Nephroprotective effect of apilarnil in lipopolysaccharide-induced sepsis through TLR4/NF-κB signaling pathway

TLR4型 脂多糖 败血症 肿瘤坏死因子α 药理学 医学 免疫组织化学 NF-κB 炎症 免疫系统 内科学 化学 内分泌学 免疫学
作者
Nihal İnandıklıoğlu,Züleyha Doğanyiğit,Aslı Okan,Emin Kaymak,Sibel Sılıcı
出处
期刊:Life Sciences [Elsevier BV]
卷期号:284: 119875-119875 被引量:35
标识
DOI:10.1016/j.lfs.2021.119875
摘要

In this study, we aimed to investigate the protective effect of apilarnil on kidney damage in the sepsis model induced by LPS.64 Sprague Dawley adult male rats were randomly divided into eight groups; control group, groups in which 0.2, 0.4 and 0.8 g/kg/bw apilarnil (API) was applied by oral gavage method for 10 days, LPS group in which 30 mg/kg/bw lipopolysaccharide (LPS) administered as intraperitoneally, groups in which LPS + 0.2, LPS+ 0.4 and LPS +0,8 API was applied. Six hour after the last administration the rats were anesthetized for euthanasia and kidney tissues were removed for RT-PCR analysis, immunohistochemical analysis and histopathologic analysis.According to the results of RT-PCR expression levels of IL-6, IL-1β, NF-κB, TNF-α and TLR4 were significantly reduced in the LPS + 0,8 API group. Immunoreactivity of TLR4, pNF-κB and TNF-α levels in the LPS + 0.8 apilarnil group were significantly lower than in the LPS and LPS + 0.2 apilarnil groups. Histologically, compared to the LPS group the glomerular damage score tended to decrease in the LPS + 0,4 API and LPS+ 0,8 API groups, while the tubulointerstitial injury score decreased especially in the LPS + 0,8 API group.In the present study, 0,8 g/kg dose of apilarnil promoted potential renoprotective effects which were achieved, at least in part, by the modulation of important markers of the local immune response in the model of LPS-induced sepsis.
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