UNIVERSITAS AIRLANGGA



Detail Article

Folia Medica Indonesiana

ISSN 0303-7932

Vol. 41 / No. 1 / Published : 2005-01

Order : 5, and page :18 - 28

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Original Article :

The effect of 5α reductase inhibitor and estrogen in prostate proliferation. an experimental study in rats

Author :

  1. Soetojo *1
  2. Doddy M Soebadi *2
  3. Hendromartono *3
  4. I Ketut Sudiana*4
  1. Department of Urology, Airlangga University School of Medicine, Dr Soetomo Teaching Hospital, Surabaya
  2. Department of Urology, Airlangga University School of Medicine, Dr Soetomo Teaching Hospital, Surabaya
  3. Department of Internal Medicine, Airlangga University School of Medicine, Dr Soetomo Teaching Hospital, Surabaya
  4. Department of Pathology, Airlangga University School of Medicine, Dr Soetomo Teaching Hospital, Surabaya

Abstract :

This was an experimental study using posttest control group design involving Wistar strain Rattus norwegicus as experimental animal. The purpose of this study was to explain the mechanism of BPH in elderly. Samples were randomly divided into 2 groups, 1- and 2-month group, each comprising 26 rats. Each group was divided further into two subgroups, one group received combined estrogen and finasteride, and the other, receiving finasteride only, served as control group. Each subgroup consisted of 13 rats. After treatment for 1 and 2 months, the prostate was removed and examined for TGF-ß1, EGF, FGF, and proliferation. Immunohistochemistry was used for examining TGF-ß1, EGF, FGF, and the examination of proliferation was carried out using graticulae. This study employed univariate analysis with 2 sample t test as TGF-ß1, EGF, and FGF had no correlation. Data analysis used in this research was univariate analysis with 2 sample t test. Analysis result showed that estrogen could reduce TGF-ß1 significantly in 1 month and 2 month groups (p < 0.05) and estrogen also stimulated significant increase of EGF in 2 month groups (p < 0.05). Estrogen also increased proliferation significantly in both 1 and 2 month groups (p < 0.05) but estrogen did not increase FGF significantly in both groups. Multiple regression analysis on the effect of TGF-ß1, EGF, FGF and estrogen to proliferation revealed that only TGF-ß1 had negative feedback. This indicated that TGF-ß1 decreased, so that the proliferation increased. Estrogen had positive impact in proliferation, indicating that increased estrogen would also increase proliferation. In conclusion, estrogen increased the proliferation of the prostate cell and EGF significantly and decreased the expression of TGF-ß1 significantly. This leads to inhibition of proliferation, and finally may cause the occurrence of BPH.

Keyword :

prostate, estrogen, TGF-ß1, EGF, FGF, BPH,


References :

Kirby R, Fitzpatrick, Kirby M, Fitzpatrick A,(1994) Shared Care for Prostatic Diseases Oxford : MSD

Kirby RS, Christmas TJ,(1997) Benign Prostatic Hyperplasia, 2nd edition - : Mosby





Archive Article

Cover Media Content

Volume : 41 / No. : 1 / Pub. : 2005-01
  1. Editorial Vol 41 No 1 2005
  2. Opinion: Research In The Development Of Medical Science And Technology
  3. The Association Of Mitochondrial Dna Mutation G3316a And T3394c With Diabetes Mellitus
  4. The Effects Of Unilateral Testicular Torsion Upon Immunity Modulation And Apoptosis Of Germinal Cells In The Contralateral Testis. An Experimental Study In Rats
  5. The Effect Of 5α Reductase Inhibitor And Estrogen In Prostate Proliferation. An Experimental Study In Rats
  6. Quality Of Refilled Drinking Water In Surabaya City
  7. Adequate Help For Patients With Cervical Cancer? The Referral System In Indonesia. A Descriptive Comparison Study In Four Provinces
  8. In Vitro Drug Sensitivity Of Trypanosoma Evansi Bangkalan Isolates
  9. Comparison Of Dead Victims Due To Burn Between Periods
  10. Serum Osmolal Gap In Healthy Persons. Comparison Of Eleven Formulas For Calculating Osmolality
  11. Traumatic Optic Neuropathy In The Division Of Neuro-ophthalmology, Department Of Ophthalmology, Dr Soetomo Teaching Hospital, Surabaya
  12. The Potential Role Of α-lipoic Acid In The Management Of Diabetes Mellitus. Possible Molecular Mechanism
  13. Review Article And Clinical Experience: Metabolic Syndrome Vs Insulin Resistance Syndrome (a Cluster Of Components And Strategies For Treatment)

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