| Background:Benign prostatic hyperplasia(BPH)is a geriatric disease characterized by prostatic epithelial and stromal cell hyperplasia causing lower urinary tract symptoms.Its clinical symptoms bring poor quality of life and well-being.The main treatments for BPH are drugs,among which 5a-reductase inhibitors and a-blockers are commonly used,such as finasteride and tamsulosin.However,they can cause adverse reactions such as hypotension,ejaculation disorders,sexual dysfunction,and increased risk of prostate fibrosis.Chinese medicine treatment of BPH has been reported.Kangquan Recipe(KQR)has a unique effect in the treatment of BPH,with mild effects and small side effects.However,KQR can more deeply explore and study the mechanism of action on the treatment of BPH.Aim:To reveal the regulation of KQR on TGF-?/Smad signaling pathway in rats with BPH,thereby inhibiting EMT.To explore the possible mechanism of regulating BAMBI expression in key nodes,and to elucidate the molecular response mechanism of KQR in inhibiting EMT of BPH.Methods:48 SD male rats were randomly divided into 6 groups,8 in each group.In addition to the normal control group(N group),the remaining 40 rats were subcutaneously injected with testosterone propionate to form a model of BPH,and were randomly divided into high-dose KQR group(G group)and medium-dose KQR group(Z group),low-dose KQR group(D group),positive drug control group(F group),and BPH group(M group).The high,medium and low dose KQR group were given 14g/kg,7g/kg and 3.5g/kg respectively;the positive drug was given finasteride O.5mg/kg;the normal control group and BPH group were given Saline 10ml/kg.The administration method was intragastric administration,and the administration volume was 1 mL/100 g once a day for 30 days.Samples were taken after the intervention.The weight of the rat,the wet weight of the prostate were weighed,the prostate volume was measured,the prostate index was calculated,the pathological changes of the prostate tissue were observed by microscopy,and the active components contained in KQR side were analyzed by high performance liquid chromatography(HPLC);Method WB for detection of BAMBI protein in hypothalamus and pituitary tissues and TAM-?,TGF-?R1,TGF-PR2,p-Smad2,p-Smad3,BAMBI,E-cadherin and N-cadherin protein expression in prostate tissues;qRT-PCR was used to detect the expression of BAMBI mRNA and TGF-?,TGF-?R1,BAMBI,Smad2,E-cadherin and N-cadherin mRNA in rat serum and prostatic fluid.Results:1.The active ingredients contained in KQR are Nortrachelogenin-8'-O-?-glucoside,Trachelogenin,Arctigenin,Luteolin-4'-glucoside,Nortrachelogenin-5'-C-?-glucoside,Luteoloside,Apigenin-7'-glucoside,Tracheloside,Nortrachelogenin,Isoquercitrin.2.KQR can reduce the wet weight,volume and index of prostate in rats with BPH.By pathological observation,KQR can reduce the glandular cavity of the prostate,reduce the secretion in the cavity,reverse the proliferation of prostatic epithelial cells,and reduce the proliferation of interstitial tissue.Improve the intracellular environment and inhibit the proliferation of prostate tissue.Kangquan side promoted the expression of BAMBI protein in hypothalamic-pituitary-prostate tissue of BPH rats;increased the expression of BAMBI mRNA in blood,prostatic fluid and prostate tissue of rats,the effect of high-dose KQR group was the most obvious,and the regulation effect was Dose-effect relationship.Kangquan prescription can increase the expression of TGF-(?,TGF-?R1,TGF-?R2,p-Smad2,p-Smad3,BAMBI and E-cadherin in prostatic tissue of rats with BPH,and decrease the expression of N-cadherin protein.The expression levels of TGF-?,TGF-?R1,Smad2,BAMBI and E-cadherin in prostate tissues were increased,and the expression of N-cadherin mRNA was decreased.Conclusion:1.KQR prescription can treat BPH in rats.2.The mechanism by which Kangquanfang regulates BAMBI expression may be related to the hypothalamic-pituitary-prostate axis.3.One of the mechanisms of KQR's treatment of BPH is to inhibit the proliferation of epithelial mesenchyme of prostate hyperplasia by BAMBI regulation of TGF-?/Smad signaling pathway. |
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