The Effect of Apilarnil on The Autophagia Against Lipolysaccarite-Based Sepsıs in Liver

Year 2020, Volume: 1 Issue: 2, 84 - 89, 30.09.2020

Züleyha Doğanyiğit , Betül Köklü , Arda Uner , Aslı Okan Emin Kaymak , Sibel Silici

Abstract

Sepsis, triggered by highly bacterial lipopolysaccharide (LPS) endotoxins, exhibits high morbidity and mortality despite medical advances. Damage to the liver occurs due to the production of highly reactive oxygen compounds (ROS) and the release of various proinflammatory cytokines. It is suggested that autophagy, which regulates inflammation and selectively destroys damaged mitochondria, suppresses apoptosis and provides a possible protective mechanism in the endotoxic liver. However, apilarnil, a bee product, is known to have high antioxidant activity and positive effects against various diseases thanks to its polyphenols. In this study, it is aimed to reveal the potential protective effect of apilarnil on the autophagy mechanism in the endotoxic liver model LPS-induced. 64 male Sprague dawley rats weighing 200-250; control, apilarnil treated groups (0.2, 0.4 and 0.8 g / kg), LPS (30 mg / kg) group and LPS + apilarnil treated groups (LPS + 0.2 g / kg, LPS + 0.4 g / kg and LPS + 0.8 g / kg) are randomly divided into eight groups. Beclin-1, LC3 and P62 proteins were analyzed immunohistochemically in order to determine the activity level of autophagy pathway in the liver tissues taken after the completion of the experiment protocol. The data obtained showed that Beclin-1 immunoreactivity decreased while LC3 and P62 expression increased in the tissues of the LPS group compared to the control group. When apilarnil was applied with LPS, it was determined that there was an increase in Beclin-1 level (p> 0.05) and a decrease in P62 levels (p <0.05) depending on the dose increase. Apilarnil increases the activity of the autophagy pathway and shows potential positive effects by providing a significant decrease on LC3 and P62 protein expression increased by LPS. However, the role of apilarnil in the autophagy pathway, which is a possible protector against LPS-induced sepsis, should be further investigated.

Keywords

Beclin-1, LC3, P62, Apilarnil, LPS, Liver

Supporting Institution

Yozgat Bozok University Project Coordination Application and Research Center

Project Number

6602a-TF / 20-375

References

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