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PubMed1995

Louisianins A, B, C and D: non-steroidal growth inhibitors of testosterone-responsive SC 115 cells. II. Physico-chemical properties and structural elucidation.

New non-steroidal growth inhibitors of testosterone-responsive SC 115 cells, louisianins A (MW: 189; C11H11NO2), B (MW: 191; C11H13NO2), C (MW: 173; C11H11NO) and D (MW: 173; C11H11NO) were isolated from the cultured broth of Streptomyces sp. WK-4028. Their structures were determined on the basis of spectroscopic data. The structure of louisianin A in particular was confirmed by X-ray crystallographic analysis. The four compounds commonly possess a unique pyrindine skeleton in the molecule.

5-alpha Reductase Inhibitors↗
PubMedDate not supplied

[The mechanism of antiarrhythmic action of a new ammonium derivative of lidocaine (LKhT-12-02)].

The results of electrophysiological investigation of the effects of LKhT-12-02 (a quaternary ammonium derivative of lidocaine) on the intact cat heart and the isolated ion channels of Lymnaea stagnalis snail showed that this compound belongs to class 1B antiarrhythmic agents (Vaughan - Williams classification). The drug does not suppress the automatic nonmonotonic rhythm driver, does not influence the conductance in ventricles, auricles, and atrioventricular node in the sinus rhythm, and does not elongate the effective refractory period of the auricles and atrioventricular node. LKhT-12-02 decreases the rate of fast depolarization of the action potential, while not reducing its duration. The compound does not influence the conduction of sodium ion channels.

Action Potentials↗
PubMed2007

Garlic compounds induced calpain and intrinsic caspase cascade for apoptosis in human malignant neuroblastoma SH-SY5Y cells.

Malignant (N-type) neuroblastoma continues to defy current chemotherapeutic regimens. We tested the garlic compounds diallyl sulfide (DAS) and diallyl disulfide (DADS) for induction of apoptosis in human malignant neuroblastoma SH-SY5Y cells. Viability of human primary neurons was unaffected after 24 h treatment with 50 and 100 microM DAS and 50 microM DADS but slightly affected with 100 microM DADS. Treatment with 50 and 100 microM DAS or DADS significantly decreased viability in SH-SY5Y cells. Wright staining showed morphological features of apoptosis in SH-SY5Y cells treated with 50 and 100 microM DAS or DADS for 24 h. ApopTag assay demonstrated DNA fragmentation in apoptotic cells. Apoptosis was associated with an increase in [Ca(2+)](i), increase in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, increase in cytosolic Smac/Diablo, and down regulation of inhibitor-of-apoptosis proteins and nuclear factor kappa B (NFkappaB). Activation of caspase-9 and caspase-3 indicated involvement of intrinsic pathway of apoptosis. Calpain and caspase-3 activities produced 145 kD spectrin break down product (SBDP) and 120 kD SBDP, respectively. Also, caspase-3 activity cleaved inhibitor of caspase-activated DNase (ICAD). Results strongly suggested that the garlic compounds DAS and DADS suppressed anti-apoptotic factors and activated calpain and intrinsic caspase cascade for apoptosis in SH-SY5Y cells.

Allyl Compounds↗
PubMed2005

Effects of garlic oil and two of its major organosulfur compounds, diallyl disulfide and diallyl trisulfide, on intestinal damage in rats injected with endotoxin.

Garlic and its active components are known to possess antioxidant and antiinflammatory effects. The present study investigated the effects of garlic oil and its organosulfur compounds on endotoxin-induced intestinal mucosal damage. Wistar rats received by gavage 50 or 200 mg/kg body weight garlic oil (GO), 0.5 mmol/kg body weight diallyl disulfide or diallyl trisulfide, or the vehicle (corn oil; 2 ml/kg body weight) every other day for 2 weeks before being injected with endotoxin (i.p., 5 mg/kg body weight). Control rats were administered with corn oil and were injected with sterile saline. Samples for the measurement of proinflammatory cytokines were collected 3 h after injection, and all other samples were collected 18 h after injection. The low dose of GO suppressed endotoxin-induced inducible nitric oxide synthase (iNOS) activity, ulceration, and apoptosis in the intestinal mucosa (P < 0.05). The high dose of GO significantly lowered the peripheral level of nitrate/nitrite and endotoxin-induced iNOS activity in the intestinal mucosa (P < 0.05) but worsened intestinal mucosal damage accompanied by elevated peripheral proinflammatory cytokines. Diallyl trisulfide but not diallyl disulfide showed similar toxic effect as that of high-dose GO. These results suggest the preventive effect and possible toxicity of garlic oil and its organosulfur compounds in endotoxin-induced systemic inflammation and intestinal damage.

