Regulation of rosmarinic acid on NF-κB and p38 MAPK signaling path-ways in rats with sepsis and acute kidney injury
The aim of this study is to explore the protective effect and mechanism of rosmarinic acid(RA)on rats with sepsis and acute kidney injury.The kidney injury models of sepsis were constructed by cecal ligation and puncture(CLP)and the rats were randomly divided into sham operation group,model group,RA groups(12.5,25,50 mg/kg),and dexamethasone(Dex,1 mg/kg)group.H-E staining of kidney tissues,renal function indexes,oxidative stress indexes,apoptosis of kidney tissues,and expressions of NF-κB and p38 MAPK signaling pathway proteins were compared among the groups.The results showed that compared to the model group,the RA groups(25,50 mg/kg)and Dex group had significantly decreased levels of serum creatinine(Scr),blood urea nitrogen(BUN),neutrophil gelatinase-associated lipocalin(NGAL),kidney injury molecule 1(KIM-1),TNF-α,IL-1β,IL-6,malondialdehyde(MDA),number of apoptosis cells in kidney tissues,cleaved Caspase-3/Caspase-3,cytochrome c(Cyt c),cleaved poly(ADP-ribose)polymerase(cleaved PARP),phosphorylated p65(p-p65)/p65 and phosphorylated p38(p-p38)/p38(P＜0.05).In contrast,the levels of superoxide dismutase(SOD)and glutathione perox-idase(GSH-Px)were significantly increased in RA groups(25,50 mg/kg)and Dex group(P＜0.05).In addition,the improvement of the above indexes was more significant in RA group(50 mg/kg)and Dex group(P＜0.05).The study suggests that RA inhibits NF-κB and p38 MAPK signaling pathways,alleviates inflammation response and oxidative stress,and reduces apoptosis of kidney tissues to improve sepsis and acute kidney injury.
rosmarinic acidsepsis and acute kidney injuryinflammatory responseapoptosisnuclear factor κB p65p38 mitogen-activated protein kinase
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