IgA nephropathy benefits from compound k treatment by inhibiting NF-κB/NLRP3 inflammasome and enhancing autophagy and SIRT1

Chung Yao Wu, Kuo Feng Hua, Wan Han Hsu, Yusuke Suzuki, Lichieh Julie Chu, Yu Chieh Lee, Akiko Takahata, Sheau Long Lee, Chia Chao Wu, David J. Nikolic-Paterson, Shuk Man Ka, Ann Chen

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)


IgA nephropathy (IgAN), the most common primary glomerular disorder, has a relatively poor prognosis yet lacks a pathogenesisbased 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.

Original languageEnglish
Pages (from-to)202-212
Number of pages11
JournalJournal of Immunology
Issue number1
Publication statusPublished - 1 Jul 2020

Cite this