Objective To explore the expression of vascular endothelial growth factor(VEGF) and Survivin in nasopharyngeal carcinoma.Methods Immunohistochemical method staining for the paraffin sections(SP method) were used to assess the expression of VECF and Survivin expression in 80 cases of nasopharyngeal carcinoma tissues and 24 cases of nasopharyngeal chronic inflammation tissues.Results The overexpression rate of VEGF protein was 75.76% (61/80) in nasopharyngeal carcinoma tissues,and 25.00% (6/80) in nasopharyngeal chronic inflammation tissues(P<0.01) ;The overexpression rate of Survivin protein was 67.50% (54/80) in nasopharyngeal carcinoma tissues,and 16.67% (4/80) in nasopharyngeal chronic inflammation tissues(P<0.01).The expression of VEGF was related to TNM stage,T stage,lymph node metastasis and distant metastasis (P<0.05) ,and there was a close relation between the expression of Survivin and TNM stage,T stage,lymph node metastasis and distant metastasis (P<0.05).Conclusion Detecting the expression levels of VEGF and Survivin proteins simultaneously in nasopharyngeal carcinoma had certain reference value for judging biological behavior and evaluating prognosis of patients with nasopharyngeal carcinoma.

AIM AND METHODSTo investigate the role of modulation by angiotensin AT1 receptor in sodium and water excretion induced by cholinergic agonist carbachol. Tyrosine hydroxylase immunoreactivity (TH-IR) in hypothalamus were also observed.

RESULTSThe natriuretic and diuretic effect induced by carbachol (CBC) were partially inhibited by pretreatment of losartan, a specific blocker of angiotensin AT1 receptor (P < 0.05). Immunohistochemistry showed that both TH-IR density and number of TH-IR positive neurons were markedly increased in PaPo, Arc, Pe and AHP of hypothalamus at 40 min after carbachol administration, as compared with NS group (P < 0.05). However, in losartan pretreated group, the number and the density of TH-IR were significantly decreased in such nuclei mentioned above except PaPo.

CONCLUSIONThe results above suggest that brain AT1 receptor appears to be involved in mediating natriuresis induced by cholinergic stimulus. The blockade of AT1 receptor may down regulate the excitability of adrenergic neurons in Arc, Pe and AHP induced by CBC. We postulate that brain adrenergic and angiotensinergic pathway get involved in natriuresis induced by brain cholinergic stimulus together. Moreover, angiotensinergic neurons may influence the activity of adrenergic neurons in hypothalamus.

Angiotensin-Converting Enzyme Inhibitors ; pharmacology ; Animals ; Brain ; metabolism ; Carbachol ; pharmacology ; Losartan ; pharmacology ; Male ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 ; metabolism ; Receptors, Cholinergic ; metabolism ; Sodium ; metabolism ; Water ; metabolism