language Türkçe
Article 2021 · 8 citations

Effect of betulinic acid administration on TLR-9/NF-κB /IL-18 levels in experimental liver injury

Dokumacioglu, Eda, Iskender, Hatice, Kapakin, Kubra Asena Terim, Yenice, Guler, Mokthare, Behzat, Bolat, Ismail, Hayirli, Armagan

Abstract

Background/aim: Acetaminophen (APAP), used in the composition of thousands of preparations, is the most commonly used analgesic and antipyretic drug. The present study aimed to investigate the potential protective effects of the betulinic acid (BA) treatment through an APAP-induced hepatotoxicity rat model, using inflammatory, biochemical, and histopathological parameters. Materials and methods: The study consisted of four groups: control group, APAP group, BA group, and APAP+BA group. Experimental studies continued for fifteen days. Serum samples were analysed for glucose, total cholesterol (TChol), triglyceride (TG), low density lipoprotein (LDL), high density lipoprotein (HDL), aspartate amino transferase (AST), malondialdehyde (MDA), toll-like receptor-9 (TLR-9), nuclear factor kappa B (NF-kappa B), and interleukin-18 (IL-18). Results: TLR9, IL-18, NF-kappa B, and MDA levels increased significantly in liver injury groups. These increases considerably decreased by the BA treatment. All groups showed immunopositivity for 8-hydroxy-2'-deoxyguanosine (8-OHdG) and interleukin (IL-1 beta) in the hepatocytes, inflammatory cells, and epithelial cells of bile ducts. Conclusion: BA can be used as an effective agent in the prevention and treatment of acute liver diseases due to its inhibitory properties in multiple pathways and its potent antioxidant effects.

Keywords
Acetaminophen betulinic acid interleukin-18 nuclear factor kappa B toll-like receptor-9 NF-KAPPA-B ACETAMINOPHEN-INDUCED HEPATOTOXICITY OXIDATIVE STRESS INFLAMMATION EXPRESSION CHITOSAN DAMAGE IL-18 NRF2 TLR
WoS Categories
Medicine, General & Internal
Sustainable Development Goals
Citation
Journal
TURKISH JOURNAL OF MEDICAL SCIENCES
Year
2021
Volume
51
Issue
3
Pages
1544-1553
ISSN
1300-0144
eISSN
1303-6165
DOI
10.3906/sag-2004-184
WoS UID
WOS:000668257500016
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