Chlormadinone Acetate (CMA) Induces Apoptosis on Canine Spontaneous Benign Prostatic Hyperplasia (BPH)
| Autor: | Rie Ikeda, Takaharu Nakayama, Norio Fukui, Masanori Murakoshi |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Histology
Physiology business.industry Cell Biology Hyperplasia medicine.disease Biochemistry Beagle Pathology and Forensic Medicine Steroidal antiandrogen Andrology Chlormadinone acetate chemistry.chemical_compound medicine.anatomical_structure Atrophy chemistry Prostate Apoptosis Medicine Benign prostatic hyperplasia (BPH) business |
| Zdroj: | ACTA HISTOCHEMICA ET CYTOCHEMICA. 34:223-228 |
| ISSN: | 1347-5800 0044-5991 |
| DOI: | 10.1267/ahc.34.223 |
| Popis: | The effect of a synthetic steroidal antiandrogen, chlormadinone acetate (CMA), on spontaneous benign prostatic hyperplasia (BPH) in dogs was investigated. Male beagle dogs (5-8 years old) were divided into four experimental groups. Group 1 consisted of untreated controls. Groups 2 to 4 received CMA 0.03, 0.1, and 0.3 mg/kg/day, p.o., respectively, for 6 months. In group 1, glandular hyperplasia of the prostate was clearly detected. In groups 2 to 4, CMA produced marked atrophy of the glandular epithelium. The interacinar fibro-muscular stroma was prominent. To evaluate the frequency of apoptosis, we counted the positive cells stained by the nick end labeling method. In group 1, the apoptotic index was 0.76±0.03%. In groups 2 to 4, apoptotic indices were 15.41±1.26%, 2.63±0.98% and 1.45±0.85%, respectively. Apoptotic cell death was mainly observed in the glandular epithelial cells. Based on our data, regression of BPH after treatment with CMA may be apoptotic cell death. |
| Databáze: | OpenAIRE |
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