[Inhibitory effect of losartan on prostatic hyperplasia in spontaneous hypertension rats and its pathophysiological mechanism].

OBJECTIVE: To investigate the effect of losartan on prostatic hyperplasia in spontaneous hypertension rats (SHRs) and its pathophysiological mechanism. METHODS: We randomly divided 36 male SHRs into three groups of equal number to be treated intragastrically with high-dose losartan (30 mg per kg per d), low-dose losartan (15 mg per kg per d) and distilled water (control group). After 6 weeks of intervention, we measured the body weight and tail artery blood pressure of the rats and compared them with the baseline data. We collected blood from the heart for determination of the levels of serum angiotensin II (Ang II), insulin-like growth factor-1 (IGF-1) and interleukin-6 (IL-6) by enzyme-linked immunosorbent assay (ELISA), and harvested their prostates for measurement of their weight, observation of the tissue ultrastructures under the electron microscope and detection of the expression of endothelial nitric oxide synthase (eNOS) in the prostate tissue by immunohistochemistry. RESULTS: Compared with the control group, the low- and high-dose losartan groups showed significant decreases in systolic blood pressure ([203.75 +/- 10.28] vs [184.54 +/- 16.90] mmHg, P = 0.013; [203.75 +/- 10.28] vs [166.88 +/- 14.74] mmHg, P = 0.001) and diastolic blood pressure ([151.58 +/- 9.96] vs [136.71 +/- 14.28] mmHg, P = 0.022; [151.58 +/- 9.96] vs [122.71 +/- 11.56] mmHg, P < 0.001) of the lower tail artery after treatment, as well as in the prostate weight ([0.73 +/- 0.08] vs [0.64 +/- 0.10] mg, P = 0.011; [0.73 +/- 0.08 ] vs [0.50 +/- 0.17] mg, P < 0.001). Electron microscopy revealed edema of the basal and columnar epithelial cells, concentrated and marginated heterochromatin and widened nuclear gap of interstitial fibroblast nuclei, and reduced mitochondria and endoplasmic reticula in the low-dose losartan group, and even more obvious in the high-dose group. The level of serum Ang II was remarkably higher in the low- and high-dose losartan groups than in the control ([61.32 +/- 2.49] vs [54.85 +/- 7.20] pg/ml, P = 0.021; [65.49 +/- 6.78] vs [54.85 +/- 7.20] pg/ml, P < 0.001]) , that of serum IGF-1 was lower in high-dose losartan than in the control group ([1.50 +/- 0.11] vs [1.60 +/- 0.10] ng/ml, P = 0.03), but the serum IL-6 levels exhibited no significant differences among the three groups. The expression of eNOS in the prostate tissue was significantly higher in the losartan groups than in the controls (P = 0.022), even higher in the high-dose than in the low-dose group. CONCLUSION: Losartan can suppress the progression of prostate hyperplasia in spontaneous hypertension rats by inhibiting RAS, IGF-1 and angiogenesis.

[Effects of curcumin on secretion of adiponectin and interleukin-6 in human adipose tissues: an in vitro study].

OBJECTIVE: To investigate the effects of different concentrations of curcumin on secretion of adiponectin (APN) and interleukin-6 (IL-6) in human adipose tissues cultivated in vitro. METHODS: Seven male patients with kidney stones were admitted. Abdominal subcutaneous adipose tissue and perirenal adipose tissue were collected from the operating-patients, and were cultivated with different concentrations of curcumin (10 and 100 microg/ml) in vitro. The contents of APN and IL-6 in the culture medium of adipose tissue cells were measured by enzyme-linked immunosorbent assay (ELISA) after they were cultured for 6 and 24 hours. RESULTS: Compared with the blank control group, the content of APN in the adipose tissue culture medium was increased by 100 microg/ml curcumin (P<0.05) after 6-hour culture, and the content of IL-6 was significantly decreased by 100 microg/ml curcumin after 6- and 24-hour culture (P<0.05). CONCLUSION: 100 microg/ml curcumin can increase APN secretion and decrease IL-6 secretion in human adipose tissues cultivated in vitro.