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Hirudin ameliorates myocardial ischemia-reperfusion injury in a rat model of hemorrhagic shock and resuscitation: roles of NLRP3-signaling pathway.
Bai, Yang; Bai, Jing; Lu, Peng; Jing, Yu-Mo; Zheng, Wei-Chao; Wang, Lu-Ying; Wang, Jian-Hua; Wang, Feng.
Afiliación
  • Bai Y; Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
  • Bai J; Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, China.
  • Lu P; Department of Cardiovascular Disease, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Hebei University of Chinese Medicine, Cangzhou, China.
  • Jing YM; Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
  • Zheng WC; Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
  • Wang LY; Department of Anesthesia and Trauma Research, Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
  • Wang JH; Department of Anesthesiology, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China.
  • Wang F; Department of Cardiovascular Disease, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine, Cangzhou, China. ecoco2021@163.com.
Mol Cell Biochem ; 479(1): 63-72, 2024 Jan.
Article en En | MEDLINE | ID: mdl-36988778
Severe hemorrhage shock and resuscitation (HSR) has been reported to induce myocardial ischemia-reperfusion injury (MIRI), resulting in a poor prognosis. Hirudin, an effective thrombin inhibitor, can offer protection against MIRI. This study aimed to determine if hirudin administration ameliorates HSR-induced MIRI and the underlying mechanism. A rat model of HSR was established by bleeding rats to a mean arterial blood pressure of 30-35 mmHg for 45 min and then resuscitating them with all the shed blood through the left femoral vein. After HSR, 1 mg/kg of hirudin was administrated immediately. At 24 h after HSR, the cardiac injury was assessed using serum CK-MB, cTnT, hematoxylin-eosin (HE) staining, echocardiography, M1-polarized macrophages, and pyroptosis-associated factors, including cleaved caspase-1, Gasdermin D (GSDMD) N-terminal, IL-1ß, and IL-18 were measured by immunofluorescence and western blot assays. Nigericin, a unique agonist, was utilized to evaluate the responsibilities of NLRP3 signaling. Under the HSR condition, rats exhibited a significant increase in myocardial injury score, an elevation of serum cTnT, CK-MB levels, an aggrandization of M1-polarized macrophages, an upregulation of pyroptosis-associated factors, including cleaved caspase-1, GSDMD N-terminal, IL-1ß, and IL-18, but a significant decrease in left ventricular ejection fraction (EF%) and a reduction of left ventricular fractional shortening (FS%), while hirudin administration partially restored the changes. However, the NLRP3 agonist nigericin reversed the cardioprotective effects of hirudin. We determined the cardioprotective effects of hirudin against HSR-induced MIRI. The mechanism may involve the inhibition of NLRP3-induced pyroptosis.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Choque Hemorrágico / Daño por Reperfusión Miocárdica Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Mol Cell Biochem Año: 2024 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Choque Hemorrágico / Daño por Reperfusión Miocárdica Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Mol Cell Biochem Año: 2024 Tipo del documento: Article País de afiliación: China