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Updated: Mar 15, 2026
A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
Published on: June 22, 2022
Morroniside promotes angiogenesis and further improves microvascular circulation after focal cerebral
Tingting Liu1, Benxu Xiang1, Deyu Guo1
1Department of Experimental Animal Center, Xuanwu Hospital of Capital Medical University, Beijing 100053, PR China.
Abstract:
Preservation of cerebral microvascular functional integrity is crucial for protecting and repairing the brain after stroke. Our previous study demonstrated that morroniside promoted angiogenesis 7days after stroke. The current study aimed to further evaluate the long-term effects of morroniside on angiogenesis and to examine whether angiogenesis induced by morroniside could improve blood flow velocity. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO), and morroniside was then administered once per day at a dose of 270mg/kg. New vessel formation and the expression of ephrinB2/VEGFR2 signaling pathway components were examined 14days after MCAO to examine angiogenesis and the associated mechanisms. The dynamics of regional cerebral blood flow (rCBF) and the number of vessels of the leptomeningeal anastomoses were analyzed to characterize microvascular circulation 3days after MCAO. We demonstrated that morroniside promoted angiogenesis by regulating the ephrinB2/VEGFR2 signaling pathway 14days post-ischemia. By 3days post-ischemia, morroniside improved rCBF and increased the number of vessels of the leptomeningeal anastomoses. Moreover, morroniside decreased the infarct volume and improved neurological function 14days after MCAO. Our findings suggest that morroniside promoted long-term angiogenesis, thereby improving microvascular circulation and neurological function. It suggested that the angiogenic mechanism of morroniside might be mediated by the ephrinB2/VEGFR2 signaling pathway.
Insights
Morroniside promotes long-term brain angiogenesis and improves blood flow after stroke by regulating the ephrinB2/VEGFR2 pathway. This enhances neurological function and reduces infarct volume, offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Pharmacology
- Cardiovascular Research
Background:
- Cerebral microvascular integrity is vital for brain repair post-stroke.
- Previous research indicated morroniside promotes early-stage angiogenesis (7 days post-stroke).
- The long-term effects and mechanisms of morroniside on angiogenesis require further investigation.
Purpose of the Study:
- To evaluate the long-term impact of morroniside on angiogenesis after stroke.
- To determine if morroniside-induced angiogenesis improves cerebral blood flow velocity.
- To elucidate the molecular mechanisms underlying morroniside's angiogenic effects.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in Sprague-Dawley rats.
- Administration of morroniside (270 mg/kg/day).
- Assessment of angiogenesis (14 days), ephrinB2/VEGFR2 signaling, regional cerebral blood flow (rCBF) (3 days), leptomeningeal anastomoses, infarct volume, and neurological function (14 days).
Main Results:
- Morroniside significantly promoted angiogenesis by regulating the ephrinB2/VEGFR2 signaling pathway 14 days post-MCAO.
- Morroniside improved rCBF and increased leptomeningeal anastomoses by 3 days post-MCAO.
- Morroniside reduced infarct volume and improved neurological function 14 days post-MCAO.
Conclusions:
- Morroniside facilitates long-term angiogenesis, enhancing microvascular circulation and neurological recovery after stroke.
- The ephrinB2/VEGFR2 signaling pathway is implicated in the angiogenic mechanism of morroniside.
- Morroniside demonstrates potential as a therapeutic agent for stroke recovery.
