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Sevoflurane alleviates inflammation, apoptosis and permeability damage of human umbilical vein endothelial cells induced by lipopolysaccharide by inhibiting endoplasmic reticulum stress via upregulating RORα.
Ni, Weiwei; Zou, Zhiwei; Jiang, Ping; Wang, Shuo.
Afiliación
  • Ni W; Department of Anesthesiology, Wujin Hospital Affiliated with Jiangsu University, Changzhou, Jiangsu 213000, China; Department of Anesthesiology, The Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu 213000, China.
  • Zou Z; Department of Anesthesiology, Wujin Hospital Affiliated with Jiangsu University, Changzhou, Jiangsu 213000, China; Department of Anesthesiology, The Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu 213000, China.
  • Jiang P; Department of Anesthesiology, Wujin Hospital Affiliated with Jiangsu University, Changzhou, Jiangsu 213000, China; Department of Anesthesiology, The Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu 213000, China.
  • Wang S; Department of Anesthesiology, Wujin Hospital Affiliated with Jiangsu University, Changzhou, Jiangsu 213000, China; Department of Anesthesiology, The Wujin Clinical College of Xuzhou Medical University, Changzhou, Jiangsu 213000, China. Electronic address: WangShuodoc@163.com.
Prostaglandins Other Lipid Mediat ; 172: 106821, 2024 Jun.
Article en En | MEDLINE | ID: mdl-38373554
ABSTRACT
Endothelial dysfunction often accompanies sepsis. Sevoflurane (Sev) is a widely used inhaled anesthetic that has a protective effect on sepsis-associated damage. We aimed to elucidate the role of Sev in endothelial dysfunction by using a model of LPS induced HUVECs. Sev increased the viability and decreased the apoptosis of HUVECs exposed to LPS. Inflammation and endothelial cell adhesion were improved after Sev addition. Besides, Sev alleviated LPS-induced endothelial cell permeability damage in HUVECs. RORα served as a potential protein that bound to Sev. Importantly, Sev upregulated RORα expression and inhibited endoplasmic reticulum (ER) stress in LPS-treated HUVECs. RORα silencing reversed the impacts of Sev on ER stress. Moreover, RORα deficiency or tunicamycin (ER stress inducer) treatment restored the effects of Sev on the viability, apoptosis, inflammation and endothelial permeability damage of HUVECs exposed to LPS. Taken together, Sev ameliorated LPS-induced endothelial cell damage by targeting RORα to inhibit ER stress.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación hacia Arriba / Lipopolisacáridos / Apoptosis / Miembro 1 del Grupo F de la Subfamilia 1 de Receptores Nucleares / Células Endoteliales de la Vena Umbilical Humana / Estrés del Retículo Endoplásmico / Sevoflurano / Inflamación Límite: Humans Idioma: En Revista: Prostaglandins Other Lipid Mediat Asunto de la revista: ENDOCRINOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación hacia Arriba / Lipopolisacáridos / Apoptosis / Miembro 1 del Grupo F de la Subfamilia 1 de Receptores Nucleares / Células Endoteliales de la Vena Umbilical Humana / Estrés del Retículo Endoplásmico / Sevoflurano / Inflamación Límite: Humans Idioma: En Revista: Prostaglandins Other Lipid Mediat Asunto de la revista: ENDOCRINOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos