FOOD SCIENCE ›› 2013, Vol. 34 ›› Issue (9): 287-291.doi: 10.7506/spkx1002-6630-201309058

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Effect and Mechanism of Angiotensin-converting Enzyme 2 on Diabetic Renal Injury in Rats

WANG Shan-shan,MA Chang,ZHANG Wei,WANG Yan-xia,ZHANG Yuan-shu*   

  1. Key Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural University, Nanjing 210095, China
  • Received:2013-01-19 Revised:2013-04-15 Online:2013-05-15 Published:2013-05-07
  • Contact: ZHANG Yuan-shu E-mail:wangshanshan2544@126.com

Abstract:

Objective: To compare the expression levels of ACE- AngⅡ-AT1/ACE2- Ang1-7-Mas and related regulatory
factors involved in the RAS (renin–angiotensin system) in order to explore the role and mechanism of ACE2 in the
occurrence and development of diabetes-induced renal in rats. Methods: Diabetes was induced in rats by intraperitoneal
injection of streptozotocin (STZ). The rats in the control group 1 and the model group 1 were guillotined 15 d later, and those
in the control group 2 and the model group 2 were guillotined 30 d later for measurement of the renal expression lelvels of
ACE, AT1, ACE2 and Mas mRNA and determination of the contents of AngⅠ and AngⅡ in local renal tissues. Results:
Compared with the control groups, the expression levels of ACE2 and Mas receptor mRNA were elevated in the model
group 1, ACE mRNA expression showed no significant difference, while AT1 mRNA expression and ACE/ACE2 mRNA
ratio decreased; renal ACE2 mRNA expression was lower in the model group 2 than in the control group 2, no obvisous
difference in Mas receptor mRNA expression existed, whereas the expression of ACE mRNA and AT1 receptor presented
an increasing trend and the ACE/ACE2 mRNA ratio of the modle group 2 was higher than that of the control group 2 with a
significant difference. The model group 1 showed a decrease in renin activity and AngⅠ content in local renal tissues with
a signficant difference (P < 0.05) but an increase in AngⅡ content with no significant difference (P > 0.05) as compared
to the control group 1. Compared with the control group 2, extremely significantly higher levels (P < 0.01) of renin activity
and AngⅠ content togeterh with a significant higher level (P < 0.05) of AngⅡ were observed in the model group 2.Conclusion: Abnormal expression of ACE and ACE2 is one of the reasons for the occurrence and development of diabetesinduced
renal injury in rats. The ACE2-Ang (1-7)-Mas axis activation is dominant at the initial stage of renal injury, which
is replaced by the ACE-AngⅡ-AT1 shaft activation at the serious stage. ACE2 plays a protective role by degrading AngⅠ
against the incidence of early renal disease.

Key words: angiotensin converting enzymeⅡ(ACE2), diabetes, kidney injury, angiotensin converting enzymeⅠ(ACE)-AngⅡ-AT1 axis, angiotensin converting enzymeⅡ- Ang-(1-7)-Mas axis

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