[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.

[The study of soluble P-selectin levels and it's correlation to the severity of coronary artery lesions in coronary heart disease].

OBJECTIVE: To investigate the difference of soluble P-selectin levels in different subtype of coronary heart disease and the relationship between soluble P-selectin levels with the severity of coronary artery lesions. METHODS: Enzyme linked immuoserbent assay (ELISA) was used to measure the plasma soluble P-selectin levels in 69 patients with angiocardiography documented coronary heart disease and 19 normal coronary arteries persons without angiocardiography detectable coronary artery disease (control group). The coronary artery lesions score was recorded according to single, double and triple-vessel lesions while the American College of Cardiology and the American Heart Association proposed type A, B, C lesion and Gensini scoring system. The relationships between plasma soluble P-selectin levels and the coronary artery score (the severity of coronary heart disease) were assessed. RESULTS: (1) The level of plasma soluble P-selectin was obviously higher in the coronary heart disease group than in the control group (180.6 +/- 60.5 ng/L vs. 145.3 +/- 21.7 ng/L, P<0.05). (2) The level of plasma soluble P-selectin was significantly higher in the acute coronary syndrome group (191.4 +/- 63.7 ng/L) than in the control group (145.3 +/- 21.7 ng/L, P< 0.01) and in the stable angina pectoris group (141.3 +/- 17.9 ng/L, P<0.01). (3) The level of plasma soluble P-selectin was high in multi-vessel coronary artery lesions group than in single-vessel group (190.1 +/- 64.2 ng/L vs. 157.2 +/- 43.4 ng/L, P < 0.05). The level of plasma soluble P-selectin was positively correlated with the Gensini score (r = 0.391, P = 0.001); the numbers of vessels lesions (rs = 0.349, P = 0.003); Type A, B and C lesions (rs = 0.358, P = 0.002). CONCLUSION: The positive correlation between the level of soluble P-selectin and the coronary artery score may indicate that soluble P-selectin levels might reflect the severity of coronary heart disease. The elevated soluble P-selectin level in acute coronary syndrome suggested the possible relation of P-selectin to the pathogenesis of acute coronary syndrome, which may save as a potential marker of plaque unstability.