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Arch Pharm Res. 2011 Jun;34(6):971-8. Epub 2011 Jul 2.
Rhododendrin, an analgesic/anti-inflammatory arylbutanoid glycoside, from the leaves of Rhododendron aureum.
Kim MH, Nugroho A, Choi J, Park JH, Park HJ.
Department of Pharmaceutical Engineering, Sangji University, Wonju, 220-702, Korea.
To identify an analgesic/anti-inflammatory component from the leaves of Rhododendron aureum (Ericaceae), phytochemical isolation and pharmacological assays (writhing assays and vascular permeability assay for analgesic action in mice; carrageenan-induced paw edemaand TPA-induced ear edema assays of anti-inflammatory action in rats) were performed. Four compounds were isolated from the active fraction (BuOH fraction) by silica gel column chromatography and identified as (-)-rhododendrol, (-)-rhododendrin, avicularin and hyperoside by spectroscopic methods. Rhododendrin, the main compound of the BuOH fraction, exhibited significant analgesic actions in mice and anti-inflammatory actions in rats. This compound accounted for 3.1% of the MeOH extract and 0.48% of dried leaves, respectively, on HPLC analysis. These results suggest that rhododendrin is the major biologically active substance in the leaves of R. aureum with analgesic/anti-inflammatory activity.
Pharmacol Rep. 2010 Sep-Oct;62(5):949-55.
Anti-apoptotic effects of hyperoside via inhibition of NR2B-containing NMDA receptors.
Zhang XN, Li JM, Yang Q, Feng B, Liu SB, Xu ZH, Guo YY, Zhao MG.
Department of Pharmacology, School of Pharmacy, TangDu Hospital, Fourth Military Medical University, Xi'an 710032, China.
Hyperoside (Hyp) is a flavonoid compound isolated from a folk remedy, Rhododendron ponticum L. leaves. It has been shown to have neuroprotective effects both in vivo and in vitro. However, little is known about the effects of Hyp on the neuronal apoptosis induced by glutamate. The present study showed that Hyp significantly attenuated, in a concentration-dependent manner, the apoptosis induced by the exposure of cultured neurons to NMDA. Western blot analysis revealed that Hyp antagonized the expression of excess NR2B-containing NMDA receptors; however, it had no effect on the expression of NR2A-containing NMDA receptors. Our results demonstrate that the neuroprotective effect of Hyp owes, at least partially, to its differential modulation of NR2A- and NR2B-containing NMDA receptors.