Abstract:

Objective To investigate the relationship between the protective effect of angiotensin (Ang) （1-7） and the protein expression of intermediate conductance Ca2+ -activated K+ channels (KCa3.1) in renal fibrosis. Methods Totally 60 male mice were randomly divided into 5 groups: control group (WT); Ang Ⅱ group: mice received Ang Ⅱ ［1.4 mg/(kg.d)］by hypodermic injection; Ang Ⅱ blocker group (Losartan): mice received Ang Ⅱ ［1.4 mg/(kg.d)］and Losartan ［40 mg/(kg.d)］by hypodermic injection; Ang （1-7） group: mice received Ang Ⅱ ［1.4 mg/(kg.d)］and Ang （1-7） ［0.14 mg/(kg.d)］by hypodermic injection; diminazene aceturate(DIZE) group: mice received Ang Ⅱ ［1.4 mg/(kg.d)］and DIZE ［10 mg/(kg.d)］by hypodermic injection. After 4 weeks of continuous administration, the related indicators were detected. Masson staining was used to detect the collagen content, and Western blotting was used to detect the protein expression of collagen type Ⅰ, collagen type Ⅲ and KCa3.1 channel. Results Collagen deposition in renal tissue increased significantly after 4 weeks of hypodermic injection of Ang Ⅱ (n=12，P<0.01) compared with the WT group, which suggested that the model of renal fibrosis was successfully reproduced. Ang Ⅱ significantly increased the synthesis of collagen type Ⅰ and Ⅲ (n=6,P<0.01) and increased the expression of KCa3.1 channel protein (n=6，P<0.01) in renal tissues, while Ang （1-7） and ACE2 activator DIZE significantly inhibited those exchanges (n=12 or 6，P<0.01). Conclusion Ang （1-7） plays a protective role in the process of renal fibrosis, which may be related to the downregulation of KCa3.1 channel protein expression in renal tissue.

Key words: Fibrosis, Renal, Angiotensin （1-7）, Intermediate conductance Ca2+ activated K+ channel, Western blotting, Mouse