Catalpol protects mice against renal ischemia/reperfusion injury via suppressing PI3K/Akt-eNOS signaling and inflammation.

摘要: Renal ischemia/reperfusion-injury (IRI) is a common disease in clinic, which also the most cause of acute kidney failure. Previous investigations has illustrated that catalpol neuroprotective, anti-inflammatory, and anti-hepatitis virus effects. This study was designed to investigate protective effect on renal IRI mice through suppressing phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt)-endothelial nitric oxide synthase (eNOS) against inflammation, possible underlying mechanism. Firstly, we used model analyze blood urea nitrogen serum creatinine levels mice. Next, real-time PCR western blotting were detect expression KIM-1 PI3K, Akt eNOS IRI, respectively. In addition, activities tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) interleukin-10 (IL-10) measured with respective TNF-α, IL-1β, IL-6 IL-10 ELISA kits. Our results showed clearly reduced nitrogen, Meanwhile, found markedly group. Suppressing PI3K/Akt-eNOS involved IRI. Collectively, protected via inhibiting signaling inflammatory responses.