Protective effect and mechanism of IL-10 on renal ischemia–reperfusion injury

• DOI: 10.1038/s41374-018-0162-0
• Publication Date: 2019-01-30T17:15:17Z
• Authors: Kenji Sakai; Yuji Nozaki; Yoshinori Murao; Tomohiro Yano; Jinhai Ri; Kaoru Niki; Koji Kinoshita; Masanori Funauchi; Itaru Matsumura
• Keywords: Blood urea nitrogen; Proinflammatory cytokine; Renal ischemia

Interleukin (IL)-10, a cytokine with anti-inflammatory effects, is produced by blood cells and of various organs. Ischemia-reperfusion injury (IRI) systemic inflammatory disease caused circulation pro-inflammatory cytokines chemokines from or organs damaged ischemia. Apoptosis, key event after IRI, correlated the degree injury. Here we investigated effects mechanism IL-10 in renal IRI. Compared to wild-type (WT) mice knockout (IL-10 KO) IRI demonstrated decreased function as represented urea nitrogen serum creatinine, upregulated early acute kidney (AKI) biomarkers such molecule-1 (Kim-1), increased mRNA expression IL-1β, IL-6, IL-18 chemokine (regulated on activation, normal T cell expressed secreted; RANTES), pro-apoptosis factors Bax cleaved caspase-3. When tubular epithelial (TECs) KO were put hypoxic state added recombinant IL-10, their decreased. Our findings that suppressed production cytokines, dysfunction,