%A Yan Cao, Xiao-jie He, Wei Xiang, Zhu-wen Yi %T Protective effect of catechin on renal microvessels in 5/6 nephrectomized rats and its mechanism %0 Journal Article %D 2009 %J Journal of Integrative Medicine %R 10.3736/jcim20090612 %P 557-562 %V 7 %N 6 %U {http://www.jcimjournal.com/CN/abstract/article_671.shtml} %8 2009-06-20 %X

Objective

To investigate the effects of catechin on angiotensin-converting enzyme (ACE) activity, angiotensin Ⅱ(Ang Ⅱ) content and microvessel density (MVD) in renal tissues of 5/6 nephrectomized rats.
Methods

Sixty SD rats were divided into 3 groups: sham-operated group, untreated group and catechin group. Animal model was reproduced by 5/6 nephrectomy. After 8- and 12-week administration, rats were sacrificed. Renal MVD was measured by immunohistochemical method with CD34 marking. Activities of ACE in plasma and renal cortices were measured by ultraviolet spectrophotometer, and Ang Ⅱ contents in plasma and renal cortices were measured by radioimmunoassay. Glomerular sclerosis index (GSI) and tubule interstitial score (TIS) were calculated by semiquantitative integration with hematoxylin and eosin staining and periodic acid-Schiff staining.
Results

After 8- and 12-week administration, the GSI and TIS in the catechin group were much less than those in the untreated group (P<0.05, P<0.01). MVDs around glomerulus and tubule at the end of the 8th and 12th week in the untreated group and the catechin group were much less than those in the sham-operated group (P<0.01). The ACE activities and Ang Ⅱcontents in plasma and renal cortices in the catechin group were much less than those in the untreated group (P<0.01). By Pearson correlation analysis, we found that MVD had negative correlation with GSI, TIS, Ang Ⅱ content, and ACE activity(P<0.01), however, the ACE activity and Ang Ⅱ content had positive correlation with GSI, TIS (P<0.01).
Conclusion

Catechin can prevent the 5/6 nephrectomized rats from decreasing of MVD and inhibit the progress of glomerular sclerosis and interstitial fibrosis by inhibiting the activity of ACE and reducing the production of Ang Ⅱ.