Acute kidney injury (AKI) is often accompanied by
inflammation. Echinacea
polysaccharide (EP) is an active ingredient that has been demonstrated to possess anti‑oxidative, anti‑inflammatory, antimicrobial and immunomodulatory functions. However, the role of EP in AKI has not been examined. The present study investigated the effects of EP on
lipopolysaccharide (LPS)‑induced AKI. Western blotting, immunohistochemistry and immunofluorescence analyses were performed to detect
protein expression levels. Administration of EP significantly attenuated LPS‑induced renal tissue injury, along with a decrease in blood
urea nitrogen and
creatinine levels. EP decreased the levels of
inducible nitric oxide synthase and cyclo‑oxygenase‑2 in LPS‑treated mice. Furthermore, LPS‑induced
inflammation was inhibited by EP in renal tissues and HBZY‑1 cells, as demonstrated by the downregulation of
tumor necrosis factor‑α,
interleukin (IL)‑1β, IL‑6,
nitric oxide and
prostaglandin E2 levels. Similarly, EP administration decreased oxidative stress (OS) via decreasing
reactive oxygen species,
malondialdehyde and
oxidized glutathione levels, and increasing
superoxide dismutase,
catalase,
glutathione reductase and
reduced glutathione activity. Notably, EP induced a marked decrease in the expression levels of phospho‑extracellular signal‑regulated
protein kinase (p‑ERK), phospho‑c‑Jun N‑terminal
kinase (p‑JNK) and p‑p38 in vivo and in vitro. In addition, in LPS‑treated HBZY‑1 cells, EP enhanced cell viability and inhibited nuclear translocation of p‑ERK, p‑JNK and p‑p38. Overall, the present findings demonstrated that EP alleviated LPS‑induced AKI via the suppression of
inflammation, OS and the mitogen‑activated
protein kinase signaling pathway, providing insight into potential avenues for the treatment of AKI.