OBJECTIVETo observe the effect of Yifei Qinghua Granule (YQG) on vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), angiostatin, and endostatin in tumor tissue of Lewis Lung cancer mice, and to explore its anti-tumor mechanisms.

METHODSTotally 70 C57BL/6 mice were randomly divided into the model group, the low, medium, and high dose YQG groups, the gefitinib group, the gefitinib plus medium dose YQG group, and the cyclophosphamide (CTX) group, 10 in each group. The models were established by subcutaneously injecting Lewis lung cancer cells from the right axilla of C57BL/6 mice. Mice in the model group were given with 0.4 mL pure water by gastrogavage, once daily. Mice in the low and medium dose YHG groups were given with YHG at the daily dose of 5 and 10 g/kg by gastrogavage, once daily. Those in the high dose YHG group were given with YHG at 10 g/kg by gastrogavage, twice daily. Those in the gefitinib group were given with gefitinib 100 mg/ kg by gastrogavage, once daily. Those in the gefitinib plus medium dose YHG group were given with gefitinib at 100 mg/kg by gastrogavage in the morning and YHG at 10 g/kg by gastrogavage in the afternoon. All medication was started from the 2nd day of inoculation, lasting 14 successive days. Those in the CTX group were given CTX at 60 mg/kg by peritoneal injection on the 3rd and the 7th day of the experiment. Mice were sacrificed at the fifteenth day of the experiment. Tumors were taken out. Expressions of VEGF, bFGF, angiostatin, and endostatin in the tumor tissue were detected using immunohistochemical assay.

RESULTSCompared with the model group, the expression of VEGF significantly decreased, expressions of angiostatin and endostatin significantly increased in each group (P < 0.01). The expression of bFGF significantly decreased in the gefitinib group (P < 0.05). There was no statistical difference in VEGF among all groups (P > 0.05). The angiostatin expression was significantly higher in the CTX group than in the low dose YQG group (P < 0.01). The expression of endostatin was significantly higher in the high dose YQG group and the gefitinib plus medium dose YQG group than in the low and the medium dose YQG groups (P < 0.01). The expression of endostatin was significantly higher in the gefitinib plus medium dose YQG group than in the gefitinib group (P < 0.05).

CONCLUSIONThe action mechanism of YQG in treating lung cancer might be achieved through reducing the expression of angiogenesis promoting factor VEGF and increasing expressions of angiogenesis inhibitors angiostatin and endostatin.

Angiostatins ; metabolism ; Animals ; Carcinoma, Lewis Lung ; drug therapy ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Endostatins ; metabolism ; Fibroblast Growth Factor 2 ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Phytotherapy ; Vascular Endothelial Growth Factor A ; metabolism

PURPOSE: To identify factors predicting the presence of overactive bladder syndrome (OAB)-wet, compared with OAB-dry. METHODS: Between September 2007 and September 2013, the medical records of 623 women with OAB who completed a 3-day bladder diary and underwent urodynamic studies in a medical center were retrospectively reviewed. OAB-wet was diagnosed in patients who complained of at least one episode of urgency incontinence in the previous month; otherwise, OAB-dry was diagnosed. Multivariable logistic regression analysis was used to predict the presence of OAB-wet. RESULTS: Age (odds ratio [OR], 1.05; P<0.001), maximal flow rate (Qmax) (OR,1.06; P<0.001), voided volume (OR, 0.996; P=0.001), detrusor pressure at maximal flow rate (PdetQmax) (OR, 1.02; P=0.003), urgency episodes (OR, 1.04; P<0.001) and urodynamic stress incontinence (OR,1.78; P=0.01) were independent predictors for the presence of OAB-wet vs. OAB-dry. If we use bladder contractility index as a variable for multivariable logistic regression analysis, bladder contractility index (OR, 1.012; P<0.001) become an independent predictor for OAB-wet. CONCLUSIONS: A smaller bladder capacity and more frequent urgency episodes were predictors of OAB-wet, and the above findings indicate that OAB-wet and OAB-dry might be a continuum of OAB. Old age, high Qmax, high PdetQmax and urodynamic stress incontinence were also predictors for OAB-wet, and the above results reveal that OAB-wet and OAB-dry have partially different clinical and urodynamic features. Further studies might be performed to elucidate whether different treatment strategies between OAB-dry and OAB-wet can improve treatment efficacy.
Female ; Humans ; Logistic Models ; Medical Records ; Retrospective Studies ; Treatment Outcome ; Urinary Bladder ; Urinary Bladder, Overactive ; Urodynamics

OBJECTIVE: To study the effects of total ginsenosides (TG) extract from Panax ginseng on neural stem cell (NSC) proliferation and differentiation and their underlying mechanisms. METHODS: The migration of NSCs after treatment with various concentrations of TG extract (50, 100, or 200 µ g/mL) were monitored. The proliferation of NSCs was examined by a combination of cell counting kit-8 and neurosphere assays. NSC differentiation mediated by TG extract was evaluated by Western blotting and immunofluorescence staining to monitor the expression of nestin and microtubule associated protein 2 (MAP2). The GSK-3β/β-catenin pathway in TG-treated NSCs was examined by Western blot assay. The NSCs with constitutively active GSK-3β mutant were made by adenovirus-mediated gene transfection, then the proliferation and differentiation of NSCs mediated by TG were further verified. RESULTS: TG treatment significantly enhanced NSC migration (P<0.01 or P<0.05) and increased the proliferation of NSCs (P<0.01 or P<0.05). TG mediation also significantly upregulated MAP2 expression but downregulated nestin expression (P<0.01 or P<0.05). TG extract also significantly induced GSK-3β phosphorylation at Ser9, leading to GSK-3β inactivation and, consequently, the activation of the GSK-3β/β-catenin pathway (P<0.01 or P<0.05). In addition, constitutive activation of GSK-3β in NSCs by the transfection of GSK-3β S9A mutant was found to significantly suppress TG-mediated NSC proliferation and differentiation (P<0.01 or P<0.05). CONCLUSION TG promoted NSC proliferation and neuronal differentiation by inactivating GSK-3β.
Animals ; Cell Differentiation ; Cell Proliferation ; Ginsenosides/pharmacology* ; Glycogen Synthase Kinase 3 beta/metabolism* ; Neural Stem Cells/metabolism* ; Panax ; Plant Extracts/pharmacology* ; Rats ; beta Catenin/metabolism*