Aloin Preconditioning Attenuates Hepatic IschemiaReperfusion Injury via Inhibiting TLR4MyD88NF-κB Signal Pathway In Vivo and In Vitro
Joint Authors
Du, Yichao
Qian, Baolin
Gao, Lin
Tan, Peng
Chen, Hao
Wang, Ankang
Zheng, Tianxiang
Pu, Shilin
Xia, Xianming
Fu, Wenguang
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-11-20
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
Background.
Aloin exerts considerable protective effects in various disease models, and its effect on hepatic ischemia-reperfusion (HIR) injury remains unknown.
This research is aimed at conducting an in-depth investigation of the antioxidant, anti-inflammatory, and antiapoptosis effects of aloin in HIR injury and explain the underlying molecular mechanisms.
Methods.
In vivo, different concentrations of aloin were intraperitoneally injected 1 h before the establishment of the HIR model in male mice.
The hepatic function, pathological status, oxidative stress, and inflammatory and apoptosis markers were measured.
In vitro, aloin (AL, C21H22O9) or lipopolysaccharide (LPS) was added to a culture of mouse primary hepatocytes before it underwent hypoxia/reoxygenation (H/R), and the apoptosis in the mouse primary hepatocytes was analyzed.
Results.
We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response.
Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).
American Psychological Association (APA)
Du, Yichao& Qian, Baolin& Gao, Lin& Tan, Peng& Chen, Hao& Wang, Ankang…[et al.]. 2019. Aloin Preconditioning Attenuates Hepatic IschemiaReperfusion Injury via Inhibiting TLR4MyD88NF-κB Signal Pathway In Vivo and In Vitro. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1203395
Modern Language Association (MLA)
Du, Yichao…[et al.]. Aloin Preconditioning Attenuates Hepatic IschemiaReperfusion Injury via Inhibiting TLR4MyD88NF-κB Signal Pathway In Vivo and In Vitro. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-14.
https://search.emarefa.net/detail/BIM-1203395
American Medical Association (AMA)
Du, Yichao& Qian, Baolin& Gao, Lin& Tan, Peng& Chen, Hao& Wang, Ankang…[et al.]. Aloin Preconditioning Attenuates Hepatic IschemiaReperfusion Injury via Inhibiting TLR4MyD88NF-κB Signal Pathway In Vivo and In Vitro. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-14.
https://search.emarefa.net/detail/BIM-1203395
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203395