Jaceosidin, a methylated trihydroxyflavone, can induce apoptosis in cancer cells via activating Bax and also could block signaling pathways related to inflammation. It is first isolated from the Compositae family.
Jaceosidin is a flavonoid isolated from Artemisia vestita that has been reported to possess anti-tumor and anti-proliferative activities in many cancer cells. Jaceosidin induced apoptosis in multiple human renal carcinoma cells (Caki, ACHN, A498, and 786-O), lung cancer cells (A549) and glioma cells (U251MG). Treatment with jaceosidin also caused loss of mitochondrial membrane potential (MMP) and Bax activation, which led to the release of cytochrome c into the cytosol[3]. Jaceosidin is a more potent inhibitor of cell growth than cisplatin in human endometrial cancer cells. In contrast, jaceosidin-induced cytotoxicity in normal endometrial cells was lower than that observed for cisplatin. Jaceosidin induced G2/M phase cell cycle arrest and modulated the levels of cyclin B and p-Cdc2 in Hec1A cells. Jaceosidin shows cytostatic activity to HES and HESC cells with IC50s of 52.68 and 55.10 μM, and is less cytotocxic on Hec1 A and KLE (IC50, 70.54, 147.14 μM, respectively), after treatment for 48 h[4]. Jaceosidin could improve ER (endoplasmic reticulum) stress and attenuate insulin resistance via SERCA2b (sarco-endoplasmic reticulum Ca2+-ATPase 2b) upregulation in mice skeletal muscles[5]. Mice were orally administrated with Jaceosidin (15, 30 and 60 mg/kg) after LPS challenge. 24 h after LPS (lipopolysaccharide) challenge, Jaceosidin could significantly decrease the lung wet-to-dry weight (W/D) ratio and the protein concentration in bronchoalveolar lavage fluid (BALF) [6].
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