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At least 379 records · Page 21Linked to original sources
PubMed1982

Protective effect of saikosaponin-d isolated from Bupleurum falcatum L. on CCl4-induced liver injury in the rat.

The effects of saikosaponin-d extracted from the roots of Bupleurum falcatum L. on carbon tetrachloride-induced hepatic injury were studied in rats. Pretreatment with saikosaponin-d produced a remarkable inhibitory action on acute hepatic injury by CCl4. A significant inhibition of lipid peroxidation induced by an acute dose of CCl4 in the liver of rats pre-treated with saikosaponin-d was also noted. Continuous injection of CCl4 caused liver cirrhosis in rats but the severity of cirrhosis was reduced in rats treated simultaneously with CCl4 and saikosaponin-d.

Animals↗
PubMed1998

Production of antibody against saikosaponin a, an active component of bupleuri radix.

High titer rabbit polyclonal antibodies (pAbs) which show a specificity for saikosaponin a (SSA), have been generated. The immunogen used was a conjugate of SSA linked through its glucose moiety to bovine serum albumin by periodate oxidation method. The antibody titers obtained from two rabbits, inoculated with the immunogen, reached a plateau after the fourth and third booster injection, respectively. The specificity of the pAbs was determined by hapten inhibition assays using several SSA-like structures. SSA competitively inhibited the binding of the rabbit anti-SSA pAbs to SSA-ovalbumin on solid phase, a coated antigen on the well. The antibodies showed high specificity to SSA, exhibiting no significant cross-reactivity with any of SSA analogues tested.

Animals↗
PubMed2003

Differential effect of bovine serum albumin on ginsenoside metabolite-induced inhibition of alpha3beta4 nicotinic acetylcholine receptor expressed in Xenopus oocytes.

Ginsenosides, major active ingredients of Panax ginseng, that exhibit various pharmacological and physiological actions are transformed into compound K (CK) or M4 by intestinal microorganisms. CK is a metabolite derived from protopanaxadiol (PD) ginsenosides, whereas M4 is a metabolite derived from protopanaxatriol (PT) ginsenosides. Recent reports shows that ginsenosides might play a role as pro-drugs for these metabolites. In present study, we investigated the effect of bovine serum albumin (BSA), which is one of major binding proteins on various neurotransmitters, hormones, and other pharmacological agents, on ginsenoside Rg2-, CK-, or M4-induced regulation of alpha3beta4 nicotinic acetylcholine (ACh) receptor channel activity expressed in Xenopus oocytes. In the absence of BSA, treatment of ACh elicited inward peak current (I(ACh)) in oocytes expressing alpha3beta4 nicotinic ACh receptor. Co-treatment of ginsenoside Rg2, CK, or M4 with ACh inhibited I(ACh) in oocytes expressing (alpha3beta4 nicotinic ACh receptor with reversible and dose-dependent manner. In the presence of 1% BSA, treatment of ACh still elicited I(ACh) in oocytes expressing alpha3beta4 nicotinic ACh receptor and co-treatment of ginsenoside Rg2 or M4 but not CK with ACh inhibited I(ACh) in oocytes expressing alpha3beta4 nicotinic ACh receptor with reversible and dose-dependent manner. These results show that BSA interferes the action of CK rather than M4 on the inhibitory effect of I(ACh) in oocytes expressing alpha3beta4 nicotinic ACh receptor and further suggest that BSA exhibits a differential interaction on ginsenoside metabolites.

Acetylcholine↗
PubMed2004

Role of the Fas/Fas ligand death receptor pathway in ginseng saponin metabolite-induced apoptosis in HepG2 cells.

This research team found in previous studies, that the ginseng saponin metabolite IH901 induces apoptosis in HepG2 cells via a mitochondrial-mediated pathway, which resulted in the activation of caspase-9 and subsequently of caspase-3 and -8. Based on these results, the involvement of the Fas/Fas ligand (FasL) death-receptor pathway, in IH901-induced apoptosis in HepG2 cells, was investigated. Levels of Fas and the Fas ligand (FasL) mRNA or protein were not increased by IH901, rather they were decreased significantly at 18 h post treatment. Soluble FasL (sFasL) was detectable by immunoprecipitation analysis in the medium of HepG2 cells treated with IH901. Increased levels of sFasL were inversely correlated with the levels of FasL. Preincubation of HepG2 cells with antagonistic anti-Fas antibody showed little protective effect, if any, on IH901-induced cell death. At a 30 microM (24 and 48 h) and 40 microM (24 h) concentration of IH901, the cytotoxic effect of IH901 was less then 50%, anti-Fas antibody prevented IH901-induced cell death. However, at a 60 microM (24 and 48 h) and 40 microM (48 h) concentration of IH901, cell death rates were about 80% or more and most of the chemopreventive and chemotherapeutic effects of IH901 were manifested. Blocking the Fas receptor did not influence IH901-induced cell death. These results indicate that the Fas/FasL system is engaged, but not required for IH901-induced cell death, at pharmacologically significant concentrations.

