Chemical constituents and biological activities of Viburnum macrocephalum f. keteleeri.

Three new compounds (1-3) and seven known compounds (4-10) have been isolated from the ethanolic extract of Viburnum macrocephalum f. keteleeri using bioactivity-guided fractionation and identified as methyl (2-α-L-rhamnopyranosyloxy)acetate (1), methyl (2R-3-α-L-rhamnopyranosyloxy)glycerate (2), methyl (3R-4-α-L-rhamnopyranosyloxy-3-hydroxy)butanoate (3), bridelionoside B (4), (6S,7E,9R)-roseoside (5), linarionoside A (6), 3,7,11-trimethyl-1,6-dodecadien-3,10,11-triol (7), (+)-8-hydroxylinalool (8), ß-sitosterol (9) and daucosterol (10). The structures of 1-3, including absolute configurations, were determined by spectroscopic data (1H and 13C NMR, HSQC, HMBC and ORD) and chemical methods. In addition, compounds 1-8 were assayed for their insecticidal and antimicrobial activities. Compounds 7 and 8 exhibited moderately insecticidal effects against Mythimna separata with LD50 values of 180 and 230 µg g-1, respectively. Compounds 2, 3, 7 and 8 showed varying antimicrobial activities with IC50 values ranging from 125 to 529 µM.

Insecticidal and α-glucosidase inhibitory activities of chemical constituents from Viburnum fordiae Hance.

The ethanolic extract of the stems of Viburnum fordiae Hance showed insecticidal and α-glucosidase inhibitory activities and then was fractionated by bioactivity-guided fractionation to obtain a rare C13-norisoprenoid (1), together with a new phenolic glycoside (2), and seven known compounds, alangionoside C (3), pisumionoside (4), koaburaside (5), 3,5-dimethoxy-benzyl alcohol 4-O-ß-d-glucopyranoside (6), 3,4,5-trimethoxybenzyl-ß-d-glucopyranoside (7), arbutin (8), and salidroside (9). The previously undescribed compounds were elucidated as (3R,9R)-3-hydroxy-7,8-didehydro-ß-ionyl 9-O-α-d-arabinopyranosyl-(1→6)-ß-d-glucopyranoside (1) and 2-(4-O-ß-d-glucopyranosyl)syringylpropane-1,3-diol (2) by spectroscopic data (1H and 13C NMR, HSQC, HMBC, 1H-1H COSY, HSQC-TOCSY, HRESIMS, IR and ORD) and chemical methods. Compound 1 showed potent insecticidal effect against Mythimna separata with LD50 value of 140 µg g-1. Compounds 2, 5, 6, 8 and 9 showed varying α-glucosidase inhibitory activity with IC50 values ranging from 148.2 to 230.9 µM.

Effect of arginine vasopressin on acupuncture analgesia in the rat.

Arginine vasopressin (AVP) has been proven to be involved in the process of pain regulation. This communication was designed to investigate the effect of AVP on acupuncture analgesia in the rat model. The results showed that intraventricular injection (icv) of AVP could enhance acupuncture analgesia in a dose-dependent manner, whereas icv of anti-AVP serum decreased acupuncture analgesia. However, neither intrathecal (ith) nor intravenous injection (iv) of AVP or anti-AVP serum could influence acupuncture analgesia. Electrical acupuncture of "Zusanli" points (St. 36) decreased AVP concentration in the hypothalamic paraventricular nucleus (PVN), and increased AVP concentration in the hypothalamic supraoptic nucleus (SON), periaqueductial gray (PAG), caudate nucleus (CdN) and raphe magnus nucleus (RMN), but did not change AVP concentration in the pituitary, spinal cord and plasma. The effect of AVP on acupuncture analgesia was partly reversed by pretreatment with naloxone, an opiate receptor antagonist. These data suggested that AVP in the brain played a role in the process of acupuncture analgesia in combination with the endogenous opiate peptide system.

Effect of hypothalamic supraoptic nucleus on acupuncture analgesia in the rat.

Hypothalamic supraoptic nucleus (SON) has been demonstrated to involve in pain modulation. Acupuncture analgesia is a very useful clinical skill for pain relief, which has over 2500-year history in China. The present study investigated the effect of SON on acupuncture analgesia in the rat. Electrical stimulation of the SON or microinjection of a small dose L-glutamate sodium into the SON enhanced acupuncture analgesia in a dose-dependent manner, while cauterization of the SON weakened acupuncture analgesia. Pituitary removal did not influence the effect of L-glutamate sodium that enhanced acupuncture analgesia in the SON. The data suggested that the neurons and not the nerve fibers in the SON played an important role in acupuncture analgesia, which effect might be through the central nervous system rather than the hypothalamo-neurohypophyseal system.

