Search
- Page Path
-
HOME
> Search
Original Articles
- Pharmacology, Drug Therapy, and Toxicology
- Effect of Progesterone on COX-2 Expression and Proliferation of Prostate Stromal Cell.
-
Soo Ryun Jung, Sung Han Kim, E Hwa Choi, Ji Eun Park, Eun Mi Jeon, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi
-
Yeungnam Univ J Med. 2006;23(1):62-70. Published online June 30, 2006
-
DOI: https://doi.org/10.12701/yujm.2006.23.1.62
-
-
Abstract
PDF
- BACKGROUND
Benign prostatic hyperplasia (BPH) is the most common benign tumor in older men; the etiology of this disease remains poorly understood. Testosterone and dihydrotestosterone (DHT) both act as androgen via a single androgen receptor. Testosterone is converted to DHT by 5alpha-reductase in prostatic stromal cells. Progesterone has been reported to inhibit DHT conversion; howevwe, its effect on prostatic stromal cells remains to be elucidated. MATERILAS AND METHODS: In this experiment, we investigated the effect of progesterone on androgen receptor expression induced by DHT. We also tested the effect of progesterone on cyclooxygenase-2 (COX-2) expression, as well as prostate stromal cell proliferation using the cell count kit-8. RESULTS: Progesterone did not cause an increase of prostate stromal cell proliferation. The mRNA expression of the androgen receptor and COX-2 were not changed by progesterone; the expressions of androgen receptor and COX-2 proteins were decreased by progesterone in prostate stromal cells. CONCLUSION: These results suggest that in prostate stromal cells, progesterone decreases androgen receptor protein expression, which results in decrement of COX-2 protein expression. This effect might be mediated by post-transcriptional regulation.
- Endocrinology, Diabetes, and Metabolism
- Insulin Resistance in Late Pregnant Rats.
-
Myung Heup Chun, Yong Woon Kim, So Young Park, Jong Yeon Kim, Suck Kang Lee
-
Yeungnam Univ J Med. 1995;12(2):319-330. Published online December 31, 1995
-
DOI: https://doi.org/10.12701/yujm.1995.12.2.319
-
-
Abstract
PDF
- The influence of normal late pregnancy on insulin action and insulin secretion was studied in the Sprague-Dawley female rats. On 20th day after mating, intravenous glucose tolerance test(IVGTI) was performed in non pregnant control and pregnant rats. As results of IVGTT, glucose disappearance rate was not significantly different in both groups, but secretory response of insulin was significantly(p<0.05) increased in pregnant rat. And the ratio of insulin/ .glucose was significantly higher in pregnant rats, which means existence of insulin resistance. These insulin resistance was overcomed by increased secretory response of pancreatic insulin. Insulinogenic index( A insulin/glucose - 5 min) was highly significantly (r=0.62, p<0.01) correlated with progesterone concentration. Glycogen level and amounts of "C-glucose incorporated into glycogen after IVGTT were significantly(p<0. 05) decreased in the liver, but were not changed significantly in soleus. Glycogen synthase activity of soleus and liver was not differ significantly in the both groups. Insulin binding at varying concentrations of insulin to crude membrane of pregnant liver was not significantly different from control. In conclusions, although these pregnant rats were normal glucose tolerance due to increased secretory response of insulin, that was correlated with progesterone concentration, pregnant rat had insulin resistance. The mechanisms of insulin resistance were not related to defect of insulin binding phase and glycogen synthase, but suggest pre-receptor and/or postreceptor phase.
TOP