Hirudin alleviates acute ischemic stroke by inhibiting NLRP3 inflammasome-mediated neuroinflammation: In vivo and in vitro approaches
Animal model study published in International Immunopharmacology (2022)
Abstract
Acute ischemic stroke is a severe condition that a vessel supplying blood to the brain is abruptly blocked mostly due to cerebral thrombosis and embolism. There is a dearth of the effective prevention and early intervention strategies. NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediated neuroinflammation plays a crucial role in the pathophysiology of ischemic stroke. Hirudin is a secretion from the salivary glands of the leech Hirudo medicinalis and has a role in regulating inflammation. In this study, hirudin with a dose of 10-40 mg/kg was given to middle cerebral artery occlusion/reperfusion mice. Hirudin markedly constrained cerebral infarct area in a dose-dependent manner, and significantly improved locomotor disability at 40 mg/kg dose. Similar to MCC950, a selective NLRP3 inflammasome inhibitor, hirudin inhibited M1 polarization and promoted M2 polarization. It also strikingly suppressed the ischemia-induced overexpression of NLRP3 and its downstream components, caspase-1, apoptosis-associated speck-like protein (ASC), and interleukin-1β (IL-1β). Hirudin and MCC950 equivalently protected viability and death of BV-2 microglia cells against oxygen-glucose deprivation/reperfusion (OGD/R), an in vitro cell model of brain ischemia. Both agents had similar effects in normalizing the OGD/R-evoked aberrant microglial profiles and NLRP3 pathway dysregulation as observed in the mice. These results demonstrated anti-ischemic effects of hirudin and its association with the inhibition of microglial NLRP3 inflammasome-mediated neuroinflammation. Hirudin is a promising agent for the early intervention of acute ischemic stroke.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Zusammenfassung
Hirudin (10-40 mg/kg) dose-dependently reduced cerebral infarct area in middle cerebral artery occlusion mice via inhibition of NLRP3 inflammasome, M1 microglial polarization, and IL-1β release — extending hirudin's role beyond anticoagulation to neuroinflammation.
Warum dies für die Hirudotherapie relevant ist
This study investigated whether hirudin—a secretion from the salivary glands of the leech Hirudo medicinalis that has a role in regulating inflammation—alleviates acute ischemic stroke by inhibiting NLRP3 inflammasome-mediated neuroinflammation. Using both in vivo (middle cerebral artery occlusion/reperfusion mice, 10–40 mg/kg) and in vitro (BV-2 microglia oxygen-glucose deprivation/reperfusion) approaches, hirudin dose-dependently reduced cerebral infarct area, improved locomotor function at 40 mg/kg, suppressed M1 microglial polarization, promoted M2 polarization, and reduced NLRP3, caspase-1, ASC, and IL-1β expression, with effects comparable to the NLRP3 inhibitor MCC950. This is relevant to ASH's domain as the abstract identifies hirudin as a leech salivary secretion and characterizes an anti-inflammatory mechanism in stroke. However, these are preclinical findings from mouse and cell culture models; no clinical or human data are presented.
Zitation
Hirudin alleviates acute ischemic stroke by inhibiting NLRP3 inflammasome-mediated neuroinflammation: In vivo and in vitro approaches.
Li WQ et al. · International Immunopharmacology, 2022
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