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Protective Effect of Alpha 1-Antitrypsin on Renal Ischemia-Reperfusion Injury

Jeong, Kye-Hwa ; Lim, Jeong-Hoon ; Lee, Kyung-Hee ; Kim, Min-Jung ; Jung, Hee-Yeon ; Choi, Ji-Young ; Cho, Jang-Hee ; Park, Sun-Hee ; Kim, Yong-Lim ; Kim, Chan-Duck

Transplantation proceedings, 2019-10, Vol.51 (8), p.2814-2822 [Periódico revisado por pares]

United States: Elsevier Inc

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  • Título:
    Protective Effect of Alpha 1-Antitrypsin on Renal Ischemia-Reperfusion Injury
  • Autor: Jeong, Kye-Hwa ; Lim, Jeong-Hoon ; Lee, Kyung-Hee ; Kim, Min-Jung ; Jung, Hee-Yeon ; Choi, Ji-Young ; Cho, Jang-Hee ; Park, Sun-Hee ; Kim, Yong-Lim ; Kim, Chan-Duck
  • Assuntos: alpha 1-Antitrypsin - pharmacology ; alpha 1-Antitrypsin - therapeutic use ; Animals ; Apoptosis - drug effects ; Blood Urea Nitrogen ; Creatinine - blood ; Cytokines - metabolism ; Disease Models, Animal ; Inflammation - pathology ; Kidney - blood supply ; Kidney Diseases - pathology ; Kidney Diseases - prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention & control ; Serine Proteinase Inhibitors - pharmacology ; Serine Proteinase Inhibitors - therapeutic use
  • É parte de: Transplantation proceedings, 2019-10, Vol.51 (8), p.2814-2822
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
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  • Descrição: α1-Antitrypsin (AAT) is an important protein in the anti-inflammatory response that functions to regulate the activity of serine proteinases. We aimed to evaluate the protective effect of AAT on ischemia-reperfusion injury (IRI) in a mouse model. We investigated the effects of AAT in a C57BL/6 mouse model of IRI by dividing them into 4 groups: normal control, sham operated, ischemia-reperfusion (IR), and IR after AAT pretreatment (IR-AAT). In the IR-AAT group, mice were pretreated with AAT (80 mg/kg/d) for 3 days before renal ischemia was induced by clamping the bilateral renal vascular pedicles for 30 minutes. At 24 hours after IRI, biochemistry, histology, inflammatory cytokines, and apoptosis were assayed. Blood urea nitrogen and serum creatinine levels were significantly lower in the IR-AAT group than in the IR group. Neutrophil gelatinase-associated lipocalin and kidney injury molecule 1 protein levels were significantly lower in the IR-AAT group than in the IR group. In addition, there were fewer tubular injuries and less interstitial fibrosis in the IR-AAT group than in the IR group, and the expression levels of transforming growth factor β, interleukin 1β, and interleukin 6 were significantly lower in the IR-AAT group than in the IR group. When compared with the IR group, there were fewer terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay–positive cells, lower caspase 3 activity and B-cell lymphoma 2-associated X protein (Bax), and higher B-cell lymphoma 2 (Bcl–2) in the IR-AAT group. α1-Antitrypsin preserved renal function, attenuated tubular injuries and interstitial fibrosis, and inhibited inflammation and apoptosis after renal IRI. Our results suggest that AAT has protective effects against renal IRI by inhibiting inflammatory and apoptosis pathways. •α1-Antitrypsin (AAT) is an important protein in the anti-inflammatory response that functions to regulate the activity of serine proteinases.•Treatment with AAT before renal ischemia-reperfusion injury (IRI) reduced IRI, as shown by the significantly lower levels of blood urea nitrogen, serum creatinine,•Neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, and fewer tubular injuries and interstitial fibrosis were in the AAT pretreatment group compared with the ischemia-reperfusion group.•With respect to the mechanisms underlying the protective effect of AAT against renal IRI, administration of AAT before renal IRI decreased inflammation, as demonstrated by the reduced expression of transforming growth factor β, interleukin 1β, and interleukin 6.•In addition, apoptosis, as measured by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, caspase 3 activity, and the expression of B-cell leukemia/lymphoma 2-associated X protein, was inhibited by AAT pretreatment.•Based on these results, AAT protects against ischemia reperfusion–induced kidney damage through anti-inflammatory and antiapoptotic pathways.
  • Editor: United States: Elsevier Inc
  • Idioma: Inglês
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