Related Experiment Video
Updated: Dec 2, 2025
Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
Methionine selenium antagonizes LPS-induced necroptosis in the chicken liver via the miR-155/TRAF3/MAPK axis
Zhao Zhirong1, Zhang Qiaojian1, Xu Chunjing2
1Department of Basic Veterinary Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin, People's Republic of China.
Abstract:
Organic selenium has antioxidation and disease treatment effects. To explore the mechanisms of how methionine selenium alleviates necroptosis in the liver and whether this process is related to microRNA (miRNA) and the mitogen-activated protein kinase (MAPK) pathway, an animal model of methionine selenium and the lipopolysaccharide (LPS) interaction was established. The morphology, inflammatory factor (tumor necrosis factor-α [TNF-α]), necroptosis-related genes (RIP1, RIP3, MLKL, and caspase 8), MAPK pathway-related genes (JNK, ERK, and p38, p-JNK, p-ERK, and p-p38), gga-miR-155, TRAF3 (predicted target of gga-miR-155), and oxidative stress-related indicators (SOD, MDA, CAT, GSH, and GSH-Px) were analyzed from the perspective of the miR-155/TRAF3/MAPK axis to elucidate the mechanism of methionine selenium on the LPS-induced necroptosis mechanism in the chicken liver. The current results suggested that methionine selenium antagonizes oxidative stress, inflammation, and the MAPK pathway, thereby antagonizing the occurrence of necroptosis through multiple mechanisms. At the same time, methionine selenium affects miR-155/TRAF3/MAPK signaling, reduces miR-155 expression, and upregulates TRAF3 expression to inhibit necroptosis. This information provided new ideas and a theoretical basis for the practical application of methionine selenium, and it also enriched the study of miRNAs in birds and provided a reference for comparative medicine.
Insights
Methionine selenium alleviates liver necroptosis by reducing oxidative stress and inflammation. It modulates the miR-155/TRAF3/MAPK pathway, offering a new therapeutic strategy.
Area of Science:
- Animal models
- Molecular biology
- Biochemistry
Background:
- Organic selenium compounds, like methionine selenium, possess antioxidant and therapeutic properties.
- Necroptosis, a form of programmed cell death, is implicated in liver disease.
- MicroRNAs (miRNAs) and the mitogen-activated protein kinase (MAPK) pathway are involved in cellular regulation and disease processes.
Purpose of the Study:
- To investigate the protective mechanisms of methionine selenium against lipopolysaccharide (LPS)-induced necroptosis in chicken liver.
- To determine the role of the miR-155/TRAF3/MAPK signaling axis in methionine selenium's effects.
- To elucidate how methionine selenium influences oxidative stress and inflammation.
Main Methods:
- Establishment of an animal model using methionine selenium and LPS.
- Analysis of liver morphology, inflammatory factors (TNF-α), necroptosis markers (RIP1, RIP3, MLKL, caspase 8), and MAPK pathway components (JNK, ERK, p38).
- Quantification of oxidative stress indicators (SOD, MDA, CAT, GSH, GSH-Px) and assessment of gga-miR-155 and TRAF3 expression.
Main Results:
- Methionine selenium demonstrated protective effects against LPS-induced liver injury.
- It significantly antagonized oxidative stress, inflammation, and MAPK pathway activation.
- Methionine selenium treatment led to reduced gga-miR-155 expression and increased TRAF3 expression, inhibiting necroptosis.
Conclusions:
- Methionine selenium exerts protective effects against liver necroptosis through multiple mechanisms, including mitigating oxidative stress and inflammation.
- The study highlights the involvement of the miR-155/TRAF3/MAPK signaling pathway in methionine selenium's therapeutic action.
- These findings provide a theoretical basis for the application of methionine selenium and contribute to the understanding of miRNA functions in avian species.
