Ang-(1-7) in animal models of stroke

Type of stroke inducedAnimal modelMain findingReferences
Ischemic strokeEndothelin1-induced middle cerebral artery occlusion (MCAO)- Ang-(1-7) central administration reduced the brain infarct size and neurological alteration 72 h after the insult.
- Beneficial actions of Ang-(1-7) were mediated by MasR.
Mecca et al., 2011 [109]
Permanent middle cerebral artery occlusion (pMCAO)- Intracerebral infusion of Ang-(1-7) decreased infarct volume and improved neurological alteration after 24 h following the insult.
- Ang-(1-7) had an antioxidant effect, inhibited NF-κB activity and decreased pro-inflammatory cytokines and COX-2 in the peri-infarct areas.
- Beneficial actions of Ang-(1-7) were mediated by MasR.
Jiang et al., 2012 [93]
- Intracerebral infusion of Ang-(1-7) for 4 weeks reduced infarct size and neurological alteration after pMCAO.
- Ang-(1-7) increased cerebral capillary density via stimulation of endothelial cell proliferation and eNOS activation.
- Beneficial effects of Ang-(1-7) were mediated by MasR.
Jiang et al., 2014 [126]
- Ang-(1-7) infusion exerted a direct neuroprotective action during l ischemic injury in the brain by reducing cell swelling and death. These effects were mediated by decreased NOX expression with the consequent reduction of ROS production.
- The beneficial effect of Ang-(1-7)/MasR stimulation on cerebral ischemic injury showed a greater protective effect in older animals.
- Neuroprotective effects of Ang-(1-7) were mediated by MasR.
Zheng et al., 2014 [128]
Hemorrhagic strokeStroke-prone SHRs (spSHRs)- ICV Ang-(1-7) infusion into spSHRs fed a high-sodium (4%) diet for 6 weeks decreased the number of hemorrhages in the striatum, enhanced neurological status, reduced the striatal microglia and increased survival.
- Ang-(1-7) effects were partly prevented by ICV infusion of the MasR blocker, A-779.
Regenhardt et al., 2014 [127]
Intracerebral hemorrhage- ICV infusion of Ang-(1-7) enhanced neurological function compared with rats that received control solution.Del Bigio et al., 1996 [129]

COX-2: cyclooxygenase 2; eNOS: endothelial nitric oxide synthase; NOX: NADPH oxidase; ROS: Reactive oxygen species