Allyl Compounds↗
PubMed2005

Prokinetic effect of a Kampo medicine, Hange-koboku-to (Banxia-houpo-tang), on patients with functional dyspepsia.

Limited evidence is available as to whether Kampo medicine modifies gastrointestinal function in humans. We investigated the effect of a Kampo medicine, Hange-koboku-to (Banxia-houpo-tang, HKT), on patients with functional dyspepsia (FD) and on healthy volunteers with regard to gastric motility. The gastric emptying rate (GER) in FD patients was significantly lower than in the healthy subjects. GER in FD patients and in healthy volunteers showed a significant increase after 2 weeks of medication with HKT. Furthermore, gastrointestinal symptoms improved significantly in the FD patients after the administration of HKT. These results suggest that HKT improves delayed gastric emptying and acts as a prokinetic agent.

Adult↗
PubMed2002

Down-modulation of Bcl-XL, release of cytochrome c and sequential activation of caspases during honokiol-induced apoptosis in human squamous lung cancer CH27 cells.

Honokiol is a phenolic compound purified from Magnolia officinalis, which induced the apoptotic cell death in several types of human cancer cells. In the present study, the molecular mechanism of honokiol-mediated apoptotic process was examined in human squamous lung cancer CH27 cells. Here, we found that honokiol-induced apoptotic cell death was accompanied by upregulation of Bad and downregulation of Bcl-XL, while honokiol had no effect on the levels of Bcl-2, Bcl-XS, Bag-1, Bax and Bak proteins. Moreover, honokiol treatment caused the release of mitochondrial cytochrome c to cytosol and sequential activation of caspases. Proteolytic activation of caspase-3 and cleavage of PARP, an in vivo substrate for caspase-3, were observed in honokiol-treated CH27 cells. Furthermore, treatment with caspase inhibitors z-DEVD-fmk and z-VAD-fmk markedly blocked honokiol-induced apoptosis. These results demonstrated that modulation of Bcl-XL and Bad proteins, release of mitochondrial cytochrome c and activation of caspase-3, participated in honokiol-triggered apoptotic process in human squamous lung cancer CH27 cells.

Antineoplastic Agents, Phytogenic↗
PubMed1997

In vitro and in vivo protective effect of honokiol on rat liver from peroxidative injury.

Honokiol, a compound extracted from the Chinese medicinal herb Magnolia officinalis, has a strong antioxidant effect on the inhibition of lipid peroxidation in rat heart mitochondria. To investigate the protective effect of honokiol on hepatocytes from peroxidative injury, oxygen consumption and malondialdehyde formation for in vitro iron-induced lipid peroxidation were assayed, and the mitochondrial respiratory function for in vivo ischemia-reperfusion injury were evaluated in rat liver, respectively. The inhibitory effect of honokiol on oxygen consumption and malondialdehyde formation during iron-induced lipid peroxidation in liver mitochondria showed obvious dose-dependent responses with a concentration of 50% inhibition being 2.3 x 10(-7) M and 4.96 x 10(-7) M, respectively, that is, 550 times and 680 times more potent than alpha-tocopherol, respectively. When rat livers were introduced with ischemia 60 min followed by reperfusion for 60 min, and then pretreated with honokiol (10 micrograms/kg BW), the mitochondrial respiratory control ratio (the quotient of the respiration rate of State 3 to that of State 4) and ADP/O ratio from the honokiol-treated livers were significantly higher than those of non-treated livers during reperfusion. The dose-dependent protective effect of honokiol on ischemia-reperfusion injury was 10 microgram-100 micrograms/Kg body weight. We conclude that honokiol is a strong antioxidant and shed insight into clinical implications for protection of hepatocytes from ischemia-reperfusion injury.

Animals↗
PubMed2005

Honokiol induces apoptosis via cytochrome c release and caspase activation in activated rat hepatic stellate cells in vitro.

