Zhonghua nan ke xue = National journal of andrology · 2010
[Expressions of transforming growth factor-beta(1) and Smad4 in rat models of chronic nonbacterial prostatitis and their clinical significance].
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Wang Yang-Min, Lu Shou-Lin, Zhao Zhi-Qiang, Zhao Yu-Hai, Wang Nan, Jing De-Shan, Dong Yong-Chao
Аннотация
OBJECTIVE: To investigate the expressions of transforming growth factor-beta(1) and Smad4 in the prostatic tissue of rat models of chronic nonbacterial prostatitis (CNP), and to explore the mechanisms of CNP and its fibrosis.
METHODS: Sixty 6-month-old SD rats were randomly allocated into three groups of equal number: normal control, 30 d CNP model and 45 d CNP model, the models made by castration + high-dose intramuscular injection of estradiol benzoate. The expressions of TGF-beta1 and Smad4 in the prostatic tissue were detected by immunohistochemistry and Western blot.
RESULTS: Compared with the normal controls, the 30 d and 45 d CNP rat models showed a significantly increased expression of TGF-beta1 and decreased expression of Smad4 (P < 0.05), even more significantly in the 45 d than in the 30 d group. And the expression of TGF-beta1 was negatively correlated with that of Smad4 in the CNP rat models.
CONCLUSION: TGF-beta1 and Smad4 may be involved in the pathogenesis of CNP, and prostatic fibrosis may make the condition difficult to cure.
METHODS: Sixty 6-month-old SD rats were randomly allocated into three groups of equal number: normal control, 30 d CNP model and 45 d CNP model, the models made by castration + high-dose intramuscular injection of estradiol benzoate. The expressions of TGF-beta1 and Smad4 in the prostatic tissue were detected by immunohistochemistry and Western blot.
RESULTS: Compared with the normal controls, the 30 d and 45 d CNP rat models showed a significantly increased expression of TGF-beta1 and decreased expression of Smad4 (P < 0.05), even more significantly in the 45 d than in the 30 d group. And the expression of TGF-beta1 was negatively correlated with that of Smad4 in the CNP rat models.
CONCLUSION: TGF-beta1 and Smad4 may be involved in the pathogenesis of CNP, and prostatic fibrosis may make the condition difficult to cure.