In the present study, we investigated the roles of TGF-β signaling pathway in a rat benign prostatic hyperplasia （BPH） model treated with cetrorelix. TGF-β1 and c-Myc expression were measured by qRT-PCR and Western blotting in the proximal and distal region of ventral prostatic lobes, respectively. We observed that treatment with cetrorelix led to a significant reduction of ventral prostate weight in a dose-dependent manner. In the proximal region, after cetrorelix treatment, the expression of TGF-β1 was dramatically increased （P〈0.05）, while the expression of c-Myc was significantly decreased （P〈0.05）. In comparison with the control group, the cetrorelix groups had more TUNEL-positive cells. Our findings strongly suggest that the TGF-β signaling pathway may be one of the major causes responsible for prostate volume reduction in BPH rats after cetrorelix treatment.
Objective： To construct a recombinant lentivirus vector which carries SD rat transducer of regulated CREB activity-1（TORC1） gene and examine its ability to express the TORC 1 gene in vitro. Methods： The coding sequence of SD rat TORC 1 gene was amplified using PCR and cloned into pGC-FU vector. 293T cells were transfected using Lipofectamine 2000 and packaged for the recombinant lentivirus particles. When the cloned sequence was identified to be right, the recombinant lentivirus particles were amplified in a large quantity. The titer of virus was determined by real-time PCR and the level of TORC1 expression was examined by Western blot. Results： The recombinant lentivirus vector carrying TORC1 was constructed successfully and could express TORC1 at a high level in 293T cells in vitro, and the titer determined by real-time PCR was 2 × 10^8 TU/ml. Conclusion： The recombinant lentivirus vector could express TORCl gene at a high level, and was very helpful in the study of exploring the effect of TORC1 on spinal cord injury.
