Angiotensin (1-7) participating in renal fibrosis by inhibiting intermediate conductance Ca2+-activated K+ channels protein expression / 解剖学报

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 (KCa3. 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 DI and KCa3. 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 DI (n=6,P<0.01) and increased the expression of Kca3. 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 downregulation of KCa3. 1 channel protein expression in renal tissue.