White crystalline powder
(3β,6α,12β,24R)-3,12,25-Trihydroxy-20,24-epoxydammaran-6-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-mannopyranoside/pseudo-ginsenoside-Fll/GINSENOSIDE A1/β-D-Mannopyranoside, (3β,6α,12β,24R)-20,24-epoxy-3,12,25-trihydroxydammaran-6-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-/(3b,6a,12b,24R)-20,24-Epoxy-3,12,25/PSEUDOGINSENOSIDE/Pseuginsenoside F11/(24R)-Pseudoginsenoside F11/24(S)-pseudo-ginsenoside-F11/Pseudoginsenoside FII/Pseudoginsenoside-F11/Pseuginsensoside F11/Pseudoginsenoside F11
885.3±65.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:69884-00-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Pseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside, has been reported to exert wide-ranging neuroprotective properties. The aim of this study was to investigate the effect and potential mechanisms of PF11 on the autophagic/lysosomal pathway following ischemic stroke.
Male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO). Cerebral ischemia outcome, TUNEL staining, Fluoro-Jade B staining were carried out 24 hours poststroke. The autophagic/lysosomal-related proteins were measured.
A single administration of PF11 significantly decreased the infarct area, reduced the brain water content, and improved neurological functions, even 4 hours after the onset of pMCAO. Meanwhile, PF11 lessened the ischemic insult-mediated loss of neurons and activation of astrocytes and microglia. Furthermore, PF11 attenuated pMCAO-induced accumulations of autophagosomes and apoptosis. We further observed a remarkable effect of PF11 in reversing the ischemic insult-induced accumulation of autophagosomes (LC3-II) and abnormal aggregation of autophagic proteins (SQSTM1 and ubiquitin). Furthermore, PF11 was capable of improving lysosomal function and lysosome/autophagosome fusion following pMCAO, and this change was reversed by the lysosomal inhibitor chloroquine. Also, the improvement of ischemic outcome and the antiapoptotic effect induced by PF11 was reversed by CQ.
These findings indicate that the autophagic flux is impaired in a rat model of pMCAO, and that PF11 exerts an excellent protective effect against ischemic stroke by alleviating autophagic/lysosomal defects.
© 2017 John Wiley & Sons Ltd.
PF11; apoptosis; autophagic/lysosomal defects; permanent cerebral ischemia
Pseudoginsenoside-F11 attenuates cerebral ischemic injury by alleviating autophagic/lysosomal defects.
Liu YY1, Zhang TY1, Xue X2, Liu DM1, Zhang HT1, Yuan LL1, Liu YL1, Yang HL1, Sun SB1, Zhang C1, Xu HS1, Wu CF1, Yang JY1.
Pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, has been reported to have anti-inflammatory properties, but the effects of PF11 on acute lung inflammation were unknown. The present study aimed to investigate the protective effects and potential mechanisms of PF11 on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in male BALB/c mice. After being treated with PF11 (3, 10, and 30 mg/kg, intravenous) once a day for 3 consecutive days, the mice were challenged by intratracheal instillation of LPS, and then their lung tissues and bronchoalveolar lavage fluid (BALF) were collected for further analysis. The results showed that PF11 attenuated LPS-induced ALI, with alleviated histopathological damage, decreased lung wet/dry weight ratio, and reduced protein concentration and inflammatory cells number in BALF. Moreover, PF11 reversed the LPS-induced increases of mRNA expression and protein levels of interleukin-6, tumor necrosis factor-α, and interleukin-1β. Meanwhile, PF11 decreased LPS-induced myeloperoxidase activity and neutrophil infiltration in lung tissue by reducing the expression of macrophage inflammatory protein-2 and intercellular adhesion molecule-1, as well as enhanced neutrophil clearance by accelerating neutrophils apoptosis and their phagocytosis by alveolar macrophages. In conclusion, these results indicated that PF11 significantly attenuated LPS-induced ALI through suppressing neutrophil infiltration and accelerating neutrophil clearance, suggesting its potential in the treatment of ALI.
acute lung injury; lipopolysaccharide; neutrophil; pseudoginsenoside-F11
Pseudoginsenoside-F11 Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Suppressing Neutrophil Infiltration and Accelerating Neutrophil Clearance.
