Estrogen inhibits colon polyp formation by reducing angiogenesis in a carcinogen-induced rat model.

Objective. To study the effects of estrogen on colon polyp formation, proliferation, and angiogenesis on a rat model of colon cancer induced by dimethylhydrazine (DMH). Methods. Thirty-six female ovariectomized (OVX) rats were randomly divided into 3 groups: (I) control group (administrated with vehicles weekly), (II) DMH group (administrated with DMH weekly), and (III) DMH + E2 group (administrated with DMH and 17ß-estradiol weekly). The incidence, volumes, and multiplicity of colon polyps in each group were evaluated. The microvessel density (MVD), the expressions of Proliferating Cell Nuclear Antigen (PCNA), and the expressions of HIF-1 α and VEGF in polyps were detected in each group. Results. Estrogen reduced the multiplicity, volumes, and the PCNA expressions of DMH-induced colon polyps. The MVD in DMH + E2 group was significantly lower than that in DMH group. Estrogen treatment decreased the HIF-1 α and VEGF expressions at both mRNA and protein level. Conclusion. Estrogen replacement was protective for ovariectomized rats from DMH-induced carcinogenesis, and one of the mechanisms for this was due to estrogen's inhibitive effects on blood vessel formation by downregulating VEGF and HIF-1 α expressions.

[Expression of hepatic Bcl-2 and Bax proteins in schistosome-infected mice and the role of pentoxifylline].

OBJECTIVE: To study the expression of hepatic Bcl-2 and Bax proteins in mice infected with Schistosoma japonicum and the role of pentoxifylline (PTX) in the expression. METHODS: Forty mice were randomly divided into 4 groups: one normal control group,mice in the other three groups were all infected each with 25 cercariae, the infected control group was fed for 10 weeks after infection, and 2 weeks after infection, the high dose PTX group was given PTX 360 mg/(kg x d) for 8 weeks and the low dose PTX group was given PTX 180 mg/(kg x d)also for 8 weeks. At the end of 10 weeks all the mice were killed. Bcl-2 and Bax proteins expression was detected by immunohistochemisty. RESULTS: Compared with the normal control group, the expression of Bcl-2 and Bax was significantly higher in the infected control group (P < 0.05). Bcl-2 was significantly higher in high (dose PTX group than in the infected control group and in low dose PTX group (P < 0.05). However there was no significant difference in the expression of Bax among the groups (P > 0.05). CONCLUSION: PTX treatment can significantly increase the expression of Bcl-2 in liver tissue of schistosome-infected mice in a dose-dependent manner, and may play a role against liver inflammation and schistosomiasis-related liver fibrosis.

Effects of carbon dioxide and nitrogen on adhesive growth and expressions of E-cadherin and VEGF of human colon cancer cell CCL-228.

AIM: To study the effects of carbon dioxide on the metastatic capability of cancer cells, and to compare them with that of nitrogen. METHODS: The colon cancer cell CCL-228 was treated with 100 % carbon dioxide or nitrogen at different time points and then cultured under normal condition. Twelve hours after the treatment, the survival rates of suspension cells and the expressions of e-cadherin and VEGF were examined. RESULTS: After 60 min of carbon dioxide and longer time of nitrogen treatment, the suspended cells increased and the expression of e-cadherin decreased while the expression of VEGF was enhanced significantly. And the effects of nitrogen were similar to, but weaker than, those of carbon dioxide. CONCLUSION: Carbon dioxide may improve the metastatic capability of cancer cells and its effects are significantly stronger than that of nitrogen. A sequential use of carbon dioxide and nitrogen in pneumoperitoneum may take the advantage of both gases.

Effects of pentoxifylline on the hepatic content of TGF-beta1 and collagen in Schistosomiasis japonica mice with liver fibrosis.

AIM: To study the effects of pentoxifylline (PTX) on the content of hepatic TGF-beta1, type I and type III collagen in schistosomiasis japonica mice with liver fibrosis and its mechanism of anti-fibrosis. METHODS: Forty mice with schistosomiasis were divided into four groups: one group as control without any treatment, other three were treated with Praziquantel 500 mg/(kg x d)for 2 d, high dose PTX 360 mg/(kg x d) for 8 wk, and low dose PTX 180 mg/(kg x d) for 8 wk respectively. Immunohistochemical technique and multimedia color pathographic analysis system were applied to observe the content change of hepatic TGF-beta1, type I and type III collagen in schistosomiasis japonica mice with liver fibrosis before and after PTX treatment. RESULTS: Effects of PTX on the content change of hepatic TGF-beta1, type I and type III collagen in schistosomiasis japonica mice with liver fibrosis were related to the dosage of PTX, high dose PTX treated group could significantly reduce the content of TGF-beta1 (0.709+/-0.111), type I (0.644+/-0.108) and type III (0.654+/-0.152) collagen compared with those of control group (0.883+/-0.140, 0.771+/-0.156, 0.822+/-0.129) with statistical significance (P<0.05). Low dose PTX could also reduce the hepatic content of TGF-beta1 (0.752+/-0.152), type I (0.733+/-0.117) and type III (0.788+/-0.147) collagen, but without statistical significance (P>0.05). Both high dose and low dose PTX groups have significant differences on the content of TGF-beta1, type I and type III collagen (P<0.05, P<0.05, P<0.01, respectively). CONCLUSION: High dose of PTX treatment could reduce the content of hepatic TGF-beta1, type I and type III collagen significantly in schistosomiasis japonica mice with liver fibrosis, and thus plays its role of antifibrosis.