Effect of oxytocin on acupuncture analgesia in the rat.

Oxytocin has been demonstrated to be involved in pain modulation. Acupuncture analgesia is a very useful clinical tool for pain relief, which has over 2500-year history in China. The present study investigated the role of oxytocin in acupuncture analgesia in the rat through oxytocin administration and measurement. Central administration of oxytocin (intraventricular injection or intrathecal injection) enhanced acupuncture analgesia, while central administration of anti-oxytocin serum weakened acupuncture analgesia in a dose-dependent manner. However, intravenous injection of oxytocin or anti-oxytocin serum did not influence acupuncture analgesia. Electrical acupuncture of "Zusanli" (St. 36) reduced oxytocin concentration in the hypothalamic supraoptic nucleus, and elevated oxytocin concentration in the hypothalamic suprachiasmatic nucleus, hypothalamic ventromedial nucleus, thalamic ventral nucleus, periaqueductal gray, raphe magnus nucleus, caudate nucleus, thoracic spinal cord and lumbar spinal cord, but did not alter oxytocin concentration in the hypothalamic paraventricular nucleus, anterior pituitary, posterior pituitary and plasma. The data suggested that oxytocin in central nervous system rather than in peripheral organs is involved in acupuncture analgesia.

Only arginine vasopressin, not oxytocin and endogenous opiate peptides, in hypothalamic paraventricular nucleus play a role in acupuncture analgesia in the rat.

Our previous study proved that hypothalamic paraventricular nucleus (PVH) plays an important role in acupuncture analgesia. The effect of acupuncture on the concentrations of arginine vasopressin (AVP), oxytocin (OXT), leucine-enkephaline (L-Ek), beta-endorphin (beta-Ep) and dynorphinA(1-13) (DynA(1-13)) was investigated in rat PVH. Electrical acupuncture of "Zusanli" points (St. 36) 30 min increased the AVP, not OXT, L-Ek, beta-Ep and DynA(1-13) concentrations in PVH tissue using micropunch and radioimmunoassay, which showed a negative relationship between the pain threshold and AVP concentrations in PVH tissue. Electrical acupuncture could elevate the AVP concentrations in PVH perfuse liquid during acupuncture, and then reduce the AVP concentrations in PVH perfuse liquid after acupuncture. But no change in OXT, L-Ek, beta-Ep and DynA(1-13) concentrations was detected in PVH perfuse liquid. Electrical acupuncture decreased the number of AVP, not OXT, L-Ek, beta-Ep and DynA(1-13) immunoreactive cells in PVH using immunocytochemistry. The results suggested that only AVP, not OXT and endogenous opiate peptides in PVH involved acupuncture analgesia in the rat.

Through central arginine vasopressin, not oxytocin and endogenous opiate peptides, glutamate sodium induces hypothalamic paraventricular nucleus enhancing acupuncture analgesia in the rat.

Our previous study proved that the hypothalamic paraventricular nucleus (PVH) plays an important role in acupuncture analgesia. The neuropeptides involving in the PVH regulation of acupuncture analgesia was investigated in the rat. The changes of pain threshold, which was induced by electrical acupuncture of "Zusanli" points (St. 36), were measured as acupuncture analgesia. Microinjection of l-glutamate sodium into the PVH, which only excites the PVH neurons, could dose-dependently enhance the acupuncture analgesia, but microinjection of l-glutamate sodium into the area nearby the PVH did not alter acupuncture analgesia. Removing pituitary did not influence this effect of l-glutamate sodium. Microinjection of l-glutamate sodium into the PVH only increased the arginine vasopressin (AVP), not oxytocin (OXT), leucine enkephaline (L-Ek), beta-endorphine (beta-Ep) and dynorphinA(1-13) (DynA(1-13)) concentrations in the PVH perfuse liquid using radioimmunoassay. Intraventricular injection of anti-arginine vasopressin serum (AAVPS) could completely reverse the effect of microinjection of l-glutamate sodium into the PVH enhancing acupuncture analgesia. Intraventricular injection of naloxone, one opiate peptide antagonist, partly attenuated this effect of l-glutamate sodium, and intraventricular of anti-oxytocin serum (AOXTS) did not change this effect of l-glutamate sodium. The results suggested that l-glutamate sodium induces the PVH enhancing acupuncture analgesia only through AVP, not OXT and endogenous opiate peptides in central nervous system.