Investigation of the role of hepatic oval cell in primary hepatocarcinogenesis using specific Y chromosome / 中华外科杂志

<p><b>OBJECTIVE</b>To determine the role of hepatic oval cell in primary hepatocarcinogenesis using specific Y chromosome.</p><p><b>METHODS</b>The model of hepatic oval cell proliferation was established by feeding 30 male Wistar rats with 0.06% 3'3-diaminobenzidine (DAB) for 4 weeks. Another 40 female Wistar rats were equally randomized into two groups: control group and experimental group. Experimental group was inoculated with oval cells suspension from the prepared male rats under the hepatic amicula and fed with DAB for 14 weeks continuously to promote hepatocarcinogenesis. Control group was fed with DAB for 14 weeks. After primer fragments were worked out on the male rats' SRY genes using the software of primer design, DNAs were extracted from the hepatic carcinomas of the female rats of the two groups and then amplified with PCR. Electrophoretic analysis was performed on the products.</p><p><b>RESULTS</b>After 14 weeks, primary hepatocarcinogenesis was found in the livers of all the 40 female rats. Electrophoresis showed the positive straps from the experimental group with the same length to the designed segments, whereas no positive straps were seen in the control group.</p><p><b>CONCLUSIONS</b>The hepatic oval cells can differentiate into hepatic cancer cells, which provides the evidence that the hepatocellular carcinoma has its source from the hepatic oval cells.</p>

Rosiglitazone inhibits atherosclerosis in apolipoprotein E-knockout mice / 中华心血管病杂志

<p><b>OBJECTIVE</b>To study the effect of rosiglitazone on atherosclerosis and potential mechanism in ApoE-knockout mice.</p><p><b>METHODS</b>Thirty-two 6-week-old ApoE-knockout mice were used as atherosclerosis model in two groups: rosiglitazone group (n = 18) and control group (n = 14). Each group contained equal numbers of male and female mice. All mice were fed with normal chow diet. In addition to normal diet, rosiglitazone group received rosiglitazone 17 mg/kg of body weight/day. Venous bloods were collected for plasma glucose and lipid analysis, and aorta were prepared for morphologic and immunohistochemical analysis after 14 weeks. Aortic root (1 cm) was cut and prepared for paraffin slice. The histomorphometric analysis of atherosclerotic lesion was performed by means of HE; positive percentage of macrophage cell and tumor necrosis factor-alpha were measured by means of immunohistochemistry in cross section. The ratio of lesion/aortic wall surface in the rest aorta was measured by means of Sudan IV staining in longitudinal section.</p><p><b>RESULTS</b>The amount of fatty streak in rosiglitazone group was significantly greater than that of control group; the gross number of lesions and the number of fibrous plaque and atheromatous plaque were similar in two groups. There were no differences in percentage of lesions in cross section in two groups. Rosiglitazone could significantly reduce the extend of atherosclerosis of longitudinal section, decrease the amount of macrophage cell and the level of tumor necrosis factor-alpha in lesions. The plasma glucose was normal and similar in two groups, and total cholesterol, LDL-cholesterol and triglyceride were significantly higher in rosiglitazone group.</p><p><b>CONCLUSION</b>Rosiglitazone suppresses the expression of tumor necrosis factor-alpha, reduces the number of macrophage cell in lesion, and inhibits the development of atherosclerosis.</p>