Effects of Artesunate prevent nephritis via the Toll-like receptor 4/nuclear factor-κB signaling pathway in rats

Abstract

The active ingredient in Artemisia carvifolia, artemisinin, may alleviate inflammation and toxicity. Artemisinin and its derivatives are first-line anti-malarial drugs currently, which have rapid effects on fever caused by malaria parasites with fewer side effects. The present study investigated the effects of Artesunate in a mouse nephritis model. Mice were injected intraperitoneally with 500 μl pristine to induce nephritis, and were treated with 28.8 mg/kg Artesunate. Subsequently, proteinuria, renal function, and tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels were assessed to evaluate the effects of Artesunate on nephritis. Western blot analysis was used to measure the protein expression levels of α-smooth muscle actin (SMA), TLR4, myeloid differentiation primary response gene 88 (MyD88), NF-κB p65 and transforming growth factor (TGF)-β1 to investigate the underlying mechanisms of Artesunate on nephritis. The results demonstrated that Artesunate reduced proteinuria and preserved renal function in nephritis mice. Artesunate attenuated TNF-α and IL-6 levels, suppressed α-SMA, TLR4, MyD88, NF-κB p65 and TGF-β1 protein expression, and decreased caspase-3 activity in nephritis mice. These results indicated that the effects of Artesunate may prevent nephritis and inhibit inflammation via the TLR4/NF-κB signaling pathway in mice. Therefore, Artesunate may be a potential therapeutic agent to prevent nephritis.