ArticleBiomedical reports2014
Effect of benazepril on the transdifferentiation of renal tubular epithelial cells from diabetic rats.
Article in Biomedical reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 4 citations in OpenAlex.
- Inhibitor of IGF1 receptor alleviates the inflammation process in the diabetic kidney mouse model without activating SOCS2.Drug design, development and therapy · 2018Article
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5 authors at 1 institution in 1 country.
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Abstract
The aim of this study was to investigate the effect of benazepril on the transdifferentiation of renal tubular epithelial cells from diabetic rats. Thirty male Sprague-Dawley rats were included in the present study. Eight of the 30 rats were randomly selected and served as the normal control group (N group), while the remaining 22 rats, injected with streptozotocin (STZ), comprised the diabetic rat model. Rats with diabetes were randomly divided into the diabetic (DM group) and benazepril (B group) groups. The total course was conducted over 12 weeks. Blood glucose, body weight, kidney/body weight, 24-h urinary protein, serum creatinine and blood urea nitrogen were measured at the start and end of the study. We observed the tubulointerstitial pathological changes, and applied immunohistochemistry and western blotting to detect the expression of α-smooth muscle actin (α-SMA) in renal tissue. The levels of blood glucose, kidney/body weight, 24-h urinary protein, serum creatinine, blood urea nitrogen and tubulointerstitial damage index (TII) in the DM group were significantly higher than that in the N group (p<0.01). Except for blood glucose and kidney/body weight, the remaining indices were lower in the B group compared with those in the DM group (p<0.01). Immunohistochemical staining results revealed the expression of α-SMA in renal tubular epithelial cells to be significantly higher in the DM and B groups compared with the control (N) group (p<0.01). Western blot analysis revealed that the expression of α-SMA in diabetic renal tissue increased 3.27-fold compared with that of the N group, while the expression of α-SMA in the B group decreased 45% compared with that in the DM group. In conclusion, benazepril significantly reduced the expression of α-SMA in renal tubular epithelial cells obtained from diabetic rats, inhibited the transdifferentiation of renal tubular epithelial cells and played an important role in kidney protection.
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