPPRg1 (HPPRg1-H, 20 mg??kg^-1) and high dosage of HPPRg1 (HPPRg1-H, 40 mg??kg^-1) groups, respectively. Through evaluating inhibition rates of tumors, organ indices, and levels of TNF-??, IFN-?? and IL-2 to observe the anti-tumor effect of HPPRg1. In addition, H&E and Hoechst 33258 straining were used to observe the apoptosis of H₂₂ tumor cell. RESULTS Compared with the model group, the three dose groups of HPPRg1 can inhibit tumor proliferation. Mainly through the inhibition of tumor cell proliferation and pro-apoptosis to exert anti-tumor effect. CONCLUSION HPPRg1 has a significantly inhibitory effect on H₂₂ tumor-bearing mice, the mechanism may related to promote apoptosis of tumor cells and improve immunity.     

Efficacy of Ciji Hua'ai Baosheng formula on the expressions of vascular endothelial growth factor,kinase insert domain-containing receptor and basic fibroblast growth factor in mouse models of H_22 hepatocellular carcinoma

OBJECTIVE: To investigate the efficacy of Ciji Hua'ai Baosheng formula(CHBF) on microvessel density(MVD) and vascular endothelial growth factor(VEGF), kinase insert domain-containing receptor(KDR) and basic fibroblast growth factor(b FGF) expression in serum and tumor tissue of mice receiving chemotherapy for the treatment of H22 hepatocellular carcinoma.METHODS: Sixty Kunming mice were injected subcutaneously with H22 hepatoma carcinoma cell suspensions into the right anterior armpit. Seven days later, all transplanted tumor were formed and the mice were intraperitoneally injected 200 mg/kg cytoxan(CTX) to establish the models of tumor-bearing mouse chemotherapy, then they were randomly divided into model group, continuing CTX chemotherapy group(CTX group), and three CHBF(117, 58.5 and 29.25 g/kg) groups. After ten days of treatments, histology was observed, contents of VEGF, KDR and b FGF in serum and tumor tissue were measured by enzyme-linked immunosorbent assay(ELISA), VEGF and b FGF protein expression and MVD tagged by CD34 were detected by immunohistochemisty.RESULTS: MVD in CHBF(117, 58.5 g/kg) and CTX groups was significantly lower than that in model group(P 0.01); expressions of VEGF, KDR and b FGF in serum and tumor tissue in CHBF(117 g/kg)group were less than those in model group(P 0.05; P 0.01); the expressions of MVD, VEGF and b FGF in tumor tissue of CHBF(117 g/kg) groupwere also less than those in CTX group(P 0.05;P 0.01).CONCLUSION: CHBF can effectively reduce the expression of VEGF, KDR and b FGF in serum and tumor tissue, and decrease MVD and delay tumor progression.     

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??OBJECTIVE To study the antitumor effect of Pileostegia tomentella 95% alcohol extract (PTAE) on H₂₂ tumor-bearing mice and its possible mechanisms. METHODS Sixty mice were chosen and mouse models bearing H₂₂ solid tumor were established in fifty mice, and the others were as normal control. H₂₂ tumor-bearing mice were randomly divided into five groups:model control group, fluorouracil group(20 mg??kg^-1), PTAE high, middle and low-dose group(180, 90, 45 g??kg^-1 of crude drug, respectively). The mice in treatment groups were intragastric administration respectively, meanwhile, the mice in normal control and model groups were treated with the same volume of distilled water, once a day for ten days. The blood was collected from eyeball in all mice, and the serum were separated and detected by ELISA for IL-2 and TNF-??.Then the mice were put to death. Their tumors, thymuses and spleens were separated and weighted, and the tumor inhibitory rates, thymus and spleen indexes were calculated. The pathological change of tumor tissue was observed. RESULTS Compared with model control group, the tumor weights of PTAE high and middle-dose groups were significantly decreased (P??0.05, P??0.01), the tumor inhibitory rates were 37.44% and 38.46% respectively. The spleen index of PTAE middle-dose group was increased significantly (P??0.01). The level of IL-2 in serum of tumor-bearing mice in the PTAE high-dose group was increased significantly(P??0.05), and the level of TNF-?? in serum (P??0.01) could be increased significantly in the PATE high, middle and low-dose groups. CONCLUSION Pileostegia tomentella 95% alcohol extract has antitumor activity, its mechanism may be developed by immuno-regulation.     

