Alantolactone mitigates renal injury induced by diabetes via inhibition of high glucose-mediated inflammatory response and macrophage infiltration.

Background: Inflammatory response plays a crucial role in the occurrence and development of diabetic nephropathy (DN). Drugs that carry anti-inflammatory effects have the potential to treat diabetic nephropathy. It's reported that alantolactone (ALA), a natural product, has a variety of pharmacological effects against inflammation and oxidation. However, the specific effects of alantolactone on DN and the mechanisms underlying alantolactone remain elusive. Therefore, the present study aimed to probe whether ALA could mitigate inflammation as mediated by high glucose (HG) in NRK-52E cells and reduce renal injury caused by diabetic nephropathy.Materials and methods: The anti-inflammatory effect of ALA was evaluated in the present study using ELISA and RT-qPCR. Western blot and macrophage adhesion assay were then performed to confirm anti-macrophage adhesion and the protein expression of cell adhesion molecules. Finally, the effect of ALA and its underlying mechanism was evaluated in vivo.Results: Results showed that ALA curbed HG-stimulated expression of macrophage adhesion and pro-inflammatory cytokines in renal NRK-52E cells. In addition, both pro-inflammatory cytokines and NF-kappa B witnessed reduced expression or activity in oral administration with ALA in vivo, thus inhibiting the increase of serum creatinine and urea nitrogen (BUN) levels. This in consequence ameliorated fibrosis and stemmed pathological worsening of diabetic renal tissues.Conclusions: These findings suggest that ALA may hold promise in the treatment of DN, and importantly, the anti-inflammatory system may prove to be a new strategy to treat human DN.