Post Date December, 03 2023
Androgen
It is well known that androgen is an indispensable condition for benign prostatic hyperplasia, but the testosterone secreted by testicular interstitial cells cannot play a direct role. Normally, after testosterone enters the prostate cells, there are two metabolic pathways: α- Under the action of reductase, it is irreversibly transformed into 5 α- Dihydrotestosterone, reconstituted into 3 α- Androstanediol; The second step is to convert the aromatase to 1 β- Estradiol. Of which 5 α- The activity of dihydrotestosterone (DHT) is 2-3 times stronger than that of testosterone, and it is the most important androgen. It can bind to specific receptors to form a complex that enters the nucleus, and then connect to nuclear receptors and bind to chromatin, affecting the synthesis of RNA and DNA. DHT has a positive promoting effect on the formation of prostate hyperplasia, so eunuchs and castrated dogs do not develop prostate hyperplasia.
5 α- Reductase can be divided into two isoenzymes, type I and type II. Type II enzymes are dominant in humans and type I enzymes are dominant in dogs. Research has confirmed that only 5% of the prostate enzymes in humans and dogs increase with age α- Reductase content increases, and other animals show a downward trend. In fact, only humans and dogs can naturally form prostate hyperplasia, if there is 5% α- Prostate hyperplasia does not occur in people with reductase deficiency.
Estrogen
With age, the concentration of estrogen in men is stable or slightly increased, and compared to young men, the proportion of male to female in elderly men increases. Some scholars believe that this change in the balance of male and female hormones may be the cause of prostate stromal induction activity leading to prostate hyperplasia. Some studies have shown that binding estrogen in benign prostatic hyperplasia (BPH) can activate cells to synthesize and secrete extracellular matrix proteins, forming a dense layer of fibrous connective tissue around the cells, thereby participating in the occurrence and development of BPH. In the initial interstitial hyperplasia, the role of estrogen is primary; In the process of prostate hyperplasia, estrogen and androgen have a synergistic effect, so some people call estrogen a stimulator of the growth of the prostate matrix.
Since estrogen stimulates the release of prolactin from the pituitary gland, prolactin can also stimulate the absorption and utilization of androgens by prostate cells. Some studies have found that there is a positive correlation between the plasma prolactin level and the androgen receptor content in prostate cells during prostate hyperplasia, so it can be speculated that the two can also have a synergistic effect in the process of prostate hyperplasia. However, drugs that inhibit prolactin have not been able to reduce the size of the hyperplastic prostate, so the mechanism remains to be further studied.
