ArticleAmerican journal of translational research2019
Glycyrrhizin suppresses inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JUK signaling pathway in attenuating intervertebral disc degeneration.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Glycyrrhizin (GLY) and glycyrrhetinic acid (GA) as potential multi-target antimicrobials: mechanisms, biofilm disruption, and synergy against drug-resistant pathogens.Frontiers in microbiology · 2026Review
- Review
- Molecular mechanisms and treatment strategies for discogenic lumbar pain.Immunologic research · 2025Review
- Exploring the potential anti-apoptotic effects of traditional Chinese medicine in intervertebral disc degeneration: mechanisms and therapeutic prospects.Frontiers in physiology · 2025Review
- Molecular Mechanisms of Intervertebral Disc Degeneration Induced byBioMed research international · 2025Review
- Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK.Biomolecules · 2024Review
- The JNK signaling pathway in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2024Review
- Vitiligo and Mental Health: Natural Compounds' Usefulness.Antioxidants (Basel, Switzerland) · 2023Review
- Natural products can modulate inflammation in intervertebral disc degeneration.Frontiers in pharmacology · 2023Review
- Drug Candidates for Autoimmune Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Causes of and Molecular Targets for the Treatment of Intervertebral Disc Degeneration: A Review.Cells · 2022Review
- Necroptosis of nucleus pulposus cells involved in intervertebral disc degeneration through MyD88 signaling.Frontiers in endocrinology · 2022Article
- The role of miRNA, lncRNA and circRNA in the development of intervertebral disk degeneration (Review).Experimental and therapeutic medicine · 2021Review
- Glycyrrhizin Attenuates Carcinogenesis by Inhibiting the Inflammatory Response in a Murine Model of Colorectal Cancer.International journal of molecular sciences · 2021Article
- Natural Products of Pharmacology and Mechanisms in Nucleus Pulposus Cells and Intervertebral Disc Degeneration.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- p38 promoted retinal micro-angiogenesis through up-regulated RUNX1 expression in diabetic retinopathy.Bioscience reports · 2020Article
- Protein Kinase A Is Involved in Neuropathic Pain by Activating the p38MAPK Pathway to Mediate Spinal Cord Cell Apoptosis.Mediators of inflammation · 2020Article
- Current Progress in the Endogenous Repair of Intervertebral Disk Degeneration Based on Progenitor Cells.Frontiers in bioengineering and biotechnology · 2020Review
- Glycyrrhizin Ameliorates Radiation Enteritis in Mice Accompanied by the Regulation of the HMGB1/TLR4 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is associated with the nucleus pulposus (NP) cells inflammation and apoptosis. Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition. However, it is not known whether GL protects against IDD by the inhibition of HMGB1. To study the effect and mechanism of glycyrrhizin on intervertebral disc degeneration. We analyzed the expression of HMGB1 in different degree of degenerate disc tissues. Interleukin 1 beta (IL-1β) was used in stimulating the NP cells to degeneration. We used recombined human HMGB1 to resist the function of GL to explore whether GL acted via the target of HMGB1. Our study showed that the expression of HMGB1 markedly increased in severely degenerated disc tissues. IL-1β promoted the progress of IDD, and the stimulation of GL could reverse the effects of IL-1β. Moreover, p38 and p-JNK were significantly suppressed by GL stimuli. These results suggested that GL prevented NP degradation via restraining inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JNK signaling pathway. GL may become a novel cytokine for the therapy of IDD in the future.
Indexed as
Identifiers
31497226PMC6731420W2990022256What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.