The therapeutic goal in liver fibrosis is the reversal of fibrosis and the selective clearance of activated hepatic stellate cells (HSCs) by inducing apoptosis. Over the past several years, we have screened for natural products that mediate apoptosis in activated HSCs. Among the candidate compounds, honokiol, isolated from Magnoliae cortex, was found to induce apoptotic death in activated rat HSCs, while there was no cell viability change in hepatocytes, at concentrations of 12.5-50 microM. Apoptosis was identified by DNA fragmentation, activation of caspase-3 and -9, and the proteolytic cleavage of poly(ADP-ribose) polymerase, down-regulation of bcl-2 and the release of mitochondrial cytochrome c into the cytoplasm.

Animals↗
PubMed2006

Honokiol reduces oxidative stress, c-jun-NH2-terminal kinase phosphorylation and protects against glycochenodeoxycholic acid-induced apoptosis in primary cultured rat hepatocytes.

Hydrophobic bile acid-induced apoptosis plays an important role in cholestatic liver disease, and its prevention may be of therapeutic interest. The aim of this study was to investigate the protective effect of honokiol on glycochenodeoxycholic acid-induced apoptosis in primary cultured rat hepatocytes. Glycochenodeoxycholic acid is a hydrophobic bile salt that accumulates intrahepatically during cholestasis and induces hepatocyte apoptosis at pathophysiological concentrations. Primary rat hepatocytes were pretreated with honokiol at concentrations of 40, 20 and 10 microM 5 min before glycochenodeoxycholic acid treatment. Incubation of hepatocytes with glycochenodeoxycholic acid at a concentration of 100 microM for 4 h induced apoptosis as shown by DNA fragmentation, chromatin condensation and cleavage of poly(ADP-ribose) polymerase. Pretreatment with honokiol at concentrations of 40, 20 and 10 microM significantly inhibited the generation of intracellular reactive oxygen species and reduced activation of caspases-8, -9, and -3 and cleavage of poly-(ADP-ribose) polymerase. Glycochenodeoxycholic acid treatment up-regulated phosphorylation of stress-activated protein kinase/c-jun-NH2-terminal kinase which was inhibited by honokiol treatment. Inhibition of stress-activated protein kinase/c-jun-NH2-terminal kinase phosphorylation by SP600125 protected hepatocytes from apoptosis induced by glycochenodeoxycholic acid. These data indicate that honokiol protects hepatocytes from apoptosis induced by glycochenodeoxycholic acid in vitro and this protection may be due to reduced oxidative stress and inhibition of stress-activated protein kinase/c-jun-NH2-terminal kinase phosphorylation.

Animals↗
PubMed2003

Honokiol, a small molecular weight natural product, inhibits angiogenesis in vitro and tumor growth in vivo.

Natural products comprise a major source of small molecular weight angiogenesis inhibitors. We have used the transformed endothelial cell line SVR as an effective screen of natural product extracts to isolate anti-angiogenesis and anti-tumor compounds. Aqueous extracts of Magnolia grandiflora exhibit potent activity in our SVR proliferation assays. We found that the small molecular weight compound honokiol is the active principle of magnolia extract. Honokiol exhibited potent anti-proliferative activity against SVR cells in vitro. In addition, honokiol demonstrated preferential inhibition of primary human endothelial cells compared with fibroblasts and this inhibition was antagonized by antibodies against TNF alpha-related apoptosis-inducing ligand. In vivo, honokiol was highly effective against angiosarcoma in nude mice. Our preclinical data suggests that honokiol is a systemically available and non-toxic inhibitor of angiogenesis and should be further evaluated as a potential chemotherapeutic agent.

Angiogenesis Inhibitors↗
PubMed2004

Growth inhibitory effect of alk(en)yl thiosulfates derived from onion and garlic in human immortalized and tumor cell lines.

Two alk(en)yl thiosulfates, sodium n-propyl thiosulfate (NPTS) and sodium 2-propenyl thiosulfate (2PTS), are natural constituents of onion and garlic, respectively, which were identified originally as causative agents of onion- and garlic-induced hemolytic anemia in dogs. As a continuation of our studies on the beneficial functions of NPTS and 2PTS, in the present study, we investigated the antitumor effects of these compounds. They were shown to inhibit the in vitro proliferation of three human tumorigenic cell lines, WiDr, 293 and HL-60, in a dose-dependent manner. Overall, NPTS seemed to have weak activity for inhibiting cell growth compared with 2PTS, though not in WiDr cells, which were sensitive to both compounds. NPTS and 2PTS caused oxidative damage to HL-60 cells and induced apoptosis. The extent of apoptosis was approximately proportional to that of the oxidative damage and also to that of the cytotoxicity caused by these compounds. These results suggest that the alk(en)yl thiosulfates have an antitumor effect through the induction of apoptosis initiated by oxidative stress.

