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Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2017-Nov

Resveratrol improves smooth muscle carcinogenesis in the progression of chronic prostatitis via the downregulation of c-kit/SCF by activating Sirt1.

Články mohou překládat pouze registrovaní uživatelé
Přihlášení Registrace
Odkaz je uložen do schránky
Yi He
Huizhi Zeng
Yang Yu
Jiashu Zhang
Xingping Duan
Qi Liu
Bo Yang

Klíčová slova

Abstraktní

OBJECTIVE

Bladder smooth muscle cell death accompanied by hyperplasia and hypertrophy, as induced by inflammation, is the primary cause for poor bladder function. There are emerging evidences on the role of chronic inflammation as a factor involved in carcinogenesis and progression. We aim to determine the bladder smooth muscle pathological changes and dysfunction in chronic prostatitis (CP), to investigate whether resveratrol can improve the urinary dysfunction and the role of c-kit/SCF pathway, that has been associated with the smooth muscle carcinogenesis.

METHODS

Rat model of CP was established via subcutaneous injections of DPT vaccine and subsequently treated with resveratrol. H&E staining was performed to identify the histopathological changes in prostates and bladders. Western blotting and immunohistochemical staining examined the expression level of C-kit, stem cell factor (SCF), Sirt1, apoptosis associated proteins.

RESULTS

the model group exhibited severe diffuse chronic inflammation, characterized by leukocyte infiltration and papillary frond protrusion into the gland cavities, and a notable increase in prostatic epithelial height. Meanwhile, bladder muscle arranged in disorder with fracture, and cells appeared atypia. The activity of C-kit/SCF was up-regulated, the carcinogenesis associated proteins are dysregulated significantly in CP rats. Resveratrol treatment significantly improved these factors by Sirt1 activation.

CONCLUSIONS

activated c-kit/SCF and bladder muscle carcinogenesis were involved in the pathological processes of CP, which was improved after resveratrol treatment via the downregulation of c-kit/SCF by activating Sirt1.

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