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Exp Anim. 2017 Oct 30;66(4):303-312. doi: 10.1538/expanim.16-0102. Epub 2017 Jun 22.

Esculentoside A ameliorates cecal ligation and puncture-induced acute kidney injury in rats.

Author information

1
Department of Critical Care Medicine, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Harbin 150001, P.R. China.
2
Department of Nursing, Central Hospital of Heilongjiang Province Prison, No. 85, Qi Zheng Street, Nangang District, Harbin, Heilongjiang Province 150805, P.R. China.

Abstract

Esculentoside A (EsA), a saponin isolated from Phytolacca esculenta, can attenuate acute liver and lung injury. However, whether EsA has a protective effect against sepsis-induced acute kidney injury (AKI) has not been reported. In this study, EsA (2.5, 5, or 10 mg/kg) was given to rats with sepsis induced by cecal ligation and puncture (CLP). We found that EsA improved the survival of septic rats in a dose-dependent manner. In addition, EsA lowered the kidney tubular damage score and decreased blood urea nitrogen and creatinine. Moreover, EsA inhibited excessive generation of pro-inflammatory tumor necrosis factor-α, IL-1β, and IL-6 in the serum and downregulated cyclooxygenase-2 and inducible nitric oxide synthase in the renal tissues of septic rats. EsA also suppressed the production of malonaldehyde and the activity of myeloperoxidase in the septic kidney and enhanced the activity of superoxide dismutase and glutathione. The anti-inflammatory and antioxidative effects of a high dose of EsA were comparable to those of dexamethasone. Mechanically, EsA inhibited CLP-induced increases in high-mobility group box 1, Toll-like receptor-4, and myeloid differentiation primary response 88 and nuclear accumulation of nuclear factor kappa B p65 in renal tissues. In vitro, lipopolysaccharide-induced alteration of AKI-related factors in HK-2 cells, which had been evaluated in vivo, was inhibited after EsA administration. Taken together, our study suggests that EsA effectively protects rats against septic AKI caused by CLP.

KEYWORDS:

HMGB1/TLR/NF-kB pathway; acute kidney injury; esculentoside A; sepsis

PMID:
28637971
PMCID:
PMC5682342
DOI:
10.1538/expanim.16-0102
[Indexed for MEDLINE]
Free PMC Article

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