Nicotine promotes angiogenesis in mouse brain after intracerebral hemorrhage

Here we examined the effect of nicotine on angiogenesis in the brain after intracerebral hemorrhage (ICH), as angiogenesis is considered to provide beneficial effects on brain tissues during recovery from injury after stroke. Nicotine was administered to C57BL/6 mice suffering from collagenase-induced ICH in the striatum, either by inclusion in drinking water or by daily intraperitoneal injection. Nicotine administration by both routes enhanced angiogenesis within the hematoma-affected regions, as revealed by increased CD31-immunopositive area at 7 and 14 d after ICH. Double immunofluorescence histochemistry against CD31 and proliferating cell nuclear antigen revealed that nicotine increased the number of newly generated vascular endothelial cells within the hematoma. In spite of enhanced angiogenesis, nicotine did not worsen vascular permeability after ICH, as assessed by Evans Blue extravasation. These effects of nicotine were accompanied by an increased number of surviving neurons in the hematoma at 7 d after ICH. Unexpectedly, nicotine did not increase expression of vascular endothelial growth factor mRNA in the brain and did not enhance recruitment of endothelial progenitor cells from the bone marrow. These results suggest that nicotine enhances angiogenesis in the brain after ICH, via mechanisms distinct from those involved in its action on angiogenesis in peripheral tissues. (c) 2020 Elsevier B.V. and Japan Neuroscience Society. All rights reserved.

Automated summary

Nicotine enhanced angiogenesis in the brain after intracerebral hemorrhage (ICH) without worsening vascular permeability, accompanied by an increased number of surviving neurons. Surprisingly, nicotine did not increase expression of vascular endothelial growth factor mRNA in the brain or enhance recruitment of endothelial progenitor cells from the bone marrow, suggesting distinct mechanisms of action compared to peripheral tissues.