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.
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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
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