Investigation of protective effects of apilarnil against lipopolysaccharide induced liver injury in rats via TLR 4/ HMGB-1/ NF-κB pathway - 14/03/20
, Aslı Okan a , Emin Kaymak a , Dilek Pandır b , Sibel Silici c Bienvenue sur EM-consulte, la référence des professionnels de santé.
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| pages | 10 |
| Iconographies | 6 |
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Graphical abstract |
Highlights |
• | Apilarnil treatment reduced the histopathological changes caused by LPS. |
• | Expressions of TLR4 signalling pathway increased by LPS administration were regulated by apilarnil treatment. |
• | Apilarnil regulated increased apoptosis by LPS administration. |
• | Apilarnil showed protective effect against DNA damage caused by LPS application. |
• | Apilarnil showed protective effect against oxidative stress caused by LPS. |
Abstract |
Sepsis caused by infection is one of the most important problems of clinical medicine. This study aimed to determine the effect of Apilarnil (API), a bee product, on lipopolysaccharide (LPS) induced liver injury. In the study, 64 adult Sprague-Dawley rats were divided into eight groups; control, 0.2, 0.4 and 0.8 g / kg apilarnil (API) treated groups, LPS (30 mg / kg) group, LPS + 0.2, LPS + 0.4 and LPS + 0.8 g / kg API. At tissues obtained from rats, histopathological evaluation, biochemical analysis by ELISA (Catalase-CAT, malondialdehyde-MDA, superoxide dismutase-SOD, xanthine oxidase-XOD, and testican 1-TCN-1), immunohistochemical evaluation (Toll-like receptor 4 (TLR4), High Mobility Group Box Protein 1 (HMGB-1), nuclear factor kappa B (NF-κB), Tumor necrosis factor-alpha (TNF-α), Interleukin 1 beta (IL-1β), Interleukin 6 (IL-6) and Inducible nitric oxide (iNOS)), TUNEL analysis to determine the number of apoptotic cells and Comet test as an indicator of DNA damage were performed. Histopathological examination revealed dilated blood vessels, inflammatory cell infiltration, and pyknotic nuclei damaged hepatocytes in the liver tissues of the LPS group. It was found that tissue damage was decreased significantly in LPS + API treatment groups compared to the LPS group. The number of TUNEL positive cells observed in the LPS group in liver samples increased compared to control and API-treated groups only (p < 0.05). The number of TUNEL positive cells showed a statistically significant decrease compared to the LPS group in the groups treated with LPS + API. LPS treatment increased MDA, XOD, and TCN 1 levels and decreased SOD and CAT levels; this effect was reversed in the groups treated with LPS + API. In the LPS group, DNA damage was significantly increased when compared with the LPS + API. LPS treatment increased expression of TLR4, HMGB-1, NF-κB, iNOS, TNF-α, IL-1β, IL-6; in the groups treated with LPS + API reduced this increase. In conclusion, apilarnil administered in rats may be thought to prevent LPS-induced liver damage by inhibiting the TLR4 / HMGB-1 / NF-κB signaling pathway.
Le texte complet de cet article est disponible en PDF.Keywords : Apilarnil, Oxidative stress, Apoptosis, Inflammation, LPS, Liver
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Vol 125
Article 109967- mai 2020 Retour au numéro
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