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??OBJECTIVE To study the effect mechanism of tempol against hypobaric hypoxia-induced heart damage in mice. METHODS One hundred and ten BALB/c mice were randomly divided into normal control group, hypoxia model group, acetazolamide group and tempol group. After single intraperitoneal injection for 30 min, the mice were exposed to a simulated high altitude of 8 000 m for 12 h. After hypoxic exposure, blood was collected from the eye sockets and separated into serum to measure the activities of lactic dehydrogenase (LDH)and creatine kinase (CK). Then the mice were sacrificed and the content of H₂O₂ and malondialdehyde (MDA) as well as ATPase and antioxidant enzyme activity in heart were determined. HIF-1, VEGF, Nrf2, and HO-1 were detected by immunohistochemistry. RESULTS Compared with normal control group, the activities of plasma CK and LDH in hypoxia model group significantly increased. In addition, the content of H₂O₂ and MDA in hypoxia model group significantly increased while ATPase and antioxidant enzymes activity markedly decreased compared with the normal control group. Moreover, the expression of HIF-1??, VEGF, Nrf2 and HO-1 increased. Prior administration of tempol effectively decreased the activities of plasma CK and LDH as well as the content of H₂O₂ and MDA in heart tissue. Tempol could increase ATPase and antioxidant enzyme activities and decreased the expression of HIF-1?? and VEGF compared with hypoxia model, while it could further increase the expression of Nrf2 and HO-1. CONCLUSION Tempol has protective effect on heart injury induced by hypobaric hypoxia in mice. Its mechanism may be attributed to the amelioration of energy metabolism, scavenging free radical, improvement of antioxidant enzyme activity the activation of the Nrf2/HO-1 pathway as well as alleviation of oxidative stress.     

艾灸通过成纤维细胞生长因子受体1和血管内皮细胞生长因子受体2抑制肉瘤微环境血管生成

目的:观察艾灸对肉瘤微环境中成纤维细胞生长因子受体1(FGFR1)和血管内皮细胞生长因子受体2(VEGFR2)的影响,探讨艾灸防治肉瘤的作用机制.方法:将接种S180肉瘤细胞形成移植瘤的C57BL/6J小鼠分为模型组、顺铂组和艾灸组,每组10只.艾灸组直接灸移植瘤,距离3 cm,10 min/次,每日1次,治疗14 d...     

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??OBJECTIVE To investigate the protective effect and possible mechanism of schisanhenol(Sal) in SH-SY5Y cell induced by H₂O₂. METHODS SH-SY5Y cells were treated with Sal (1,10 and 50 ??mol??L^-1) for 4 h and then exposed to H₂O₂ 100 ??mol??L^-1 for 24 h. Cell viability was measured by MTT assay. The expressions of silent information regulator 1(SIRT1), PGC-1?? and p-tau (S396) protein were detected using Western blotting. RESULTS MTT results showed that Sal significantly increased the survival rate of SH-SY5Y cell damaged by H₂O₂. Western blotting analysis showed that H₂O₂ reduced the expressions of SIRT1 and PGC-1?? in SH-SY5Y cells. However, tau protein content was increased by H₂O₂ at p-tau(S396) sites. Sal treatment significantly increased the levels of SIRT1 and PGC-1?? and decreased p-tau(S396) level induced by H₂O₂ in SH-SY5Y cells. CONCLUSION These results suggest that Sal has a protective effect on H₂O₂ damaged SH-SY5Y cells, which is related to up regulating the expressions of SIRT1 and PGC-1?? protein and decreasing the phosphorylation of tau protein.     

