root of Kaempferia galangal L.
4'-O-Methylkaempferol/Kaempferol 4'-methyl ether/3,5,7-trihydroxy-2-(4-methoxyphenyl)chromen-4-one/3,5,7-Trihydroxy-2-(4-methoxyphenyl)-4H-chromen-4-one/3,5,7-trihydroxy-4'-methoxyflavone/Kaempferid/Kaempferide/3 5 7-trihydroxy-4'-methoxyflavone/4'-Methoxy-3,5,7-trihydroxyflavone/4H-1-Benzopyran-4-one, 3,5,7-trihydroxy-2-(4-methoxyphenyl)-/3,5,7-trihydroxy-4′-methoxyflavone/4'-Methylkaempferol
Methanol; Chloroform; DMSO
543.8±50.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:491-54-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
The aim of this study is to investigate both the efficacy and mechanism of action of kaempferide (Kae) as a therapy for the treatment of cardiovascular disease. A rat model of myocardial ischemia/reperfusion (I/R) injury was established by ligation of the left anterior descending coronary artery for 30 min followed by a 2 h perfusion. In our study, we show that Kae remarkably improved cardiac function, alleviated myocardial injury via a decrease in myocardial enzyme levels, and attenuated myocardial infarct size in a dose-dependent manner. In addition, preconditioning treatment with Kae was found to significantly decrease serum TNF-α, IL-6, C-reactive protein (CRP), MDA, and ROS levels, while it was found to increase serum levels of SOD. Nuclear factor erythroid 2-related factor 2 (Nrf2) and cleaved caspase-3 expression levels were observed to be downregulated, while phospho-Akt (p-Akt) and phospho-glycogen synthase kinase-3β (p-GSK-3β) expression levels were upregulated. However, cotreatment with LY294002 (a PI3K inhibitor) or TDZD-8 (a GSK-3β inhibitor) was found to abolish the above cardioprotective effects observed with the Kae treatment. The data presented in this study provides evidence that Kae attenuates I/R-induced myocardial injury through inhibition of the Nrf2 and cleaved caspase-3 signaling pathways via a PI3K/Akt/GSK 3β-dependent mechanism.
Kaempferide Protects against Myocardial Ischemia/Reperfusion Injury through Activation of the PI3K/Akt/GSK-3β Pathway.
Wang D1, Zhang X1, Li D2, Hao W2, Meng F3, Wang B2, Han J2, Zheng Q2
Kaempferide (KF) is an O-methylated flavonol, a natural plant extract, which is often found in Kaempferia galanga. It has a variety of effects including anti-carcinogenic, anti-inflammatory, anti-oxidant, anti-bacterial and anti-viral properties. In this study, we aimed to investigate whether KF effectively inhibits titanium particle induced calvarial bone loss via down regulation of the JNK signaling pathway. In the mice with titanium particle induced calvarial osteolysis, the Low dose of KF mildly reduced the resorption pits while in the high dose group, fewer scattered pits were observed on the surface of calvarium. Histological examination showed fewer osteoclasts formation in the KF group. In mouse bone marrow macrophages (BMMs) and RAW264.7 cells, KF significantly inhibited the osteoclast formation and bone resorption at 12.5 μM. However, KF does not affect the mature osteoclast F-actin ring formation. But when being co-treated with KF and anisomycin, BMMs differentiated into mature osteoclasts. At the molecular levels, the JNK phosphorylation was inhibited and the osteoclastogenesis-related specific gene expression including V-ATPase d2, TRAP, calcitonin receptor (CTR), c-Fos and NFATc1 was markedly suppressed. In conclusion, these results indicated that KF is a promising agent in the treatment of osteoclast-related diseases.
Kaempferide Prevents Titanium Particle Induced Osteolysis by Suppressing JNK Activation during Osteoclast Formation.
Jiao Z1, Xu W1, Zheng J1, Shen P1, Qin A2, Zhang S3, Yang C4
2017 Nov 30
Kaempferide (KF) is a compound of flavonoids from Alpinae oxyphylla Miq, and the herb itself is used as a classical tonic agent. This paper aims to investigate the effects of KF on cognitive function impairment and neurodegeneration in the mouse model of Alzheimer’s disease induced by intracerebroventricular (ICV) injection of Aβ1-42 . The mice were treated with KF at doses of 0.02 and 0.2 mg/kg/day (ICV) for five consecutive days after Aβ1-42 exposures. The behavioral test results showed that KF could prevent cognitive decline in mice induced by Aβ1-42 as assessed by the locomotor activity test, Y-maze test, and Morris water maze test. Furthermore, the activities of superoxide dismutase and malondialdehyde in the hippocampus and cerebral cortex were elevated by KF administration. Results of hippocampus slices showed that neurons were integrated and regularly arranged in the groups, which were administered along with KF. In addition, we found KF could boost brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element-binding (CREB) protein signal in the hippocampus. All results illustrated that KF could exert neuroprotective effects at least partly through alleviating oxidative stress and enhancing the BDNF/TrkB/CREB pathway in Aβ1-42 -induced mice.
© 2019 John Wiley & Sons, Ltd.
Alzheimer's disease; BDNF/TrkB/CREB; kaempferide; oxidative stress
Kaempferide prevents cognitive decline via attenuation of oxidative stress and enhancement of brain-derived neurotrophic factor/tropomyosin receptor kinase B/cAMP response element-binding signaling pathway.
Yan T1, He B1, Xu M2, Wu B1, Xiao F1, Bi K3, Jia Y1.
Kaempferide is an O-methylated flavonol, a type of chemical compound. It can be found in Kaempferia galanga (aromatic ginger). The enzyme kaempferol 4'-O-methyltransferase uses S-adenosyl-L-methionine and kaempferol to produce S-adenosyl-L-homocysteine and kaempferide. P-glycoproteins.