Objective To investigate the protective effect of ethanol extract from Evodia officinalis Dode(EEEO) in a rat model of acute hepatic necrosis induced by carbon tetrachloride (CCl4).Methods Wistar rats were divided into four groups (control,CCl4,EEEO + CCl4,and Silmyarin + CCl4),the four groups were given intragastrically with normal saline,EEEO for 5 d,respectively.In the last one day,these groups except for control group were injected peritoneally with CCl4.Serum levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST),alkaline phosphatase (ALP) were detected by automatic biochemistry analyzer.Pathological changes of hepatic tissues were assessed by hematoxylin-eosine (HE) staining.The levels of superoxide dismutase (SOD),catalase (CAT) and malondialdehyde (MDA) in liver homogenate were analyzed using xanthinoxidase and thio-barbituric acid,respectively.Results Compared the ALT [(345.4 ±51.6)U/ml] and AST [(621.7 ± 143.5) U/ml)] of CCl4 group with ALT [(41.1 ± 2.2) U/ml] and AST [(85.2 ± 22.2) U/ml] of control group,the serum levels of ALT and AST in the CCl4 group were increased significantly (P ＜ 0.05).HE staining of liver tissue,the degeneration and necrosis were implicated to the whole hepatic lobules in the CCl4 group.In EEEO + CCl4 group,compared the ALT [(308.1 ± 44.6) U/ml] and AST [(546.4 ± 131.6) U/ml] of low dose EEEO + CCl4 group with the ALT [(210.6 ±34.5) U/ml] and AST [(379.3 ± 112.3) U/ml] of high dose EEEO +CCl4 group the serum levels of ALT and AST were decreased significantly in low dose EEEO + CCl4 group (P ＜0.05).The denaturation and necrosis of hepatic lobules,the level of SOD,CAT were increased and MDA decreased (P ＜ 0.05) inendochylema.Concluslons EEEO can significantly relieve the CCl4-induced hepatonecrosis.The role may be related to anti-lipid peroxidation.

Objective To investigate the clinical significance of protein expression of Six1 in cervical cancer. Meth?ods The immunohistochemical (IHC) staining was applied to detect the expression of Six1 protein in normal cervical tis?sues (n=32), cervical intraepithelial neoplasia (CIN) tissues (n=49) and cervical cancer tissues (n=123). The localization of Six1 protein was detected in vitro cultured HeLa cells using immunofluorescence (IF) staining. Results The positive rate of Six1was significantly higher in cervical cancer (72.3%) than that of CIN tissues (28.6%) and normal cervical tissues (15.6%,χ2=13.118 and 10.058 respectively, P<0.01). There were significance differences in expression levels of Six1 protein be?tween different tumor sizes and metastasis of cervical cancer (P < 0.01). The Six1 protein showed positive signals in cyto?plasm and nucleoli in HeLa cells. Conclusion Six1 expression is associated with cervical cancer, which may be a potential biomarker for invasion and metastasis of cervical cancer.

OBJECTIVES: This study was conducted to examine the effects on food intake, body weight, and metabolic parameters by amisulpride administration in male and female mice, comparing the effects of risperidone and vehicle administration. METHODS: Female and male C57BL/6 mice were grouped into low dose amisulpride(1.5mg/kg), high dose amisulpride(15mg/kg), risperidone(0.1mg/kg) and vehicle. Drugs were administered once daily through intraperitoneal injection over 21days. Body weight was measured weekly and food intake was measured daily. Levels of triglyceride, glucose, insulin and prolactin were determined at the end of experiment(on day 22). RESULTS: In the female mice, low and high dose amisulpride as well as risperidone caused significant weight gains. But weight gains in amisulpride groups were numerically smaller than that of risperidone group. In male mice, only high dose amisulpride caused significant weight gain. Among weight gain groups, only weight gain of male mice with high dose amisulpride was significantly associated with increased food intake. Weight gain group in female mice did not show significant correlation with food intake. In male mice, both amisulpride groups showed significantly high plasma insulin levels compared to vehicle. In female and male mice, low and high dose amiulpride groups showed significant high plasma prolactin levels compared to vehicle. Tri-glyceride level were not significantly changed in all groups. Glucose level was changed significantly only in male risperidone group. CONCLUSIONS: Administration of amisulpride caused more significant weight gains in female and male mice than controls but changes of metabolic parameters were different according to sex of mice. Our results suggest that different mechanisms of amisulpiride are likely to affect weight gain between male and female mice.
Animals ; Body Weight ; Eating ; Female ; Glucose ; Humans ; Injections, Intraperitoneal ; Insulin ; Male ; Mice ; Plasma ; Prolactin ; Risperidone ; Sulpiride ; Weight Gain

Previous studies have demonstrated that rottlerin, a specific PKCdelta inhibitor, potentiates death receptor- mediated apoptosis through a cytochrome c-dependent or -independent pathway. However, its ability to regulate necrotic cell death, as well as the underlying mechanism, remains unknown. We found that in murine fibrosarcoma L929 cells, treatment with rottlerin protected the cells against TNF-induced necrosis, whereas it sensitized the cells to apoptosis induced by co-treatment with Hsp90 inhibitor geldanamycin and TNF, in a manner independent of its ability to inhibit PKC-delta. TNF treatment induced rapid accumulation of mitochondrial superoxide (O2") through the Nox1 NADPH oxidase when cells undergo necrosis. Moreover, pretreatment with rottlerin failed to induce the GTP-bound form of small GTPase Rac1 by TNF treatment, and subsequently suppressed mitochondrial O2(-) production and poly(ADP-ribose) polymerase activation, thus inhibiting necrotic cell death. Therefore, our study suggests that Nox1 NADPH oxidase is a new molecular target for anti-necrotic activity of rottlerin upon death-receptor ligation.
Acetophenones/*pharmacology ; Animals ; Benzopyrans/*pharmacology ; Cell Death/*drug effects ; Cell Line, Tumor ; Mice ; Protein Kinase Inhibitors/*pharmacology ; Superoxides/metabolism ; Tumor Necrosis Factor-alpha/*antagonists & inhibitors/pharmacology