White crystalline powder
(2E,4E)-5-[(1R,7S,8R,9R)-4,7-Bis(methoxycarbonyl)-9-methyl-11-oxo-10-oxatricyclo[188.8.131.52]tridec-3-en-9-yl]-2-methylpenta-2,4-dienoic acid/(2E,4E)-5-[(1S,7S,8S,9R)-7-Acetoxy-4-(methoxycarbonyl)-9-methyl-11-oxo-10-oxatricyclo[184.108.40.206]tridec-3-en-9-yl]-2-methyl-2,4-pentadienoic acid/1H-4,9a-Ethanocyclohepta[c]pyran-7-carboxylic acid, 4a-(acetyloxy)-3-[(1E,3E)-4-carboxy-1,3-pentadien-1-yl]-3,4,4a,5,6,9-hexahydro-3-methyl-1-oxo-, 7-methyl ester, (3R,4S,4aS,9aS)-/(2E,4E)-5-[(1R,7S,8R,9R)-4,7-Bis(methoxycarbonyl)-9-methyl-11-oxo-10-oxatricyclo[220.127.116.11]tridec-3-en-9-yl]-2-methyl-2,4-pentadienoic acid/1H-4,9a-Ethanocyclohepta[c]pyran-4a,7(5H)-dicarboxylic acid, 3-[(1E,3E)-4-carboxy-1,3-pentadien-1-yl]-3,4,6,9-tetrahydro-3-methyl-1-oxo-, 4a,7-dimethyl ester, (3R,4R,4aS,9aR)-/PLAB/(2E,4E)-5-[(1S,7S,8S,9R)-7-Acetoxy-4-(methoxycarbonyl)-9-methyl-11-oxo-10-oxatricyclo[18.104.22.168]tridec-3-en-9-yl]-2-methylpenta-2,4-dienoic acid/PseudolaricAcidB/Pseudolarix acid B
Methanol; Acetontrile; DMSO
613.8±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#:82508-31-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Ferroptosis is a form of programmed cell death decided by iron-dependent lipid peroxidation, but its role in glioma cell death remains unclear. In this study, we found Pseudolaric acid B (PAB) inhibited the viabilities of glioma cells in vitro and in vivo, which was accompanied by abnormal increases of intracellular ferrous iron, H2O2 and lipid peroxidation, as well as depletion of GSH and cysteine. In vitro studies revealed that the lipid peroxidation and the cell death caused by PAB were both inhibited by iron chelator deferoxamine, but exacerbated by supplement of ferric ammonium citrate. Inhibition of lipid peroxidation with ferrostatin-1 or GSH rescued PAB-induced cell death. Morphologically, the cells treated with PAB presented intact membrane, shrunken mitochondria with increased membrane density, and normal-sized nucleus without chromatin condensation. Mechanistically, PAB improved intracellular iron by upregulation of transferrin receptor. The increased iron activated Nox4, which resulted in overproduction of H2O2 and lipid peroxides. Moreover, PAB depleted intracellular GSH via p53-mediated xCT pathway, which further exacerbated accumulation of H2O2 and lipid peroxides. Thus, PAB triggers ferroptosis in glioma cells and is a potential medicine for glioma treatment.
Copyright © 2018 Elsevier B.V. All rights reserved.
Ferroptosis; Glioma; Nox4; Pseudolaric acid B; xCT
Pseudolaric acid B triggers ferroptosis in glioma cells via activation of Nox4 and inhibition of xCT.
Wang Z1, Ding Y1, Wang X1, Lu S1, Wang C1, He C1, Wang L1, Piao M2, Chi G3, Luo Y1, Ge P4.
2018 Aug 1
High hepatitis B virus (HBV) load and chronic hepatitis B infection increase the risk of developing hepatocellular carcinoma (HCC), and is also associated with recurrence of HBV-related HCC. The aim of the present study was to investigate whether pseudolaric acid B (PAB), a diterpene acid isolated from the root and trunk bark of Pseudolarix kaempferi Gordon (Pinaceae), has an inhibitory role on the HBV secretion in HBV-related HCC. By detecting HBV surface antigen (HBsAg) by ELISA it was found that PAB inhibited HBV secretion in HepG2215 compared to control group, but did not decrease the intracellular HBV level, and the results were repeated in HepG2 cell transfect with HBV gene. Therefore, our results proved that PAB had the ability to inhibit HBV secretion. Moreover, it was shown that HepG2215 cells with HBV gene accumulated more in G0/G1 phase than HepG2 cells without HBV gene through detecting cell cycle distribution by flow cytometry, which indicated that HBV replication might favor the cell cycle environment of G0/G1 phase. However, HepG2 cells entered G2/M phase earlier than HepG2215 when PAB treatment induced G2/M arrest, therefore, HBV retarded the entry of G2/M to sustain the status of G0/G1 phase, while PAB finally changed the cell cycle environment favored by HBV virus. In addition, PAB also induced HepG2215 cell apoptosis, which would be helpful to kill the cells infected by HBV and help for devouring HBV by macrophage. Therefore, PAB inhibited HBV secretion through apoptosis and cell cycle arrest. The present findings contribute to a future potential chemotherapeutic drug in the treatment of HBV-related HCC.
Pseudolaric acid B inhibits the secretion of hepatitis B virus.
Yu J1, Wang Z2, Ren P3, Zhong T4, Wang Y5, Song F6, Hou J1, Yu X6, Hua S2.
Atherosclerosis is a progressive disease of large arteries characterized with chronic inflammation and aberrant immune response. Pseudolaric acid B (PB) has been found to exert multiple effects by inhibiting inflammatory response. However, there is no comprehensive assessment of the effects of PB on atherosclerosis using relevant in vivo and in vitro models.
MATERIAL AND METHODS:
Male ApoE-/- mice were treated with PB orally with a high fat diet (HFD) to clarify its anti-atherosclerotic activities. RAW264.7 macrophage line, a well-accepted cell model of atherosclerosis, was used to investigate anti-inflammatory effects and molecular mechanisms of PB.
PB significantly attenuated atherosclerotic lesions by modulating plasma lipid profiles as well as inhibiting inflammatory responses in macrophages of atherosclerotic mice. Meanwhile, PB markedly suppressed the expression of pro-inflammatory cytokines, and regulated cholesterol efflux related genes in oxidative low density lipoprotein (ox-LDL)-loaded macrophages. The cellular uptake of Dil-labeled ox-LDL was significantly inhibited by PB either. Moreover, the ability of PB to suppress nuclear factor kappa B (NF-κB) and activate peroxisome proliferator-activated receptor gamma (PPARγ) was confirmed using luciferase reporter assays. Conversely, the selective PPARγ antagonist GW9662 reversed the influence of PB in macrophages.
Together, these findings indicate that PB exerts its protective effects on atherosclerosis by inhibiting macrophage-mediated inflammatory response and cellular ox-LDL uptake, and promoting cholesterol efflux by suppressing NF-κB activation PPARγ-dependently. Therefore, PB may be a promising agent for inflammatory and atherosclerotic diseases.
Copyright © 2018. Published by Elsevier B.V.
Atherosclerosis; Inflammation; Macrophages; NF-κB; PPARγ; Pseudolaric acid B
Pseudolaric acid B attenuates atherosclerosis progression and inflammation by suppressing PPARγ-mediated NF-κB activation.
Li T1, Wang W2, Li YX3, Li X3, Ji WJ3, Ma YQ3, Chen H4, Zhao JH5, Zhou X6.