Background Renal fibrosis is thought to be the common pathway in most cases of end-stage renal diseases. Recently, it is reported that tribble3 plays an important role in the progress of cardiac fibrosis in diabetes mellitus (DM). Therefore, TRB3 might participate in the pathogenesis of renal fibrosis of diabetes mellitus rat.
Methods 84 male Wistar rats were randomly divided into three groups: control group (n=12), high-fat diet group (HF group, n=36), DM group (n=36). The rats in DM group were injected with streptozotocin (STZ) after feeding with a high-fat diet for 4 weeks. The last two groups were re-divided into three subgroups according to injection with TRB3 siRNA adenovirus at week 17 whether or not (HF+Ad group; HF+Vector group; HF group; DM+Ad group; DM+Vector group; DM group; n=12 per group). After rats sacrificed, renal tissue was removed and stained with H&E and masson's trichrosome staining.
Results Renal fibrosis was significantly increased in DM group compared to HF group and Control group (4.1±0.87 vs 0.9±0.13 vs 0.53±0.08; p<0.05, p=0.017, respectively). The severity of fibrosis was also significantly different between three subgroups in DM group, the same to HF group. In DM group, renal fibrosis obviously ameliorate in DM+Ad group compared to DM+Vector group and DM group (1.4±0.24 vs 7.1±0.8 vs 3.7±0.8; p<0.0001, p<0.01, respectively). In HF group, renal fibrosis also noticeably improvement in HF+Ad group compared to HF+Vector group and HF group (1.3±0.24 vs 3.0±0.8 vs 0.9±0.13; p<0.05, p<0.05, respectively).
Conclusion TRB3'silence remarkably attenuates renal fibrosis and gene interference shows beneficial effect in the development of diabetic nephropathy in diabetes mellitus.
- diabetes mellitus
- renal fibrosis