Wang P1, Hou Y2, Zhang W2, Zhang H2, Che X2, Gao Y2, Liu Y2, Yang D2, Wang J2, Xiang R1, Zhao M3, Yang J4,5.
Calcium overload has been reported to trigger neuronal death following stroke. Pseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside with various neuroprotective activities, has displayed therapeutic efficacy against permanent ischemic stroke. The present study examined the protective potential of PF11 in rats subjected to 2-h transient middle cerebral artery occlusion (tMCAO) and in cultured primary cortical neuron (PCN) exposed to oxygen-glucose deprivation/reoxygenation (OGD/R). Single intravenous administration of PF11 (12 mg/kg) significantly reduced infarct volume, brain edema, neurological deficit and cortex neuron loss at 24 h after reperfusion. Immunoblotting and immunofluorescence demonstrated that PF11 inhibited the over activation of μ-Calpain and the reduction of calcium calmodulin kinase II-α, reduced the degradation of sarcoplasmic/endoplasmic reticulum ATPase-2 and alleviated endoplasmic reticulum stress (ERS) in tMCAO rats. What’s more, rats treated with PF11 (12 mg/kg) intravenously immediately after reperfusion, and then intraperitoneally every 24 h for 14 days exhibited lessened cortex neuron loss, reduced mortality and improved performances of rotarod, grip strength and gait patterns at 1, 4, 7, and 14 days after tMCAO. Furthermore, in vitro investigations showed PF11 increased cell viability, reduced neurites decline, restored ATP level and decreased calcium content in cultured PCN under OGD/R. Moreover, PF11 alleviated ERS, reversed the diminished levels of NMDA-2B subunit, postsynaptic density protein 95 and neuronal nitric oxide synthase both in vivo and in vitro. Our study indicates that PF11 produced neuroprotection and improved long-term outcomes while repressing calcium overload in model of transient focal ischemia, suggesting that PF11 might be a considerable candidate for stroke treatment.
Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.
calcium overload; cerebral ischemia; endoplasmic reticulum stress; neuronal nitric oxide synthase; pseudoginsenoside-F11; μ-calpain
Pseudoginsenoside-F11 Protects against Transient Cerebral Ischemia Injury in Rats Involving Repressing Calcium Overload.
Zhang T1, Wu C1, Yang X1, Liu Y1, Yang H1, Yuan L1, Liu Y1, Sun S1, Yang J2.
2019 Jul 15
Pseudoginsenoside-F11 (PF11), a component of Panax quinquefolium (American ginseng), has been demonstrated to antagonize the learning and memory deficits induced by scopolamine, morphine and methamphetamine in mice. IC50 value: Inhibition of diprenorphine binding with an IC50 of 6.1 μM Target:In vitro: Biochemical experiments revealed that PF11 could inhibit diprenorphine (DIP) binding with an IC50 of 6.1 μM and reduced the binding potency of morphine in Chinese hamster ovary (CHO)-μ cells .In vivo: One in vivo model of cisplatin-induced acute renal failure was performed. The results showed that pretreatment with Pseudoginsenoside F11 reduced cisplatin-elevated blood urea nitrogen and creatinine levels, as well as ameliorated the histophathological damage . We tested the effects of Pseudoginsenoside F11 on morphine-induced development of behavioral sensitization and alterations in glutamate levels in the medial prefrontal cortex (mPFC) in freely moving mice by using in vivo microdialysis. As the results shown, Pseudoginsenoside F11 antagonized the development of behavioral sensitization and decrease of glutamate in the mPFC induced by morphine .