Objective To reveal the effect of fasting insuline(FINS) and insuline resistance(IR) in the process of benign prostatic hyperplasia(BPH). Methods One hundred and seventeen outpatients( ≥60 ys)with BPH from geriatric department were enrolled into the study. The patients were divided into groups according to their FINS and insulin resistance index (HOMA-IR). The indices of BPH, including volume of prostate ( PV ),prostate specific antigen( PSA ), international prostate symptom score (IPSS), course of BPH were analyzed in both groups. Results The PV ( [ 56. 46 ± 26. 88 ] ml vs [ 44. 84 ± 17.66 ] ml, P = 0. 017 ) and the course ( [ 18. 00 ± 6. 91 ] years vs [ 13.93 ± 7. 74 ] years, P = 0. 031 ) were significantly greater in BPH combined hyperinsulinemias(HINS) group than the BPH with normal FINS group;but we found no significant differences in the comparisons of serum PSA level or IPSS between two groups. The PV( [54. 17 ± 25.38 ] ml vs [42. 26 ±14. 15]ml,P =0. 004)and the course([ 16.58 ±7. 65] years vs [13.49 ±7. 59] years,P = 0. 036) were also significantly greater in BPH combined insuline resistance gruop than the insulin sensitivity group, again we found no significant differences in the comparisons of serum PSA level or IPSS between two groups. Conclusion FINS and IR are risk factors of progressed BPH and can promote the progress of BPH.

ObjectiveTo explore the effect of metabolic syndrome (MS) on the occurrence and development of benign prostate hyperplasia (BPH).Methods 101 elderly BPH patients were divided into two groups:BPH (n = 45) and BPH with MS (n= 56)group.The effects of metabolic indexes,including body mass index (BMI),waist,high density lipoprotein cholesterol (HDL-C),fasting blood glucose (FBS) and insuline resistance index (H()MA-IR),on prostate volume(PV),prostate-specific antigen (PSA),international prostate symptom score (IPSS) and lower urinary tract symptoms (LUTS) were surveyed in BPH patients.Results BPH with MS group showed significantly higher values of PV (t = 3.22,P= 0.003)and longer course of LUTS (t= 2.02,P =0.046) than BPH group.The BPH patients with overweight and obesity had significantly higher levels of PV(49.44±26.83 ml and 51.7±22.2 ml,P=0.021 and 0.043) than BPH patients with normal weight (38.10 ± 10.64 ml).Additionally,BPH patients with abdominal obesity had significantly higher levels of PV than BPH patients without abdominal obesity(50.26±26.51 ml vs.38.99± 11.25ml,P=0.005).BPH patients with low HDL-C had significantly higher PV than BPH patients with normal HDL-C[(54.23±28.92)ml vs.(40.40± 14.87) ml,P=0.009].The values of PV,PSA in the BPH patients with elevated FBS were significantly higher than in BPH patients with normal FBS (t=3.17 and 2.4I,P= 0.035 and 0.013).BPH patients with insuline resistance (IR) had higher values of PV and longer courses of LUTS than BPH patients without IR (t= 3.43 and 3.58,P-0.001).The PV was positively correlated with BMI(r= 0.459.P= O.OOO),FINS (r= 0.42,P=O.OOI),HOMA-IR (r= 0.49,P= 0.003) and gatively correlated with HDL-C (r= 0.38,P-0.000)- Multiple linear stepwise regression analysis showed that PV was closely correlated with HOMA-IR.ConclusionsMS has evident effects on the occurrence and development of BPH.

OBJECTIVE: To investigate the effect of hypoxia on cell viability and the endothelial differentiation potential in human umbilical cord derived mesenchymal stem cells (UC-MSCs), and to assess the in vitro protective role of VEGF under low oxygen tension. METHODS: MSCs were isolated from human umbilical cords and cultured in vitro. The morphological and phenotypic characterizations of human UC-MSCs were analyzed. The hypoxia induction was performed with or without the presence of 50 ng/mL of VEGF for different lengths of time. The cell proliferation, apoptosis, and reactive oxygen species (ROS) generation were assessed. Meanwhile, the endothelial differentiation potential of the UC-MSCs was measured. RESULTS: An increased apoptosis and ROS generation but reduced proliferation rate were observed at early stages (6, 12 h) after transferring the UC-MSCs from the atmospheric condition to the hypoxia condition. However, the UC-MSCs presented equal proliferation and apoptosis levels under hypoxic condition as compared with those under the atmospheric condition at the later stages (24, 72 h). A high concentration of exogenous VEGF (50 ng/mL) attenuated the increased apoptosis and inhibited the proliferation of UC-MSCs, induced by a short-term hypoxia treatment. After 14 days of exogenous VEGF induction under the hypoxia condition, the UC-MSCs acquired an early endothelial phenotype consisting of a mature endothelial molecule and some endothelial functions. CONCLUSION UC-MSCs progressively adapt to hypoxia in a step-by-step manner and maintain differentiation potential under hypoxia condition. VEGF can protect the UC-MSCs from cell damage and induce a differentiation of UC-MSCs toward endothelial lineage under hypoxic conditions.
Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Hypoxia ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Humans ; Mesenchymal Stem Cells ; cytology ; Protective Agents ; pharmacology ; Reactive Oxygen Species ; metabolism ; Umbilical Cord ; cytology ; Vascular Endothelial Growth Factor A ; pharmacology