Article Publish Status: FREE
Abstract Title:

Echinacea polysaccharide attenuates lipopolysaccharide‑induced acute kidney injury via inhibiting inflammation, oxidative stress and the MAPK signaling pathway.

Abstract Source:

Int J Mol Med. 2020 Oct 23. Epub 2020 Oct 23. PMID: 33416087

Abstract Author(s):

Qiumei Shi, Wuying Lang, Shiyong Wang, Guangyu Li, Xue Bai, Xijun Yan, Haihua Zhang

Article Affiliation:

Qiumei Shi


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‑treatedmice. 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.

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