The Hypothesis Of Pathophysiological Ideograph Of Chronic Prostatitis And The Studies On Restoration Of Blood-prostate Barrier In Rats

Prostatitis is an extremely common syndrome that afflicts 2%-10% of men.National Institutes of Health categoriesâ… andâ…¡prostatitis result from identifiable prostatic infections,whereas patients with categoryâ…£are asymptomatic.The majority of symptomatic cases are categoryâ…¢or chronic prostatitis (CP)/CPPS.The etiology of CP/CPPS is unknown.The traditional marker of inflammation,namely white blood cells in prostatic fluids,does not correlate with the predominant symptom of pelvic pain.An imbalance toward increased proinflammatory and decreased anti-inflammatory cytokines has been implicated and a few studies have shown some correlation of this with pelvic pain.The imbalance in some men may result from polymorphisms at the cytokine loci.An autoimmune process may be involved and experimental evidence indicates that this can be under hormonal influence.Recent findings include possible defects in the androgen receptor.The prostate may not even be the source of the symptoms.Pelvic pain also correlates with the neurotrophin nerve growth factor implicated in neurogenic inflammation and central sensitization.Finally,psychological stress may produce measurable biochemical changes and influence the other processes. The role of normal prostatic bacterial flora in inciting the inflammatory response has also been reconsidered.Most researchers believe that the symptoms of CP/CPPS appear to result from an interplay between psychological factors and dysfunction in the immune,neurological and endocrine systems.We only know that infecion or trauma triggers the inflammtory cascade and then a vicious cycle results in selfmaintenance of an inflammatory process,independent of the primary etiologic agent.But up to now, no researchers has try to establish a intact pathophysiological ideograph of chronic prostatitis.It is the bottleneck in studies of prostatitis.We try to establish a intact pathophysiological ideograph of chronic prostatitis.Furthermore,we proved a important step in this ideograph using CAP rat model and explore a validated method to restorate the blood-prostate barrier in CAP rat model.The studies are as follows:Objective:To establish a intact pathophysiological ideograph of chronic prostatitis;To study the distribution of endothelial barrier antigen(EBA,or blood-brain barrier antigen) in prostate of chronic abacterial prostatitis(CAP) rat model and its changes after immunosuppressive therapy;To study synergistic effect of mepartricin combined with finasteride in reestablishment of blood-prostate barrier in chronic abacterial prostatitis rat model.Method:Specialized biomedical literatures have been found that are implicitly linked by arguments that they respectively contain, but which nonetheless do not cite or refer to each other.The combined arguments lead to new inferences and conclusions that cannot be drawn from the separate literatures.Swanson DR describ a model and an online search strategy to aid in identifying other logically related noninteractive literatures.Based on this method,a literature review for the years 2000 to 2008 was performed using the PubMed database of the United States National Library of Medicine.The endothelial barrier antigen(EBA) is a protein expressed specifically by the endothelial cells of the rat brain barrier vessels.This antigen has been described as a 'barrier protein' and is used as a marker for the competent blood-brain barrier.An experimental CAP model was induced in adult male Sprague-Dawley rats by injection of Estradiol Benzoate subcutaneously(0.25mg/kg.d) for four weeks after castration.Using immunohistochemistry method,we studied the distribution of EBA in the prostate of CAP rat model and its changes after immunosuppressive therapy.In another experiment,40 CAP rats were randomly divided into four groups:control,indomethacin, mepartricin combined with finasteride and placebo groups.All drug treatments were conducted over a period of 4 weeks.After treatment,the results were analyzed with histological findings of the prostate to compare each group. Results:We found the theoretical and experimental proof of blood-prostate barrier in various research field and posed the intact concept of blood-prostate barrier.We further establish a intact pathophysiological ideograph of chronic prostatitis based on the concept of blood-prostate barrier.We found that EBA was strongly and consistently detected in epithelial cells of the rete testis and dorsolateral prostate gland,and in a few epithelial cells of the ventral prostate gland,the seminal vesicle and the coagulating gland.In CAP rat model,EBA could not be detected. However,after immunosuppressive therapy,the epithelial cells of prostate express EBA again.In another experiment,we found Indomethacin reduce the infiltration of inflammatory cells markedly.Mepartricin combined with Finasteride showed no effect on leukocyte infiltration in the inflamed prostatic interstitium, but penetration of inflammatory cell into the ductal lumen was restricted significantly.Conclusions:We believe that the blood-prostate barrier is existing indeed and play a key role in the pathogenesy of chronic prostatitis.Based on the concept of blood-prostate barrier,we established a intact pathophysiological ideograph of chronic prostatitis.Based on the first experiment,we can concluded that the dynamic blood-prostate bariier can be destroyed by autoimmune prostatitis and the destroy is reversible.The result proved a important step in our pathophysiological ideograph of chronic prostatitis.The second experiment indicated that mepartricin combined with finasteride reestablished the barrier function of prostate duct epithelium(blood-prostate barrier) in CAP rat model, thus showed the interesting therapeutic perspective in CAP.