Related Experiment Video
Updated: Feb 3, 2026
Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model
Published on: November 9, 2018
Protective effects of dioscin against systemic inflammatory response syndromevia adjusting TLR2/MyD88/NF‑κb signal
Xuerong Zhao1, Lianhong Yin1, Lingling Fang1
1College of Pharmacy, Dalian Medical University, Western 9 Lvshun nan Road, Dalian 116044, China.
Abstract:
Development of active compounds to control inflammation against systemic inflammatory response syndrome (SIRS) is critical important. Dioscin shows anti-inflammatory effects in our previous works. However, the action of the compound on SIRS still remained unknown. In the present paper, zymosan induced generalized inflammation (ZIGI) models in mice and rats, and PMA-differentiated THP‑1 cells stimulated by lipopolysaccharide (LPS) and Pam3-Cys-Ser-Lys4 (Pam3CSK4) were used. The results showed that dioscin significantly inhibited the proliferation of THP‑1 cells stimulated by LPS and Pam3CSK4, obviously reduced the soakage of inflammatory cells and necrosis in liver, kidney and intestine of rats and mice, and reduced peritoneal ascites fluid compared with ZIGI model groups. In addition, dioscin significantly declined the levels of alanine transaminase (ALT), aspartate transaminase (AST), creatinine (Cr), blood urea nitrogen (BUN), malondialdehyde (MDA) and myeloperoxidase (MPO), increased the levels of superoxide dismutase (SOD) in rats and mice. The migration of macrophages in tissues was also suppressed by dioscin. Mechanism investigation showed that dioscin significantly inhibited the expression levels of TLR2, MyD88, NF‑κb, HMGB‑1, increased the expression levels of IKBα, and decreased the mRNA levels of interleukin‑1 beta (IL‑1β), interleukin‑6 (IL‑6) and tumor necrosis factor‑alpha (TNF‑α) in liver, kidney, intestine tissues of rats and mice, and in PMA-differentiated THP‑1 cells, which were further confirmed by TLR2 siRNA silencing in vitro. In conclusion, our data confirmed that dioscin exhibited protective effects against SIRS via adjusting TLR2/MyD88 signal pathway, which should be developed as one potent candidate to treat SIRS in the future.
Insights
Dioscin, a natural compound, effectively combats systemic inflammatory response syndrome (SIRS) by reducing inflammation and organ damage. It works by modulating the TLR2/MyD88 signaling pathway, showing promise for future SIRS treatments.
Area of Science:
- Pharmacology
- Immunology
- Natural Products
Background:
- Systemic inflammatory response syndrome (SIRS) poses a critical challenge in clinical settings.
- Dioscin has demonstrated anti-inflammatory properties in prior research.
- The specific effects of dioscin on SIRS were previously uncharacterized.
Purpose of the Study:
- To investigate the therapeutic potential of dioscin against SIRS.
- To elucidate the underlying molecular mechanisms of dioscin's action in SIRS models.
Main Methods:
- Utilized zymosan-induced generalized inflammation (ZIGI) models in mice and rats.
- Employed lipopolysaccharide (LPS) and Pam3CSK4-stimulated THP-1 cells for in vitro assays.
- Assessed organ damage markers, inflammatory cell infiltration, and key signaling pathway components (TLR2, MyD88, NF-κB).
Main Results:
- Dioscin significantly reduced inflammatory cell infiltration, necrosis, and ascites fluid in ZIGI models.
- Dioscin normalized levels of liver enzymes (ALT, AST), kidney function markers (Cr, BUN), and oxidative stress indicators (MDA, MPO, SOD).
- Dioscin suppressed the TLR2/MyD88/NF-κB pathway, decreasing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and HMGB-1, while increasing IKBα.
Conclusions:
- Dioscin demonstrates significant protective effects against SIRS in preclinical models.
- The therapeutic action of dioscin is mediated through the modulation of the TLR2/MyD88 signaling pathway.
- Dioscin represents a promising candidate for the development of novel SIRS therapeutics.
More Related Videos
10:39In Vitro Analysis of Myd88-mediated Cellular Immune Response to West Nile Virus Mutant Strain Infection
Published on: November 27, 2014
04:06Efficient and Cost Effective Electroporation Method to Study Primary Cilium-Dependent Signaling Pathways in the Granule Cell Precursor
Published on: November 30, 2021
Related Concept Videos
02:26NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
01:28Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
01:24Inflammatory Response II: Inflammatory Exudate and Tissue Repair
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
03:14Notch Signaling Pathway
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
02:33Hedgehog Signaling Pathway
01:19Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...