title: Nerolidol Protects Against LPS-induced Acute Kidney Injury via Inhibiting TLR4/NF-κB Signaling.
abstract: Acute kidney injury (AKI) is a critical care syndrome, resulting in acute reduction of renal function and up to 22% mortality of hospitalized patients. Nerolidol is a major component in several essential oils that possesses various pharmacological properties. The present study aimed to investigate the potential effect of nerolidol on lipopolysaccharide (LPS)-induced AKI. Nerolidol dose-dependently reduced the pathological injuries of kidney induced by LPS in rats. Nerolidol significantly decreased the levels of blood urea nitrogen and creatinine in LPS-treated rats in a dose-dependent manner. In addition, nerolidol inhibited LPS-induced decrease of cell viability in NRK-52E rat proximal tubular cells, which effect was concentration dependent. Nerolidol notably inhibited the increase of TNFα and IL-1β in LPS-treated rats and the mRNA expression of TNFα and IL-1β in LPS-treated NRK-52E cells. Nerolidol suppressed the increase of toll-like receptor 4 (TLR4) expression, phosphorylation and nuclear translocation of p65 NF-κB in kidneys of LPS-treated rats and LPS-treated NRK-52E cells. Overexpression of TLR4 and p65 NF-κB significantly suppressed nerolidol-induced inhibition of TNFα and IL-1β expression and increase of cell viability in LPS-treated cells. In summary, we found that nerolidol played a critical anti-inflammatory effects through inhibition of TLR4/NF-κB signaling and protected against LPS-induced AKI. Copyright © 2017 John Wiley & Sons, Ltd.
authors.affiliation: The Department of Nephrology and Rheumatology, First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, Henan, China.
authors.forename: Lu
authors.initials: L
authors.lastname: Zhang
authors.affiliation: The Department of Nephrology and Rheumatology, First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, Henan, China.
authors.forename: Dandan
authors.initials: D
authors.lastname: Sun
authors.affiliation: The Department of Nephrology and Rheumatology, First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, Henan, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Bao
authors.affiliation: The Department of Nephrology and Rheumatology, First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, Henan, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Shi
authors.affiliation: The Department of Nephrology and Rheumatology, First Affiliated Hospital of Xinxiang Medical University, Weihui, 453100, Henan, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Cui
authors.affiliation: The Department of Nephrology and Rheumatology, Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, 453000, Henan, China.
authors.forename: Minghao
authors.initials: M
authors.lastname: Guo
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced / Q000517:prevention & control*; D000818:Animals; D002478:Cells, Cultured; D003404:Creatinine / Q000097:blood; D019610:Cytoprotection / Q000187:drug effects*; D053583:Interleukin-1beta / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000009:adverse effects / Q000494:pharmacology; D008297:Male; D051379:Mice; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012717:Sesquiterpenes / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D051197:Toll-Like Receptor 4 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012717:Sesquiterpenes; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D003404:Creatinine; C037055:nerolidol
keywords: NF-κB; acute kidney injury; lipopolysaccharide; nerolidol; toll-like receptor 4