Allyl Compounds↗
PubMed2003

Selective expression of glutathione S-transferase genes in the murine gastrointestinal tract in response to dietary organosulfur compounds.

A short-term feeding regimen was designed to analyze the effects of compounds such as diallyl disulfide (DADS), diallylthiosulfinate (allicin) from garlic and butylated hydroxyanisole (BHA) on glutathione S-transferase (GST) expression in the gastrointestinal tract and liver of male mice. After animals were force-fed these compounds, tissue GSTs were purified and individual subunits resolved by HPLC and identified on the basis of mass spectrometry (ESI MS) and immunoreactivity data. The effects of DADS and allicin on GST expression were especially prominent in stomach and small intestine, where there were major coordinate changes in GST subunit profiles. In particular, the transcripts of the mGSTM1 and mGSTM4 genes, which share large segments of common 5'-flanking sequences, and their corresponding subunits were selectively induced. Levels of alpha class subunits also increased, whereas mGSTM3 and mGSTP1 were not affected. The inducible mGSTA5 and non-responsive mGSTM3 subunits had not been identified previously. Liver and colon GSTs were also affected to a lesser extent, but this short-term feeding regimen had no effect on GST subunit patterns from other organs, including heart, brain and testis. Real-time PCR (TaqMan) methods were used for quantitative estimations of relative amounts of the mRNAs encoding the GSTs. Effects on the transcripts generally paralleled changes at the protein level, for the most part, however, the greatest relative increases were observed for those mRNAs that were expressed at low abundance constituitively. Mechanisms by which the organosulfur compounds operate to affect GST transcription could involve reversible modification of certain protein sulfhydryl groups, shifts in reduced glutathione/oxidized glutathione ratios and resultant changes in cellular redox status.

Allyl Compounds↗
PubMed2005

Magnolol and honokiol enhance HL-60 human leukemia cell differentiation induced by 1,25-dihydroxyvitamin D3 and retinoic acid.

Magnolol (MG) and honokiol (HK), two lignans showing anti-inflammatory and anti-oxidant properties and abundantly available in the medicinal plants Magnolia officinalis and M. obovata, were found to enhance HL-60 cell differentiation initiated by low doses of 1,25-dihydroxyvitamin D3 (VD3) and all-trans-retinoic acid (ATRA). Cells expressing membrane differentiation markers CD11b and CD14 were increased from 4% in non-treated control to 8-16% after being treated with 10-30 microM MG or HK. When added to 1 nM VD3, MG or HK increased markers expressing cells from approximately 30% to 50-80%. When either MG or HK was added to 20 nM ATRA, only CD11b, but not CD14, expressing cells were increased from 9% to 24-70%. Under the same conditions, adding MG or HK to VD3 or ATRA treatment further enlarged the G0/G1 cell population and increased the expression of p27(Kip1), a cyclin-dependent kinase inhibitor. Pharmacological studies using PD098059 (a MEK inhibitor), SB203580 (a p38 MAPK inhibitor) and SP600125 (a JNK inhibitor) suggested that the MEK pathway was important for VD3 and ATRA-induced differentiation and also its enhancement by MG or HK, the p38 MAPK pathway had a inhibitory effect and the JNK pathway had little influence. It is evident that MG and HK are potential differentiation enhancing agents which may allow the use of low doses of VD3 and ATRA in the treatment for acute promyelocytic leukemia.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Genotoxicity and metabolism of the source-water contaminant 1,1-dichloropropene: activation by GSTT1-1 and structure-activity considerations.

