Background:
Pseudoginsenoside F11 (Ginsenoside A1), 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.
Biochemical experiments revealed that Pseudoginsenoside F11 (Ginsenoside A1) 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[1].
One in vivo model of cisplatin-induced acute renal failure was performed. The results showed that pretreatment with Pseudoginsenoside Pseudoginsenoside F11 (Ginsenoside A1) reduced cisplatin-elevated blood urea nitrogen and creatinine levels, as well as ameliorated the histophathological damage [1]. We tested the effects of Pseudoginsenoside Pseudoginsenoside F11 (Ginsenoside A1) 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 Pseudoginsenoside F11 (Ginsenoside A1) antagonized the development of behavioral sensitization and decrease of glutamate in the mPFC induced by morphine[3].
参考文献:
[1]. Wang H, et al. The pseudoginsenoside F11 ameliorates cisplatin-induced nephrotoxicity without compromising its anti-tumor activity in vivo. Scientific Reports [2014, 4:4986]
[2]. Li Zhu, et al. Pseudoginsenoside-F11 attenuates morphine-induced signalling in Chinese hamster ovary-μ cells. Neuroreport, 25 May 2001 - Volume 12 - Issue 7 - pp 1453-1456
[3]. Yue Hao, et al. Pseudoginsenoside-F11 decreases morphine-induced behavioral sensitization and extracellular glutamate levels in the medial prefrontal cortex in mice. Pharmacology Biochemistry and BehaviorVolume 86, Issue 4, April 2007, Pages 660–666
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