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At least 1,063 records · Page 59Linked to original sources
PubMed2002

A xylanase from roots of sanchi ginseng (Panax notoginseng) with inhibitory effects on human immunodeficiency virus-1 reverse transcriptase.

A xylanase with a molecular weight of 15 kDa, which is lower than those of previously reported xylanases, was isolated from the roots of the medicinal herb Panax notoginseng. The xylanase exhibits a temperature optimum of 50 degrees C and a pH optimum between 5 and 6. It inhibits HIV-1 reverse transcriptase with an IC(50) of 10 microM, but does not affect translation in a cell-free rabbit reticulocyte system when tested up to 70 microM. The enzyme is adsorbed on CM-cellulose, Affi-gel blue gel and Mono S. Previously xylanases have been isolated from seeds and not from roots, and have not been demonstrated to inhibit HIV-1 reverse transcriptase.

Chromatography↗
PubMed2000

Effect of ginsenosides, active components of ginseng, on capsaicin-induced pain-related behavior.

Our recent study demonstrated that ginsenosides had antinociceptive effects by reducing some types of pain-related behavior in mice (Yoon et al., 1998. Ginsenosides induce differential antinociception and inhibit substance P-induced nociceptive response in mice. Life Science 62, PL319-PL325). In the present study we further investigated whether ginsenosides produce antinociceptive effects through an action at central or peripheral site(s) and whether these effects are mediated by the opioid system. Intraperitoneally injected ginsenosides suppressed in a dose-dependent manner the pain-related behavior produced by capsaicin injection into the plantar surface of the hind paw; the ED(50) was 49 mg/kg [26-92 mg/kg, 95% confidence interval (C.I.)]. Intrathecally or intracerebroventricularly administered ginsenosides also suppressed the capsaicin-induced pain-related behavior in a dose-dependent manner; the ED(50)s were 1.72 mg/kg (0.8-3.72 mg/kg, 95% C.I.) and 1. 48 mg/kg (0.8-2.6 mg/kg, 95% C.I.), respectively. On the other hand, subcutaneously injected ginsenosides to the plantar surface prior to the capsaicin injection did not alter the pain-related behavior. Naloxone pretreatment was without effect in blocking the antinociceptive effect of intrathecally administered ginsenosides. Intraperitoneally injected ginsenosides also did not significantly affect the motor response of animals. These results suggest that ginsenosides produce antinociceptive effects through their action at the spinal and/or supraspinal site(s), not at nociceptors in the periphery. In addition, the results suggest that the antinociceptive effects are not mediated by opioid receptors.

Analgesics↗
PubMedDate not supplied

Majonoside-R2, a major constituent of Vietnamese ginseng, attenuates opioid-induced antinociception.

The effects of majonoside-R2 on antinociceptive responses caused by the mu-opioid receptor agonist morphine and the selective kappa-opioid receptor agonist U-50, 488H were examined by the tail-pinch test in mice. Intraperitoneal (IP) or intracerebroventricular (ICV) injection of majonoside-R2 (3.1-6.2 mg/kg, IP or 5-10 micrograms/mouse, ICV) and diazepam (0.1-0.5 mg/kg, IP or 0.5-1.0 microgram/mouse, ICV), as well as an opioid receptor antagonist naloxone (2 mg/kg, IP or 5 micrograms/mouse, ICV), dose-dependently attenuated the antinociception caused by subcutaneously administered morphine and U-50,488H. Moreover, when co-administered ICV or intrathecally (IT) with morphine (4 micrograms/mouse) or U-50,488H (60 micrograms/mouse), majonoside-R2 (5-20 micrograms/mouse) also exhibited antagonism against the antinociceptive action of these opioid receptor agonists in the tail-pinch test. The inhibitory effects of majonoside-R2 (10 micrograms/mouse, ICV) and diazepam (1 microgram/mouse, ICV) were reversed by flumazenil (2.5 micrograms/mouse, ICV), a selective benzodiazepine receptor antagonist, and picrotoxin (0.25 microgram/mouse, ICV), a GABA-gated chloride channel blocker. These results suggest that majonoside-R2 attenuates the opioid-induced antinociception by acting at the spinal and supraspinal levels, and that the GABAA receptor complex at the supraspinal level is involved in the effect of ICV administered majonoside-R2.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2002

Protective effect of ginsenosides, active ingredients of Panax ginseng, on kainic acid-induced neurotoxicity in rat hippocampus.

Ginsenosides are known to attenuate glutamate-induced cell injuries in vitro. We investigated the in vivo effect of ginsenosides on kainic acid (KA)-induced neurotoxicity in rat hippocampus using the methods of acid fuchsin (AF) staining and heat-shock protein-70 (HSP-70) immunoreactivity to detect neuronal death and stress, respectively. Pretreatment of ginsenosides (50 or 100 mg/kg for 7 days) via intraperitoneal (i.p.) administration significantly attenuated KA (10 mg/kg i.p.)-induced cell death by decreasing AF-positive neurons in both CA1 and CA3 regions of rat hippocampus compared with KA treatment alone. Pretreatment of ginsenosides (50 or 100 mg/kg for 7 days) via i.p. administration also significantly suppressed KA-induced induction of HSP-70 in both regions of rat hippocampus. These results show that ginsenosides are effective in protecting hippocampal CA1 and CA3 cells against KA-induced neurotoxicity.

Animals↗
PubMed1998

Modulation of American ginseng on brainstem GABAergic effects in rats.

Single neurons in the region of the medial nucleus tractus solitarius (NTS), responding or not responding to gastric vagal branch stimulation, were recorded in an in vitro neonatal rat brainstem-gastric preparation. The spontaneous activity of the majority of these two types of NTS units was inhibited by GABA(A) receptor agonist, muscimol (30 microM), and this inhibition (approximately 52% compared to 100% of the control level) could be antagonized by selective GABA(A) receptor antagonist, bicuculline (10 microM). Application of Panax quinquefolium L. extracts (3.0 microg/ml) into the brainstem compartment of the preparation also significantly reduced the discharge rate of these NTS neurons (approximately 27% compared to the control level), but this reduction could not be reversed by bicuculline (10 microM). Pretreatment with Panax quinquefolium L. (3.0 microg/ml) significantly decreased the NTS inhibitory effects induced by muscimol (30 microM), approximately from 51 to 33%. Our results demonstrated the interactions of Panax quinquefolium L. with ligand-bindings of GABA(A) receptors, and the modulation of the brainstem GABAergic mechanism by Panax quinquefolium L. Our data suggest that the regulation of GABAergic neurotransmission may be an important action of Panax quinquefolium L.

Animals↗
PubMed2001

Isolation of a small chitinase-like antifungal protein from Panax notoginseng (sanchi ginseng) roots.

An antifungal protein, with a molecular weight of 15 kDa and an N-terminal sequence analogous to those of chitinases, was first isolated from the Chinese medicinal material Panax notoginseng, using cation exchange chromatography and affinity chromatography. The protein was adsorbed on CM-cellulose, Affi-gel Blue Gel and Mono S. It exerted antifungal activity against Coprinus comatus, Fusarium oxysporum and Mycosphaerella arachidicola but not against Rhizoctonia solani. The protein was devoid of ribonuclease activity against yeast tRNA.

Amino Acid Sequence↗