Cornus iridoid glycoside alleviates sepsis-induced acute lung injury by regulating NF-κB and Nrf2/HO-1 pathways
- PMID: 36086972
- DOI: 10.15586/aei.v50i5.638
Cornus iridoid glycoside alleviates sepsis-induced acute lung injury by regulating NF-κB and Nrf2/HO-1 pathways
Abstract
Background: Sepsis-induced acute lung injury (ALI) is a syndrome associated with inflammation. Cornus iridoid glycoside (CIG), a bioactive component isolated from Corni Fructus, exhibits anti-inflammatory activities. However, the function and underlying mechanisms of CIG in mice with sepsis-induced ALI remain elusive.
Methods: The sepsis-elicited ALI model of mice was established by the induction of cecal ligation and puncture (CLP). The wet/dry (W/D) ratio of lung tissues was examined, and the pathological alterations were determined by hematoxylin and eosin staining. The messenger RNA (mRNA) expressions and serum levels of Interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) were measured by reverse transcription-quantitative polymerase chain reaction and enzyme-linked immunosorbent serologic assay, respectively. The concentrations of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were assessed by biochemical kits. In addition, the relative protein levels of p-p65, p65, phosphorylated- nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (p-IκBα), IκBα, nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) gene were analyzed by Western blotting analysis.
Results: CLP enhanced W/D ratio and aggravated pathological changes and scores in mice, which were obviously alleviated by the two concentrations of CIG treatment. CIG treatment notably decreased the CLP-induced mRNA expressions and serum levels of IL-1β, IL-6, TNF-α, and MDA, but enhanced the decreased concentrations (caused by CLP) of SOD and GSH-Px. Moreover, CIG treatment significantly decreased the ratios of p65/p-p65 and IκBα/p-IκBα caused by CLP, but aggravated the CLP-induced relative protein levels of Nrf2 and HO-1.
Conclusions: CIG obviously ameliorated the sepsis-induced ALI in mice by suppressing inflammation and oxidative stress, which was closely associated with nuclear factor kappa B (NF-κB) and Nrf2-HO-1 signaling pathways.
Keywords: Cornus iridoid glycoside; NF-κB; Nrf2/HO-1; acute lung injury; sepsis.
Conflict of interest statement
The authors stated that there were no conflicts of interest to disclose.
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