ABSTRACT
Objective To investigate the protective effect of ω?6 soybean oil fat emulsion on folium sennae?induced diarrhea in mice. Methods Thirty?six Kunming mice were randomly divided into three groups,including control,diarrhea,ω?6 soybean oil fat emulsion group(12 mice in each group). Besides the mice in control group,other mice were administrated folium sennae by gavage for 15 days to establish the diarrhea model. Then mice in ω?6 soybean oil fat emulsion group received ω?6 soybean oil fat emulsion by intravenously administration at a dose of 15 mL/kg daily since 6th day after intragastric administration of folium sennae for 10 days. Animals in control group and diarrhea group were intravenously adminis?tered with same volume of saline. The body weight ,general state and diarrhea index of the mice in each group were dynamically assessed. Ten days after intravenous injection,mice in every group were sacrificed and tissues were collected. Morphology of intestine mucosa was observed after HE staining. Albumin(ALB)level in plasma was evaluated by biochemical method. Proliferating cell nuclear antigen(PCNA)expression in intestine mucosa were assessed by immunohistochemical method. Results Compared with that in the diarrhea group,the general status,body weight and diarrhea index of mice in ω?6 soybean oil fat emulsion group were improved significantly. Ten days after intravenously administration ,pathological change in intestine mucosa of mice in ω?6 soybean oil fat emulsion group was improved significantly ,ALB level in plasma and PCNA expression in intestine mucosa were significantly increased(P<0.05)compared with that in diarrhea group. Conclusion ω?6 soybean oil fat emulsion has a significant protective effect on the diarrhea of mice induced by folium sennae ,which may be related to the up?regulated expression of PCNA by ω?6 soybean oil fat emulsion.
ABSTRACT
Objective To investigate the relationship between Ezrin expression and subcellular localization of E?cadherin(E?cad),and explore the clinical significance of this relationship to pathological features such as lymph nodes metastasis in breast cancer. Methods Ninety four cases of breast cancer tissue samples with lymph node metastasis were collected. The expression of Ezrin and E?cad was detected by immunohistochemi?cal method. Results The positive rates of and E?cad and Ezrin were respectively 45.7%and 58.5%in 94 nodes positive breast cancer,containing membranal expression of E?cad(E?cadm)in 20 cases and cytoplasmic expression of E?cad(E?cadc)in 23 cases;the frequency of E?cadc positive staining was significantly higher in Ezrin(+)tissues than that in Ezrin(-)tissues(P=0.025);E?cad expression level was significantly lower in TNMⅡ?Ⅲstage cases(P=0.001),and Ezrin expression(P=0.036)and E?cadc(P=0.013)was significantly increased in bigger cases;com?pared with E?cad(+),Ezrin(-),E?cadm tissues,the number of lymph node metastasis in E?cad(-)(P=0.011),Ezrin(+)(P=0.002),E?cadc (P=0.020)tissues were increased significantly;in the order of E?cad(+)/Ezrin(-),E?cad(-)/Ezrin(-),E?cad(+)/Ezrin(+),and E?cad(-)/Ezrin(+),the number of lymph node metastasis was increased significantly(P<0.001);similarly,in the order of E?cadm/Ezrin(-),E?cadc/Ezrin(-),E?cadm/Ezrin(+),and E?cadc/Ezrin(+),the number of lymph node metastasis was increased significantly(P=0.007). Conclusion Ezrin may regulate the subcellular localization of E?cad in metastatic breast cancer ,which may affect the course of breast cancer and promote the metastasis of lymph nodes.
ABSTRACT
Aim To investigate whether EGCG treat-ment ameliorates cognitive deficits in APP/PS1 trans-genic mice and, whether it has the ameliorating effect of p75 NTR signaling to neuronal apoptosis in the hippo-campus of APP/PS1 mice. Methods Morris water maze test and locomotivity test were used to predict be-havioral changes; further TUNEL staining and Fluoro-Jade B staining were applied to confirm the neuronal apoptosis and neuronal degeneration;Western blot was employed to detect protein expression levels of p75 NTR signaling in the hippocampus of APP/PS1 mice. Re-sults EGCG treatment dramatically ameliorated the cognitive impairments, and inhibited the neuronal ap-optosis in the APP/PS1 mice. Moreover, EGCG treat-ment dramatically inhibited the p75 NTR signaling by de-creasing the p75ICD expression, JNK2 phosphorylation, and cleaved-caspase 3 expression. Conclusion EGCG treatment dramatically ameliorates the cognitive impairments, and inhibits the neuronal apoptosis by in-hibiting the p75NTR signaling.