Lupus nephritis (LN) is divided into 6 classes based on the severity of the renal histopathologic lesions (1), and histologic transformation between the classes occurs frequently (2,3). Although the exact mechanisms for the histologic transformation of mild mesangial LN into severe renal conditions remain unclear, acute induction of cellular and humoral autoimmunity, including the production of anti-double-stranded DNA (antidsDNA) antibodies (4,5), overexpression of cytokines and chemokines (6,7), differential activation of B cells (8,9), abnormal T cell activation (6,10), and Dnase1 deficiency (11,12), has been implicated. In addition, abundant production of interleukin-12 (IL-12) and IL-18 is seen in the glomeruli of patients and in mouse models of LN, and Th1 cytokines are highly implicated in the development and progression of .IL-18 has also been reported to promote the migration of circulating dendritic cells to the kidney in active LN (15,16). We recently demonstrated that expression of IL-18, induced with lipopolysaccharide
Antroquinonol ( 1), an ubiquinone derivative, was isolated from the solid-state fermented mycelium of Antrodia camphorata (Polyporaceae, Aphyllophorales), a parasitic fungus indigenous to Taiwan. The structure of compound 1 was elucidated by the analysis of their spectroscopic data. Its cytotoxic activities were evaluated against MCF-7, MDA-MB-231 (human breast carcinoma), Hep3B, HepG2 (human liver carcinoma) and DU-145, LNCaP (human prostate carcinoma) cell lines, and the IC (50) values ranged from 0.13 +/- 0.02 to 6.09 +/- 0.07 microM.
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