Apoptosis↗
PubMed1980

American ginseng. III. Pharmacokinetics of ginsenosides in the rabbit.

The pharmacokinetics of ginsenosides A1, A2, B2, and C were studied in rabbits and were best described with a one-component open model. Ginsenoside C (protopanaxadiol group ginseng saponin) showed a significantly longer half-life, higher plasma protein binding, and lower metabolic and renal clearance than ginsenosides A1, A2, and B2 (protopanaxatriol group ginseng saponins). All ginsenosides except ginsenoside A1 were slowly absorbed after intraperitoneal administration. Ginsenosides were not found in rabbit plasma or urine samples after oral administration. The observed differences in the pharmacokinetics of the ginsenosides may be ascribed to differences in protein binding. Ginsenoside C was more toxic than ginsenoside A2 after intraperitoneal administration to mice. Toxicity was not observed after oral administration of any of the ginsenosides. The genins, panaxadiol and panaxatriol, were more toxic and had larger volumes of distribution than the ginsenosides.

Animals↗
PubMed2001

Efficient production of saikosaponins in Bupleurum falcatum root fragments combined with signal transducers.

An efficient system to produce saikosaponins (saikosaponin-a and -d) in Bupleurum falcatum adventitious root fragments combined with signal transducers was developed. The roots are heterogeneous in terms of size and shape and sometimes form aggregates during cultivation. When the roots were cut to lengths of about 5 mm using a scalpel and cultivated, the root fragments did not form the aggregates, and root growth and saikosaponin production were not inhibited. After screening various signal transducers, it was clear that methyl jasmonate (MeJA) markedly promoted saikosaponin production. By comparing the effect of MeJA and related substances on saikosaponin production, we conclude that both the pentenyl and carboxylmethyl group of MeJA play an important role in the promotion of saikosaponin production. Addition of both 100 microM MeJA and 20 mM CaCl2 to the medium stimulated the content of saikosaponin in the root, with levels reaching 31.7 mg/g-dry root for 15 days of cultivation. A large amount of root fragments were prepared using a blender and cultivated (23 g-dry root/l) with 400 microM MeJA and 20 mM CaCl2, resulting in a high concentration of saikosaponins (747.3 mg/l).

Acetates↗
PubMed1983

Spectrophotometric determination of lantadene A, 22 beta-angeloyloxy-3-oxoolean-12-en-28-oic acid.

The formation of a blue chromogen between sodium borohydride-treated lantadene A (22 beta-angeloyloxy-3-oxoolean-12-en-28-oic acid) and acetic anhydride-sulfuric acid (9:1) formed the basis of a spectrophotometric method for its quantitation. The chromogen had a broad absorption maximum (lambda max) at 630-645 nm. The optimum amount of sodium borohydride for lantadene A reduction was 1 mg/mg lantadene A in methanolic solution. The chromogen was stable for 5, 7, and 26 min after reaction at 25, 18, and 0 degree C, respectively. The method is convenient, sensitive, and reproducible. The amount of lantadene A in the leaves of Lantana camara collected in the month of May quantitated by the present method was found to be 13.6 mg/g dry weight of the leaves.

Oleanolic Acid↗
PubMed1984

Homogeneous enzyme immunoassay of diosgenin and its glycosides.

Homogeneous enzyme immunoassay has been used as a tool for the determination of diosgenin and its glycosides in plants. Diosgenin antisera was found to inhibit the activity of diosgenin hemisuccinate-horseradish peroxidase conjugate which was reversed by the addition of free diosgenin or its glycosides. The increase of enzyme activity was proportional to the quantity of the hapten over a certain range of hapten concentration. Thus, a minimum of 2.5 micrograms/ml of diosgenin and 11.5 micrograms/ml of diosgenin glycosides could be determined by this method. The results were comparable with those obtained by high-performance liquid chromatography and gravimetric methods.

