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Analysis of Oxidative Stress in Zebrafish Embryos
Published on: July 7, 2014
MiR-155 aggravated septic liver injury by oxidative stress-mediated ER stress and mitochondrial dysfunction via
Zhao-Bin Yang1, Wen-Wen Chen2, Hui-Ping Chen1
1Medical Intensive Care Unit, Zhangzhou Municipal Hospital of Fujian Province, Zhangzhou 363000, China.
Objective:
Liver is uniquely vulnerable during sepsis. MicroRNA-155 (miR-155) is confirmed to play crucial roles in septic liver injury. The present study aims to investigate the mechanisms of miR-155 in septic liver injury.
Methods:
The sepsis model was established by intraperitoneal injection of lipopolysaccharide (LPS) in mice. Mice were divided into four groups: Vehicle, miR-155 antagomir, LPS, LPS+ miR-155 antagomir. The survival rate and body weight were monitored. Liver injury was assessed by H&E staining. The levels of serum ALT and inflammatory cytokines were determined by ELISA kits. Oxidative stress was detected by MDA and SOD detection kits. The miR-155, Nrf-2, and markers related to oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial injury and apoptosis were detected by western blotting and qPCR. Apoptosis in liver tissues was detected by TUNELstaining.
Results:
MiR-155 antagomir alleviated liver injury as evidenced by enhancing survival rate and body weight, inhibiting inflammatory cell infiltration, liver cells necrosis and decreasing ALT level. The productions of TNF-α, IL-6 were suppressed, while anti-inflammatory cytokine IL-10 was promoted by miR-155 antagomir. Oxidative stress was inhibited by miR-155 antagomir via enhancing nuclear factor, erythroid 2-like 2 (Nrf-2) expression. ER stress and Cytochrome C (Cyto-C) release were restrained by miR-155 antagomir. Sepsis-induced apoptosis was repressed by miR-155 antagomir as manifested by the decreased levels of Bax, cleaved caspase-12, 9 and 3, and increased levels of Bcl-2 and uncleaved PARP.
Conclusion:
MiR-155 antagomir relieved septic liver injury through inhibiting oxidative stress-mediated ER stress, mitochondrial dysfunction and apoptosis via targeting Nrf-2, suggesting miR-155 as a therapeutic target for septic liver injury.
Insights
MicroRNA-155 (miR-155) inhibition protects the liver during sepsis. Targeting miR-155 reduces inflammation, oxidative stress, and apoptosis, offering a potential therapy for septic liver injury.
Area of Science:
- Hepatology
- Molecular Biology
- Immunology
Background:
- Sepsis poses a significant threat to liver function.
- MicroRNA-155 (miR-155) is implicated in the pathogenesis of septic liver injury.
Purpose of the Study:
- To elucidate the underlying mechanisms of miR-155 in sepsis-induced liver damage.
- To evaluate the therapeutic potential of targeting miR-155 in a mouse model of sepsis.
Main Methods:
- A mouse model of sepsis was induced using lipopolysaccharide (LPS).
- Mice were treated with a miR-155 antagomir to inhibit miR-155 activity.
- Liver injury, inflammation, oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and apoptosis were assessed.
Main Results:
- miR-155 antagomir treatment improved survival and alleviated liver injury markers.
- Inhibition of miR-155 reduced pro-inflammatory cytokines (TNF-α, IL-6) and enhanced IL-10.
- miR-155 antagomir mitigated oxidative stress by upregulating Nrf-2, suppressed ER stress and mitochondrial dysfunction, and repressed apoptosis.
Conclusions:
- miR-155 inhibition ameliorates septic liver injury by targeting oxidative stress-mediated ER stress, mitochondrial dysfunction, and apoptosis via Nrf-2.
- miR-155 represents a promising therapeutic target for managing septic liver injury.
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