IgA Nephropathy Benefits from Compound K Treatment by Inhibiting NF-κB/NLRP3 Inflammasome and Enhancing Autophagy and SIRT1
| Autor: | Yusuke Suzuki, Ann Chen, Chia Chao Wu, Lichieh Julie Chu, David J. Nikolic-Paterson, Yu Chieh Lee, Shuk-Man Ka, Chung Yao Wu, Wan Han Hsu, Sheau Long Lee, Akiko Takahata, Kuo Feng Hua |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Ginsenosides
Inflammasomes Kidney Glomerulus Primary Cell Culture Immunology Mice Inbred Strains urologic and male genital diseases Cell Line Nephropathy Pathogenesis Mice 03 medical and health sciences Ginseng chemistry.chemical_compound 0302 clinical medicine Immune system Sirtuin 1 NLR Family Pyrin Domain-Containing 3 Protein Autophagy medicine Animals Humans Immunology and Allergy Chemistry Macrophages NF-kappa B Glomerulonephritis IGA Glomerulonephritis Inflammasome NF-κB Dendritic Cells medicine.disease Disease Models Animal Cancer research Signal Transduction 030215 immunology medicine.drug |
| Zdroj: | The Journal of Immunology. 205:202-212 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.1900284 |
| Popis: | IgA nephropathy (IgAN), the most common primary glomerular disorder, has a relatively poor prognosis yet lacks a pathogenesis-based treatment. Compound K (CK) is a major absorbable intestinal bacterial metabolite of ginsenosides, which are bioactive components of ginseng. The present study revealed promising therapeutic effects of CK in two complementary IgAN models: a passively induced one developed by repeated injections of IgA immune complexes and a spontaneously occurring model of spontaneous grouped ddY mice. The potential mechanism for CK includes 1) inhibiting the activation of NLRP3 inflammasome in renal tissues, macrophages and bone marrow–derived dendritic cells, 2) enhancing the induction of autophagy through increased SIRT1 expression, and 3) eliciting autophagy-mediated NLRP3 inflammasome inhibition. The results support CK as a drug candidate for IgAN. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|