Chromatography, High Pressure Liquid↗
PubMed1986

Anti-inflammatory effect of saikogenin A.

Saikogenin A, an anti-inflammatory drug, is present in the crude extract of a Chinese herbal plant called Tsai-Fu. Saikogenin A was less effective in adrenalectomized rats than in normal rats in reducing the carrageenin-induced edema. Serum corticosterone and ACTH were increased in the saikogenin A-treated rats, supporting the view that stimulation of hypothalamopituitary-adrenal system is responsible for the anti-inflammatory effect of saikogenin A. This is further supported by the findings that saikogenin A did not affect the spontaneous release of corticosterone but it facilitated the ACTH-induced release. In addition, cyclic AMP in isolated pituitary and adrenal glands was increased by saikogenin A. A role for cyclic AMP as the second messenger is thus considered. Otherwise, the direct action of saikogenin A on the process of inflammation cannot be ruled out because saikogenin A also functioned in the adrenalectomized rats and it inhibited the release of histamine induced by compound 48/80. Reduction of the vascular permeability was also observed in the saikogenin A-treated rats. These results suggest that the anti-inflammatory action of saikogenin A are due to an increase in corticosterone caused by the release of ACTH and a direct effect on the process of inflammation.

Adrenocorticotropic Hormone↗
PubMed1986

Effects of saikosaponin-d on aminonucleoside nephrosis in rats.

The effects of saikosaponin-d extracted from the roots of Bupleurum falcatum L. on aminonucleoside nephrosis were studied in rats. Urine protein excretion in rats receiving aminonucleoside alone was significantly elevated on the 2nd day after the last injection of aminonucleoside and reached a peak on the 11th day. Urinary protein on the 11th day was reduced by 48 and 46%, respectively in animals treated with saikosaponin-d from the 2nd and 8th day after the last injection of aminonucleoside. Electron microscopically, the degree of abnormality, e.g. loss or fusion of foot processes, in the glomerular epitherial cells was significantly lower in the rats treated with saikosaponin-d after aminonucleoside injection than in the rats treated with aminonucleoside alone. It is concluded that saikosaponin-d prevents the development of proteinuria induced by aminonucleoside in the rat.

Animals↗
PubMed1987

In vivo and in vitro studies of hypocholesterolemic effects of diosgenin in rats.

There is evidence that diosgenin when given orally or parenterally decreases cholesterol plasma levels in rat, chicken and rabbits that have had a diet-induced hypercholesterolemia. 2. The per-oral administration of [3H]diosgenin yielded 12% of the given dose distributed throughout: liver, spleen, epididymal fat, brain and carcass of the rat. 3. In everted gut sacs, [3H]diosgenin was better absorbed than cholesterol. 4. In these tests diosgenin was recovered esterified from the tissues and the recovered cholesterol showed less esterification in the presence of diosgenin than in its absence.

Administration, Oral↗
PubMed1979

Studies on the disposition of diosgenin in rats, dogs, monkeys and man.

Rats, dogs and squirrel monkeys were given a single oral dose of [4-(14)C]diosgenin. Virtually all of the radioactivity was excreted in the feces. All of the absorbed radioactivity was eliminated via the bile. The percent of dose absorbed decreased with increasing dose. The amount of radioactivity in livers of rats given [4-(14)C]diosgenin was less than that after [4-(14)C]cholesterol, but more than after [4-(14)C]beta-sitosterol. Absorbed radioactivity in rats distributed into tissues, most notably the liver, adrenals, and walls of the gastrointestinal tract. No serum diosgenin was detected after a single large dose to rats and dogs. After multiple doses (100 mg/kg/day for 4 weeks) of diosgenin to dogs, up to 15 micrograms/ml of unchanged diosgenin was found in serum. Serum from human subjects receiving 3 g/day of diosgenin for 4 weeks contained less than 1 microgram/ml of unchanged drug. After a single dose of [14C]diosgenin, several metabolites were detected in the bile of rats and dogs; the pattern of metabolites was dissimilar in the two species. No diosgenin or 7-hydroxydiosgenin was found. One of the major biliary metabolites was diosgenin monohydroxylated in the F ring, but the location of the hydroxyl group was different in the two species. Although rat caecal contents were capable of reducing diosgenin to smilagenin in vitro, no smilagenin was present in the feces of rats given chow supplemented with diosgenin. It was concluded that diosgenin is poorly absorbed in the species tested, and that the amount which is absorbed undergoes extensive biotransformation.

Animals↗