wu cy, hua kf, hsu wh, et al. iga nephropathy benefits from compound k treatment by inhibiting nf-kappab/nlrp3 inflammasome and enhancing autophagy and sirt1.
IgA nephropathy (IgAN), the most common primary glomerular disorder that has a relatively poor prognosis yet lacks a pathogenesis based treatment.
Compound K is a great 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 self generating occurring model of spontaneous grouped ddY mice.
The potential mechanism for CK includes first- inhibiting the activation of NLRP3 inflammasome in renal tissues, macrophages and bone marrow derived dendritic cells, second -improvising the induction of autophagy through elevated SIRT1 expression, and third- eliciting autophagy-mediated NLRP3 inflammasome inhibition.
The study result support CK as a drug candidate for IgAN.
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