AT2R Agonist C21 is an angiotensin II type 2 receptor agonist. Compound 21 (0.12 mg/kg/day for 4 weeks, p.o.) treatment improved fine motor skills after MCAO (middle cerebral artery occlusion) through modulation of the microglia/macrophage inflammatory properties. In addition, C21 increased M2 polarization and reduced the M1:M2 ratio in vitro. Thus, delayed administration of C21 downregulates post-stroke inflammation in female diabetic animals[3]. AT2R agonist C21 effectively prevents the development of PSCI in aged animals[4]. The administration of C21 (0.1-10 μM/15 min) increased the surface levels of TRKB (tropomyosin-related kinase B receptors) but was not sufficient to increase the levels of phosphorylated TRKB (pTRKB) in cultured cortical neurons from rat embryos. Consistent with increased TRKB surface expression, C21 (10 μM/15 min or 3 days) facilitated the effect of BDNF (0.1 ng/mL/15 min) on pTRKB in these cells[5]. In cultured human RPE cells, activation of AT2R with C21 significantly blocked Angiotensin II, LPS and hydrogen peroxide -induced NF-κB activation and inflammatory cytokine expression[6].
搜索
