Objective:The therapic effect of caffeic acid phenethyl ester(CAPE) in neuroglioma was to be investigated in this article.Methods:Athymic mouse model was constructed for therapic observation when tumor was treated by CAPE in vivo.Then Real-time PCR was employed to detected the expressing level of c-myc and ?-catenin genes in Wnt/?-catenin signaling pathway when U251 cells were treated by CAPE.Results:CAPE could inhibit the growth of neuroglioma in athymic mouse through drug oral application.The mRNA and protein expression of ?-catenin were inhibited.Furthermore,c-myc gene,which was the downstream of?-catenin gene,was also down-regulated after the drug treatment.Conclusion:The expressing level of ?-catenin and c-myc genes were down-regulated after CAPE treatment, by which the growth of neuroglioma could be inhibited.

Humans ; Jaw Neoplasms ; pathology ; surgery ; Mouth Neoplasms ; pathology ; surgery ; Pharyngeal Neoplasms ; pathology ; surgery ; Skull Base ; pathology ; surgery

Face ; surgery ; Humans ; Mouth ; surgery ; Reconstructive Surgical Procedures ; Retrospective Studies

Humans ; Neck Dissection ; methods ; Tongue Neoplasms ; surgery

ObjectiveTo explore the molecular mechanism that LRIG1 inhibits signal transduction system of epidermal growth factor receptor(EGFR)by investigating the role of LRIG1 in glioma.MethodsThe plasmid pcDNA3.1-LRIG1 was transfected into primary glioma cells by Lipofectamine.Then,the changes of LRJG1 and EGFR in the transfected glioma cells were measured by RT-PCR and Western blot,and the cell proliferation and apoptosis were analyzed by MTT and flow cytometry.ResultsThe expression levels of LRIG1 mRNA and protein in the glioma cells transfected with pcDNA-LRIG1 were significantly higher than those of control group and pcDNA3.1 transfected glioma cells,while those of EGFR mRNA and protein were significantly lower.The expression of PKC? and Bax was up-regulated,while the expression of bcl-2 was down-regulated.The growth of glioma cells was inhibited and their apoptosis was obviously enhanced.ConclusionBy participating the construction of the negative feedback loop of EGFR,LRIG1 inhibits the occurrence and growth of tumor through several pathways.

Contraindications ; Humans ; Infant ; Infant, Newborn ; Promethazine ; adverse effects ; therapeutic use

Humans ; Oral Surgical Procedures ; instrumentation ; methods ; Robotics ; instrumentation ; methods ; Surgery, Computer-Assisted ; instrumentation

Adult ; Axilla ; Breast Neoplasms ; pathology ; surgery ; Carcinoma, Ductal, Breast ; pathology ; secondary ; surgery ; Carcinoma, Intraductal, Noninfiltrating ; pathology ; secondary ; surgery ; False Negative Reactions ; Female ; Humans ; Lymph Node Excision ; Lymph Nodes ; pathology ; surgery ; Lymphatic Metastasis ; Mastectomy ; methods ; Reproducibility of Results ; Sentinel Lymph Node Biopsy ; methods ; Technetium Tc 99m Sulfur Colloid

Objective To investigate the expression of apoptosis-related proteins in rat cerebral cortex following traumatic brain injuries(TBI)and discuss the role of oxygen free radical-mitochondria signal pathway in Edaravone treating TBI.Methods A total of 180 male adult Sprague-Dawley rats were randomly divided into TBI group,Edaravone treatment group and control group.Each group was divided into six subgroups at 1,3,6,24,48 and 72 hours after TBI.Edaravone treatment group was injected with Edaravone(10 mg/kg)and the other two groups injected with the same volume of 0.9%normal saline.The pathological change in the rat cortex following TBI was observed with HE staining.At different time points,the expressions of Cytc,Bcl-2 and Bax in rat cortex as well as cell apoptosis and MDA change were observed by means of immunohistechemistry,TUNEL and TAB.Results HE staining showed scattered degenerated and necrotic neurous in cerebral cortex six hours after neuron injury,which peaked at 24 hours.Compared with control group,intermediate product MDA of free radical was increased six hours after TBI and peaked at 48 hours in Edaravone treatment group,which was lower than TBI group especially at 24,48 and 72 hours(P＜0.05).Compared with control group,the immunity reaction of Cytc positive cells inereased at six hours and peaked at 24 hours in TBI group,with statistical difference at 3,6,24,48 and 72 hours(P＜0.05).Compared with TBI group,the immunity reaction of Cyte positive cells was decreased obviously at 24,48 and 72 hours in Edaravone treatment group.Hyperexcitability of Bcl-2 after TBI reached peak at 3 hours and decreased gradually.But the expression of Bax was increased gradually after TBI and peaked at 48 hours,when Bax/Bcl-2 reached peak too.Folowing TBI,TUNEL positive cells increased gradually and reached peak at 48 hours,with mainly type Ⅰ TUNEL cells before 24 hours and typeⅡTUNEL cells after 24 hours.Conclusions There exist necrosis and apoptosis of nerve cells in cortex after TBI,especially apoptosis.Oxygen free radical mitochondria is one of the signal transduction pathways of nerve cell apoptosis following TBI.Edaravone exerts certain therapeutic effect on TBI.

Adolescent ; Child ; Female ; Humans ; Hypertension ; blood ; Insulin ; blood ; Insulin Resistance ; Male