Abstract:

Ｏｂｊｅｃｔｉｖｅ：Macrophage infiltration is tightly contacting with hypertensive renal injury, the present study investigated renal protection of macrophage depletion by clodronate liposome (CL) in angiotensin (Ang) Ⅱinduced hypertension mice.
Ｍｅｔｈｏｄｏｌｏｇｙ：Twentyfour C57BL/6 mice were randomly divided into four groups: normal control, normal plus CL treatment (CL, 01 ml/10g BW, 2 times/week by tail vein injection), AngⅡ infusion [14 mg/（kg·day）, implanted by minipump], and AngⅡ plus CL treatment for 14 days.
Ｒｅｓｕｌｔｓ：Compared with control mice, AngⅡ infusion significantly increased systolic blood pressure (SBP), proteinuria, renal structural damage, renal macrophage infiltration associated with higher expression of proinflamamtory cytokine tumor necrosis factor (TNF) α and inteleukin (IL) 1β. CL markedly reduced renal macrophage infiltration, renal structural and functional impairment, and the expression of the proinflammatory cytokines with a mild reduction in SBP in AngⅡ mice. Furthermore, AngⅡ also induced renal fibrosis with increasing expression of fibrotic factors TGFβ1 and fibronectin as well as the expression of NADPH oxidae subunits gp91phox and p22phox, depletion of macrophage by CL effectively reversed renal fibrosis and the changes in those molecules induced by AngⅡ.
Ｃｏｎｃｌｕｓｉｏｎ：
 Macrophage was the main contributor to AngⅡ hypertensive renal injury. The underlying mechanisms may involve increased production/release of macrophagederived inflammatory cytokine and oxidative stress, macrophage depletion protects AngⅡ induced renal hypertensive injury.