Yellow crystalline powder
Artemisia argyi,Castanea mollissima,Artemisia anomala,Artemisia roxburghiana,Helichrysum arenarium
5,7,4'-trihydroxy-3',6-dimethoxyflavone/4H-1-Benzopyran-4-one, 5,7-dihydroxy-2-(4-hydroxy-3-methoxyphenyl)-6-methoxy-/5,7-dihydroxy-2-(4-hydroxy-3-methoxyphenyl)-6-methoxychromen-4-one/5,7-Dihydroxy-2-(4-hydroxy-3-methoxyphenyl)-6-methoxy-4H-chromen-4-one/5,7,4'-trihydroxy-6,3'-dimethoxyflavone/JACEOSIDINE/4',5,7-Trihydroxy-3',6-dimethoxyflavone/6-methoxyluteolin-3'-methyl ether/Jaceosidin
Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression. Jaceosidin exhibits anti-cancer, anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation.
619.0±55.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:18085-97-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Jaceosidin is a flavonoid isolated from Artemisia vestita that has been reported to possess anti-tumor and anti-proliferative activities in many cancer cells. In this study, we investigated the anti-tumor activity of jaceosodin in renal carcinoma cells. Jaceosidin induced apoptosis in multiple human renal carcinoma cells (Caki, ACHN, A498, and 786-O), lung cancer cells (A549) and glioma cells (U251MG). In contrast, jaceosidin does not induce apoptosis in normal human umbilical vein cells (EA.hy926). Apoptotic cell death was associated with the activation of caspase-3 and cleavage of poly (ADP-ribose) polymerase. 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. We also found that jaceosidin downregulated Mcl-1 and c-FLIP expression at the transcriptional level and that ectopic expression of Mcl-1 and c-FLIP blocked jaceosidin-induced apoptosis. Cumulatively, our results suggest that jaceosidin induces apoptosis in renal carcinoma cells through Bax activation and reduces Mcl-1 and c-FLIP expression.
Apoptosis; Bax; Jaceosidin; Mcl-1; Renal cancer; c-FLIP.
Jaceosidin Induces Apoptosis Through Bax Activation and Down-Regulation of Mcl-1 and c-FLIP Expression in Human Renal Carcinoma Caki Cells
Seon Min Woo 1 , Taeg Kyu Kwon 2
2016 Dec 25
Increased endoplasmic reticulum (ER) stress has emerged as a vital contributor to dysregulated glucose homeostasis, and impaired function of sarco-endoplasmic reticulum Ca2+-ATPase 2b (SERCA2b) is one of the central mechanisms underlying ER stress. In this study, we reported that SERCA2b upregulation contributed to the amelioration of ER stress and insulin resistance by a small natural compound jaceosidin. In a model of differentiated C2C12 myotubes, jaceosidin-triggered SERCA2b upregulation enhanced insulin sensitivity and decreased ER stress. Moreover, the activity of Ca2+-ATPase in thapsigargin-treated myotubes was also augmented by jaceosidin. Furthermore, jaceosidin significantly suppressed blood glucose levels, improved glucose tolerance and lowered body weight, but did not alter food intake in insulin-resistant obese mice. In addition, this compound markedly reduced lipid accumulation, suppressed the expression of lipogenic genes in liver and ameliorated liver injury. The ameliorative effects of jaceosidin were due to its ability to reduce ER stress via increasing the expression of SERCA2b in the muscles of obese mice. Taken together, jaceosidin could improve ER stress and attenuate insulin resistance via SERCA2b upregulation in mice skeletal muscles.
Apoptosis; Bax; Jaceosidin; Mcl-1; Renal cancer; c-FLIP.
A Natural Compound Jaceosidin Ameliorates Endoplasmic Reticulum Stress and Insulin Resistance via Upregulation of SERCA2b
Zijun Ouyang 1 , Wanshuai Li 1 , Qianqian Meng 1 , Qi Zhang 1 , Xingqi Wang 1 , Ahmed Elgehama 1 , Xudong Wu 1 , Yan Shen 1 , Yang Sun 1 , Xuefeng Wu 2 , Qiang Xu 3
Acute lung injury (ALI) results from various factors including uncontrolled pulmonary inflammation, oxidative damage and the over-activated complement with high mortality rates. Jaceosidin was a flavonoid compound with significant anti-complement activity. We aimed to investigate the therapeutic effects of Jaceosidin on ALI induced by lipopolysaccharide (LPS). Mice were orally administrated with Jaceosidin (15, 30 and 60 mg/kg) after LPS challenge. 24 h after LPS challenge, Jaceosidin could significantly decrease the lung wet-to-dry weight (W/D) ratio and the protein concentration in bronchoalveolar lavage fluid (BALF). Jaceosidin could down-regulate the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β), together with up-regulation the levels of interleukin-4 (IL-4) and interleukin-10 (IL-10) in BALF. Jaceosidin could significantly decrease the levels of myeloperoxidase (MPO), cyclooxygenase-2 (COX-2) and nuclear factor-κB (NF-κB), COX-2 mRNA and NF-κB p65 mRNA together with increasing the activity of catalase (CAT). Additionally, Jaceosidin attenuated lung histopathological changes, inhibited the expressions of COX-2 and NF-κB p65 and reduced complement deposition with decreasing the levels of complement 3 (C3) and complement 3c (C3c) in serum. These data suggest that Jaceocidin may dampen the inflammatory response and decrease the levels of complement together with the antioxidant activity following LPS-induced ALI.
cute lung injury; Complement; Inflammatory mediators; Jaceosidin; Oxyradicals.
The Therapeutic Effects of Jaceosidin on Lipopolysaccharide-Induced Acute Lung Injury in Mice
Xiao-Lei Huang 1 , Xiao-Chen Wei 2 , Leng-Qiu Guo 3 , Lei Zhao 1 , Xi-Hua Chen 1 , Ya-Dong Cui 1 , Jie Yuan 4 , Dao-Feng Chen 5 , Jian Zhang 6