ReferenceID 4353
Ginsenoside Rg3 Attenuates TNF-α-Induced Damage in Chondrocytes through Regulating SIRT1-Mediated Anti-Apoptotic and Anti-Inflammatory Mechanisms
Antioxidants (Basel)
The upregulation of tumor necrosis factor-alpha (TNF-alpha) is a common event in arthritis, and the subsequent signaling cascade that leads to tissue damage has become the research focus. To explore a potential therapeut
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Record Fields
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- Reference Id
- 4353
- Evidence Id
- 20943
- Core Evidence Id
- 20943
- Source Reference Id
- 1969
- Herb2 Reference Id
- HBREF002766
- Subject Paper Key
- HBIN003500_34943075
- Pubmed Id
- 34943075
- Doi
- 10.3390/antiox10121972
- Paper Title
- Ginsenoside Rg3 Attenuates TNF-α-Induced Damage in Chondrocytes through Regulating SIRT1-Mediated Anti-Apoptotic and Anti-Inflammatory Mechanisms
- Paper Abstract
- The upregulation of tumor necrosis factor-alpha (TNF-alpha) is a common event in arthritis, and the subsequent signaling cascade that leads to tissue damage has become the research focus. To explore a potential therapeutic strategy to prevent cartilage degradation, we tested the effect of ginsenoside Rg3, a bioactive component of Panax ginseng, on TNF-alpha-stimulated chondrocytes.TC28a2 Human Chondrocytes were treated with TNF-alpha to induce damage of chondrocytes. SIRT1 and PGC-1a expression levels were investigated by Western blotting assay. Mitochondrial SIRT3 and acetylated Cyclophilin D (CypD) were investigated using mitochondrial isolation. The mitochondrial mass number and mitochondrial DNA copy were studied for mitochondrial biogenesis. MitoSOX and JC-1 were used for the investigation of mitochondrial ROS and membrane potential. Apoptotic markers, pro-inflammatory events were also tested to prove the protective effects of Rg3. We showed Rg3 reversed the TNF-alpha-inhibited SIRT1 expression. Moreover, the activation of the SIRT1/PGC-1alpha/SIRT3 pathway by Rg3 suppressed the TNF-alpha-induced acetylation of CypD, resulting in less mitochondrial dysfunction and accumulation of reactive oxygen species (ROS). Additionally, we demonstrated that the reduction of ROS ameliorated the TNF-alpha-elicited apoptosis. Furthermore, the Rg3-reverted SIRT1/PGC-1alpha/SIRT3 activation mediated the repression of p38 MAPK, which downregulated the NF-kappaB translocation in the TNF-alpha-treated cells. Our results revealed that administration of Rg3 diminished the production of interleukin 8 (IL-8) and matrix metallopeptidase 9 (MMP-9) in chondrocytes via SIRT1/PGC-1alpha/SIRT3/p38 MAPK/NF-kappaB signaling in response to TNF-alpha stimulation. Taken together, we showed that Rg3 may serve as an adjunct therapy for patients with arthritis.
- Journal
- Antioxidants (Basel)
- Publish Year
- 2021
- Experiment Subject
- human; patient; tc28a2; tnf-alpha-stimulated chondrocytes; tnf-alpha-treated cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Mitochondrial Dysfunction; Tumor; Arthritis
- Paper Title Cn
- Paper Title En
- Ginsenoside Rg3 Attenuates TNF-α-Induced Damage in Chondrocytes through Regulating SIRT1-Mediated Anti-Apoptotic and Anti-Inflammatory Mechanisms
- Bilingual Status
- semi_complete