沙苑子黄酮对肿瘤血管形成的影响

 目的 观察沙苑子黄酮（ FAC ）对肿瘤血管形成的影响,并探讨其作用机制。 方法 采用四甲基偶氮唑盐蓝（ MTT ）法观察正常条件培养基和肿瘤条件培养基下 FAC 对细胞 ECV304 增殖的作用;采用鸡胚绒毛尿囊膜（ CAM ）模型和裸鼠移植瘤组织微血管密度（ MVD ）分析,观察 FAC 对肿瘤新血管生成的影响;采用免疫组织化学方法观察 FAC 对裸鼠肿瘤组织血管生成因子 (VEGF) 及其受体 Flt-1 、 Flk-1/KDR 、 Flt-4 和血管生成抑制因子内皮抑素 (ES) 蛋白表达的影响。 结果 FAC 对经人肝癌 SMMC-7721 细胞上清液处理的血管内皮细胞增殖有较明显的抑制作用,而对正常状态下的血管内皮细胞毒性较低; FAC 明显抑制 CAM 新生血管生成, FAC-a （ 400 mg·L^-1 ）组的血管指数为 67.5% ;裸鼠移植瘤 MVD 和 VEGF 及其受体 Flt-1 和 Flk-1/KDR 的蛋白表达明显降低, ES 的蛋白表达显著增强。 结论 FAC 可抑制肿瘤组织血管形成,其作用机制与下调 VEGF 及其受体的表达和上调 ES 的表达有关。     

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??OBJECITVE To study the inhibitive effect of plumbagin on Lewis lung cancer. METHODS Cell proliferation was determined by CCK8 assay. Apoptosis was determined by flow cytometry. The expression of Bcl-2 and VEGF protein was studied by Western blot assay. The model of C57BL/6 mice bearing Lewis lung cancer was established by subcutaneous seeding of Lewis lung cancer cells, and randomly divided into 5 groups (n=6). Tumor-bearing mice were injected with normal saline, plumbagin(low, medium, high dose) or cyclophosphamide (CTX) in each group. The tumor volume was measured. All mice were sacrificed on Day 22nd under aseptic condition for the tumor collection. The transplanted tumors were weighed for calculation of the tumor inhibition rate; Immunohistochemical method was applied to assessing the VEGF expression in tumor tissue. RESULTS CCK-8 assay showed that plumbagin had an obvious inhibition on Lewis lung carcinoma cells line in a dose-dependent manner(r=0.953, P<0.05). Plumbagin significantly increased cell apoptosis rate(P<0.05). The protein levels of Bcl-2 and VEGF were significantly reduced by plumbagin (0, 2.5, 5, 10 ??mol??L^-1) treatment(P<0.05). In plumbagin(low, medium, high dose) groups and CTX group, the tumour volume, tumour weight and the expression of VEGF were significantly less than those in the control group (P<0.05). CONCLUSION The plumbagin effectively inhibits Lewis lung carcinoma cells proliferation and tumor growth of Lewis lung carcinoma cells in mice. The mechanism involved is down-regulating the expression of Bcl-2 ,VEGF and inducing cell apoptosis.     

增免抑瘤颗粒剂抗卵巢癌荷瘤小鼠皮下移植瘤血管生成作用的实验研究

目的 探讨增免抑瘤颗粒剂(Zengmian Yiliu Granule, ZMYLG)抗SKOV3卵巢癌荷瘤小鼠皮下移植瘤血管生成的影响及机制。方法 建立SKOV3卵巢癌荷瘤小鼠模型,随机分为对照组、紫杉醇组、ZMYLG高、中、低剂量组（简称ZMYLG高、中、低 组),每组8只,连续给药10天。采用细胞膜分化抗原34（CD34)抗体标记新生血管内皮细胞法,计算皮下移植瘤内微血管密度（MVD);免疫组化法、RT-PCR法检测皮下移植瘤内血管内皮生长因子（VEGF)及其受体胎肝激酶-1（FLK-1)、缺氧诱导因子（HIF-1α)蛋白及mRNA表达水平。结果 与对照组比较,紫杉醇组和ZMYLG高、中、低剂量组移植瘤内MVD明显降低,差异有统计学意义（P<0.01, P<0.05)。 ZMYLG各剂量组均能下调瘤组织中VEGF、FLK-1及HIF-1α蛋白 及mRNA表达量(P<0.01, P<0.05)。结论 ZMYLG能抑制肿瘤血管新生,其机制可能与下调HIF-1α表达,改善荷瘤小鼠缺氧状态,抑制VEGF及其受体FLK-1表达,发挥抗肿瘤血管生成作用有关。