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.
Резюме
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.
Почему это важно для гирудотерапии
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.
Цитирование
Hirudin alleviates acute ischemic stroke by inhibiting NLRP3 inflammasome-mediated neuroinflammation: In vivo and in vitro approaches.
Li WQ et al. · International Immunopharmacology, 2022
Связанный клинический контекст
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