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Original Research Article | OPEN ACCESS

Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling pathway

Zhihui Zhou1, Qun Yin2

1Department of Critical Care Medicine, Chongqing General Hospital, Chongqing 401147, China; 2Department of Hospital Infection Management, Wuxi Second People's Hospital, Wuxi, Jiangsu Province 214001, China.

For correspondence:-  Qun Yin   Email: qu_yin1635@163.com   Tel:+8651068182476

Accepted: 9 May 2022        Published: 30 June 2022

Citation: Zhou Z, Yin Q. Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling pathway. Trop J Pharm Res 2022; 21(6):1237-1242 doi: 10.4314/tjpr.v21i6.15

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the protective role of aromadendrin in septic liver injury in mice, and to determine its mechanism of action.
Methods: Eight-week-old male C57BL/6 mice (n=6 for each group) were administrated with aromadendrin (SMB00175, Sigma-Aldrich) at 0 mg/kg, 30 mg/kg and 60 mg/kg via a hypodermic intraperitoneal injection. HE staining was used to examine liver histopathological structural changes in the liver while DAPI/Tunel staining was employed to evaluate liver cell apoptosis. The mRNA expression levels of TNF-α, IL-1β and IL-6 were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Moreover, enzyme-linked immunosorbent assay (ELISA)was applied to assess the levels of TNF-α, IL-1β and IL-6, as well as the activities of catalase (CAT), antioxidant glutathione (GSH), superoxide dismutase (SOD) and malondialdehyde (MDA). Moreover, the protein levels of p65, p-p65, p-IκBα and IκBα were analyzed by Western blotting.
Results: The liver tissues exhibited severe structural damages, with edema, necrosis, and neutrophil infiltration, but recovered as a result of aromadendrin treatment (p < 0.05). The increased serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in CLP mice were reduced by aromadendrin, which also attenuated liver injury and cell apoptosis. Aromadendrin inhibited the levels of TNF-α, IL-1β and IL-6 in the mice, while the activities of GSH and antioxidant enzymes (SOD and CAT) were also significantly lowered in the mice, but attenuated by aromadendrin (p < 0.05). Aromadendrin also prevented the increased level of MDA, and suppressed the phosphorylation of p65 and IκBα (p < 0.05).
Conclusion: Aromadendrin protects mouse liver from sepsis-induced injury by inhibiting NF-κB signaling in vivo, thus suggesting a potential strategy for the therapy of sepsis-induced liver injury.

Keywords: Aromadendrin, Sepsis, NF-?B, Liver injury, Cell apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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