Related Experiment Video
Updated: Aug 14, 2026
08:32
Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Magnolol Modulates the RIG-I/NF-κB Signaling Pathway to Alleviate JEV Infection-Induced ST Cell Damage
Bohan Zheng1,2, Mengzhao Jiang1,2, Hongjie Cui1,2
1College of Animal Science, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Animals : an Open Access Journal From MDPI
|August 13, 2026
Summary
Magnolol, a natural extract, protects boar testicular cells from Japanese encephalitis virus (JEV) inflammation. It inhibits the RIG-I/NF-κB pathway, reducing JEV-induced reproductive damage.
Area of Science:
- Veterinary Virology
- Immunology
- Natural Product Chemistry
Background:
- Japanese encephalitis virus (JEV) causes severe testicular inflammation and reproductive loss in breeding boars.
- Magnolol, a natural compound, possesses known anti-inflammatory and antioxidant properties.
Purpose of the Study:
- To investigate the protective effects of magnolol against JEV-induced inflammation in swine testicular (ST) cells.
- To elucidate the underlying molecular mechanisms of magnolol's action.
Main Methods:
- Swine testicular cells were infected with JEV and treated with varying concentrations of magnolol.
- Pro-inflammatory cytokine levels were measured.
- Quantitative proteomics (4D-FastDIA) identified differentially expressed proteins.
- Key molecules in the RIG-I/NF-κB pathway were analyzed at mRNA and protein levels.
- p65 nuclear translocation was visualized via immunofluorescence.
Main Results:
- JEV infection significantly increased pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8, CCL5).
- Magnolol dose-dependently reduced these cytokine levels.
- JEV activated the RIG-I/NF-κB signaling pathway, increasing IKKβ, TRAF2, TRAF6, and p65 phosphorylation.
- Magnolol treatment (16 μg/mL) significantly inhibited this pathway activation.
Conclusions:
- Magnolol effectively alleviates JEV-induced inflammatory injury in swine testicular cells.
- The protective mechanism involves the inhibition of the RIG-I/NF-κB signaling pathway.
- Magnolol shows potential as a natural therapeutic agent for mitigating JEV-induced reproductive damage in boars.
Related Concept Videos
02:26NF-kB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
02:26NF-κB-dependent Signaling Pathway
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
01:16Calmodulin-dependent Signaling
Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
01:16TGF - β Signaling Pathway
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
01:19Inhibitors of Virion Maturation and Assembly
As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
01:07MAPK Signaling Cascades
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...