The results from those studies mentioned above drew a consistent conclusion that PHB could protect the cells or tissue from reactive oxygen species (ROS) induced injury. There were some observations reported that the PHB might be observed in renal tissue and these studies found that PHB might play a protective role in kidney against renal disease. Guo et al.18 observed that PHB protein was positively expressed at normal renal tissues, strongly downregulated in renal biopsy specimens from patients, and negatively correlated with the degrees of tubulointerstitial lesions, and they also conducted a study in rat kidney fibroblasts cell line and found that the overexpression of PHB suppressed the renal interstitial

fibroblasts proliferation and cell phenotypic change induced by TGF-βl. SCH772984 molecular weight Wu et al.45 performed a study in rats with renal tubular atrophy and interstitial fibrosis induced by aristolochic acid and found that the expression of PHB protein

Tyrosine Kinase Inhibitor Library in vitro was downregulated in renal tissue of rats. Quan et al.46 observed that the expression of prohibitin-2 (homologue of PHB147) was downregulated in RTEC stimulated by elevated uric acid, which might promote trans-differentiation of RTEC, and they also noted that prohibitin-2 was associated with RTEC apoptosis due to uric acid. Those reports consistently agreed that PHB was a protective factor, and Quan et al.46 found that prohibitin-2 was associated with RTEC apoptosis in vitro. It was similar to our result in vivo. However, there was not any investigation

performed in vivo to report that there was an association between PHB expression and the expression of Caspase-3 or the cell apoptosis in renal interstitium of RIF rats. This study was performed to explore this association in RIF rats induced by UUO. Results from our study showed that protein expression of Caspase-3, TGF-βl, Col-IV or FN, indexes of RIF and cell apoptosis were more markedly increased in the GU group than those in SHO group, especially at 28 days. We also found that the impaired RTEC was the main contributor for RIF progression in the UUO Glycogen branching enzyme model. It could draw a conclusion that the RIF model induced by UUO in our study was successful. However, the pathological mechanism of RIF was not elucidated. In this study, we found that PHB was mainly located in RTEC and PHB expression was negatively correlated with protein expression of Caspase-3, TGF-βl, Col-IV or FN, index of RIF or cell apoptosis index. The PHB expression in the normal control group was more marked when compared with that in the GU group. In conclusion, PHB suppressed the development of RIF and alleviated the protein expression of Caspase-3, TGF-βl, Col-IV or FN, and weakened the indexes of cell apoptosis and RIF. As those mentioned above, PHB was associated with the expression of Caspase-3/apoptotic cell in renal interstitium of UUO rats.