Pharmacological treatment with galectin-1 protects against renal ischaemia-reperfusion injury

Autor(es)

Carlos, Carla P. ^{[1, 2]} ; Silva, Analice A. ^[1] ; Gil, Cristiane D. ^[3] ; Oliani, Sonia M. ^{[3, 1]}

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ, UNESP, Inst Biociencias Letras & Ciencias Exatas, Dept Biol, Sao Jose Do Rio Preto, SP - Brazil

^[2] FACERES Sch Med, Dept Med, Sao Jose Do Rio Preto, SP - Brazil

^[3] Univ Fed Sao Paulo, UNIFESP, Dept Morphol & Genet, Sao Paulo, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: SCIENTIFIC REPORTS; v. 8, JUN 22 2018.
• Citações Web of Science: 2

Resumo

Galectin-1 protein (GAL-1) has important anti-inflammatory properties, but related pharmacologic approaches to effectively treat or prevent renal ischaemia and reperfusion injury are highly limited. Here, we investigated the effect of GAL-1 in a renal ischaemia-reperfusion injury rat model and an in vitro hypoxia-reoxygenation model with a proximal renal tubular epithelial cell line. In vivo, pretreatment with GAL-1 attenuated the renal parameters changed by ischaemia-reperfusion/hypoxiareoxygenation, with recovery of renal function, protecting against influx of leukocytes, cell death and oxidative stress. Ischaemia-reperfusion/hypoxia-reoxygenation was also associated with increased renal endogenous expression of GAL-1 and intercellular adhesion molecule 1 (ICAM-1) plus augmented levels of proinflammatory cytokines IL-1 beta, TNF-alpha and MCP-1 and decreased anti-inflammatory IL-10 in urine, all of which were abrogated by GAL-1 treatment. In vitro studies demonstrated renal tubular epithelial cells as an important source of GAL-lduring hypoxia-reoxygenation and confirmed the protective effects of exogenous GAL-1 through downregulation of proinflammatory cytokine release by proximal renal tubular epithelial cells. Collectively, our findings confirm the important antiinflammatory role of GAL-1 in kidney ischaemia and reperfusion injury and indicate its promising use as a therapeutic approach. (AU)

• Processo FAPESP: 16/02012-4 - Investigação das atividades imunomoduladoras da proteína anexina A1 na regulação inflamatória de doenças do sistema gastrointestinal: estudo em modelos experimentais in vivo e in vitro
• Beneficiário: Sonia Maria Oliani
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 15/09858-3 - Mecanismos de ação das proteínas galectinas-1 e -3 na inflamação alérgica: Estudo em modelos experimentais in vivo e in vitro e em pacientes alérgicos
• Beneficiário: Cristiane Damas Gil
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 11/22113-6 - Mecanismo de ação da proteína anti-inflamatória galectina-1 na lesão renal induzida por isquemia e reperfusão: análises in vivo e in vitro
• Beneficiário: Carla Patrícia Carlos
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado