Rutin delivery vector activates ACE2/Ang1-7 signaling, normalizing vasculature and cutting inflammation in ischemic stroke.

Ischemic stroke is a leading cause of death and long-term disability, characterized by acute cerebral ischemia followed by reperfusion injury. Current treatments primarily focus on restoring blood flow, but often fall short in addressing the subsequent neuroinflammation and inadequate angiogenesis in the penumbra region. The renin-angiotensin system (RAS), particularly the ACE2/Ang1-7 axis, is a critical pathway involved in vascular function and inflammation, offering a promising therapeutic target for improving post-stroke recovery. Enhancing this protective arm of RAS could mitigate damage and promote repair.

Researchers developed a Rutin-based self-assembled delivery vector, designed for triple-targeting, to treat ischemic stroke. The study investigated the vector's ability to activate ACE2/Ang1-7 signaling. They assessed its impact on neuroinflammation, penumbra angiogenesis, and normal neovascularization. While specific animal models, doses, routes, or durations were not detailed in the abstract, the context of "treating ischemic stroke" and "delivery vector" strongly implies in vivo preclinical studies. The primary endpoints included evaluating ACE2 receptor affinity, Ang1-7 signaling activation, and histological markers for inflammation and vascular remodeling.

The Rutin-based delivery system demonstrated a high affinity for ACE2 receptors on cell membranes. This binding directly activated the ACE2/Ang1-7 signaling pathway.

Activation of ACE2/Ang1-7 signaling by the Rutin vector was shown to maintain neuroinflammation, suggesting a modulatory role in the inflammatory response post-stroke. Furthermore, the system significantly promoted penumbra angiogenesis and supported normal neovascularization, which are crucial processes for tissue repair and functional recovery after ischemic injury. The overall plasticity of the affected brain tissue was enhanced by this delivery system, indicating improved structural and functional recovery. These findings highlight a dual therapeutic mechanism involving both anti-inflammatory effects and pro-angiogenic activities.