OBJECTIVESTo establish the testicular fibrosis model in rats.

METHODSWistar rats were divided into control group(n = 12) and model group(n = 40) randomly. Testicular fibrosis model was built with the classical method of establishing experimental autoimmune orchitis (EAO) combined with injecting Bacille Calmette-Guerin (BCG) into left testis.

RESULTSThe incidence rate of EAO and the rate of testicular fibrosis were 100%, 11.1% and 100%, 81.5% at 80, 140 days after the first infection, respectively.

CONCLUSIONSThe model of rat testicular fibrosis was established successfully.

Animals ; Autoimmune Diseases ; pathology ; Disease Models, Animal ; Fibrosis ; Male ; Mycobacterium bovis ; Orchitis ; pathology ; Rats ; Rats, Wistar ; Testis ; pathology

OBJECTIVE: To explore the effect of curcumin on the proliferation of renal cell carcinoma and analyze its regulation mechanism. METHODS: In RCC cell lines of A498 and 786-O, the effects of curcumin (2.5, 5, 10 µ mo/L) on the proliferation were analyzed by Annexin V+PI staining. Besides, A498 was inoculated into nude mice to establish tumorigenic models, and the model mice were treated with different concentrations of curcumin (100, 200, and 400 mg/kg), once daily for 30 days. Then the tumor diameter was measured, the tumor cells were observed by hematoxylin-eosin staining, and the protein expressions of miR-148 and ADAMTS18 were detected by immunohistochemistry. In vitro, after transfection of miR-148 mimics, miR-148 inhibitor or si-ADAMTS18 in cell lines, the expression of ADAMTS18 was examined by Western blotting and the cell survival rate was analyzed using MTT. Subsequently, Western blot analysis was again used to examine the autophagy phenomenon by measuring the relative expression level of LC3-II/LC3-I; autophagy-associated genes, including those of Beclin-1 and ATG5, were also examined when miR-148 was silenced in both cell lines with curcumin treatment. RESULTS: Curcumin could inhibit the proliferation of RCC in cell lines and nude mice. The expression of miR-148 and ADAMTS18 was upregulated after curcumin treatment both in vitro and in vivo (P<0.05). The cell survival rate was dramatically declined upon miR-148 or ADAMTS18 upregulated. However, si-ADAMTS18 treatment or miR-148 inhibitor reversed these results, that is, both of them promoted the cell survival rate. CONCLUSION Curcumin can inhibit the proliferation of renal cell carcinoma by regulating the miR-148/ ADAMTS18 axis through the suppression of autophagy in vitro and in vivo. There may exist a positive feedback loop between miR-148 and ADAMTS18 gene in RCC.
Animals ; Mice ; Carcinoma, Renal Cell/metabolism* ; Curcumin/therapeutic use* ; MicroRNAs/metabolism* ; Mice, Nude ; Cell Line, Tumor ; Kidney Neoplasms/metabolism* ; Autophagy ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; ADAMTS Proteins/metabolism*