Hirudin promotes cerebral angiogenesis and exerts neuroprotective effects in MCAO/R rats by activating the Wnt/-catenin pathway
Research article published in J Stroke Cerebrovasc Dis (2025)
Abstract
OBJECTIVE: Hirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear. In this study, we aimed to investigate whether hirudin exerts neuroprotective effects by promoting angiogenesis through the regulation of the Wnt/β-catenin signaling pathway. METHODS: An in vitro model of glucose and oxygen deprivation/reperfusion (OGD/R) was established using rat brain microvascular endothelial cells (BMECs). The effects of hirudin on OGD/R cell viability were assessed using the cell counting kit-8 (CCK-8) assay. The angiogenic potential of hirudin was evaluated using Transwell and tube formation assays. In vivo, a middle cerebral artery occlusion/reperfusion (MCAO/R) model was created in rats. The neuroprotective effects of hirudin were assessed using the modified neurological severity score (mNSS), Hematoxylin and eosin (H&E) staining, 2,3,5-Triphenyltetrazolium chloride (TTC) staining, and immunofluorescence staining. Dickkopf-1 (DKK1), a specific inhibitor of this pathway, was introduced in order to investigate the role of the Wnt/β-catenin pathway. The effects of hirudin on the Wnt/β-catenin pathway were examined through immunohistochemistry, western blotting, and reverse transcription quantitative polymerase chain reaction (RT-qPCR). RESULTS: Hirudin significantly improved BMEC survival and enhanced both cell migration and tube formation in the OGD/R model. In the MCAO/R model, hirudin reduced the mNSS score, alleviated pathological damage, decreased infarction volume, and increased the expression of key angiogenic factors, including CD34, vascular endothelial growth factor (VEGF), and angiopoietin-2 (Ang-2). In addition, hirudin activated the Wnt/β-catenin pathway, leading to elevated levels of Wnt3a and β-catenin. CONCLUSION: Hirudin has substantial neuroprotective effects associated with the promotion of angiogenesis in the ischemic penumbra. This mechanism is mediated by the regulation of the Wnt/β-catenin pathway.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Zusammenfassung
Hirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear.
Warum dies für die Hirudotherapie relevant ist
This study investigated whether hirudin exerts neuroprotective effects by promoting angiogenesis through the Wnt/β-catenin signaling pathway, using an in vitro oxygen-glucose deprivation/reperfusion model in rat brain microvascular endothelial cells and an in vivo middle cerebral artery occlusion/reperfusion rat model. Hirudin improved endothelial cell survival, migration, and tube formation in vitro, and in vivo reduced neurological severity scores, infarct volume, and pathological damage while increasing expression of angiogenic factors (CD34, VEGF, Ang-2) and activating Wnt3a/β-catenin. This study is relevant to the ASH domain because it directly examines hirudin as a therapeutic agent in ischemic stroke, although the abstract does not state its biological origin or relationship to leech therapy. Caveat: This is a preclinical animal and in vitro study, and the findings have not been validated in human clinical trials.
Zitation
Hirudin promotes cerebral angiogenesis and exerts neuroprotective effects in MCAO/R rats by activating the Wnt/-catenin pathway.
He L et al. · J Stroke Cerebrovasc Dis, 2025
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