1,1-Dichloropropene (1,1-DCPe) is a contaminant of some source waters used to make drinking water. Because of this and the fact that no toxicological data were available for this compound, which is structurally similar to the rodent carcinogen 1,3-dichloropropene (1,3-DCPe), 1,1-DCPe was placed on the Contaminant Candidate List of the US Environmental Protection Agency. Consequently, we have performed a hazard characterization of 1,1-DCPe by evaluating its mutagenicity in the Salmonella assay and its DNA damaging (comet assay) and apoptotic (caspase assay) activities in human lymphoblastoid cells. In Salmonella, 1,1-DCPe was not mutagenic in strains TA98, TA100, TA1535, or TA104 +/-S9 mix. However, it was clearly mutagenic in strain RSJ100, which expresses the rat GSTT1-1 gene. 1,1-DCPe did not induce DNA damage in GSTT1-1-deficient human lymphoblastoid cells, and it induced apoptosis in these cells only at 5 mM. Consistent with its mutagenesis in RSJ100, 1,1-DCPe reacted with glutathione (GSH) in vitro, suggesting an addition-elimination mechanism to account for the detected GSH conjugate. 1,1-DCPe was approximately 5000 times more mutagenic than its ethene congener 1,1-dichloroethylene (1,1-DCE or vinylidene chloride). Neither 1,1-DCE nor 1,3-DCPe showed enhanced mutagenicity in strain RSJ100, indicating a lack of activation of these congeners by GSTT1-1. Thus, 1,1-DCPe is a base-substitution mutagen requiring activation by GSTT1-1, possibly involving the production of a reactive episulfonium ion. This bioactivation mechanism of 1,1-DCPe is different from that of its congeners 1,1-DCE and 1,3-DCPe. The presence of 1,1-DCPe in source waters could pose an ecological or human health risk. Occurrence data for 1,1-DCPe in finished drinking water are needed to estimate human exposure to, and possible health risks from, this mutagenic compound.

Allyl Compounds↗
PubMed2000

Inhibitors of nitric oxide synthesis and TNF-alpha expression from Magnolia obovata in activated macrophages.

Nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) are the major mediators produced in activated macrophages which contribute to the circulatory failure associated with septic shock. An activity-guided fractionation of an MeOH extract of stem bark of Magnolia obovata afforded two inhibitors of NO production in lipopolysaccharides (LPS)-activated macrophages by the suppression of i-NOS expression. Their structures were elucidated by spectroscopic methods to be magnolol and honokiol with IC50 values of 16.8 and 6.4 microM, respectively. They also inhibited the production of TNF-alpha in LPS-activated macrophages. Thus, these compounds may be possible candidates for the development of new drugs to treat endotoxemia accompanied by the overproduction of NO and TNF-alpha.

Animals↗
PubMed2001

Effects of the extract of the bark of Magnolia obovata and its biphenolic constituents magnolol and honokiol on histamine release from peritoneal mast cells in rats.

We have previously reported that saiboku-to, an Oriental herbal remedy composed of a mixture of 10 different herbal extracts, possesses anti-histamine release effect on mast cells in rats. This effect may be due mainly to the extract of the bark of Magnolia obovata (M. obovata), a constituent herb of saiboku-to. In the present study, it was demonstrated that the bark extract inhibited compound 48/80 (C48/80)-induced histamine release from mast cells in a concentration-dependent manner (50 % inhibitory concentration, IC(50) = 56.98 microg/ml). Furthermore, the inhibitory activity was found in the methanol fraction, but not in water and 50 % aqueous methanol fractions derived from the bark extract. Magnolol and honokiol isolated from the methanol fraction inhibited C48/80-induced histamine release from mast cells. The potency of magnolol (IC(50) = 1.04 microg/ml) was greater than that of honokiol (IC(50) = 2.77 microg/ml). Furthermore, the actual amount of magnolol (49.76 +/- 1.14 mg) contained in the bark of M. obovata (5 g) was greater than that (8.58 +/- 0.19 mg) of honokiol. Taken together, the present results suggest that magnolol may be responsible for the biological efficacy of the bark extract of M. obovata.

Animals↗
PubMed2003

The mechanism of honokiol-induced and magnolol-induced inhibition on muscle contraction and Ca2+ mobilization in rat uterus.

The effects of honokiol and magnolol extracted from the Magnolia officinalis on muscular contractile responses and intracellular Ca(2+) mobilization were investigated in the non-pregnant rat uterus. Honokiol and magnolol (1-100 micromol/l) were observed to inhibit spontaneous and uterotonic agonists (carbachol, PGF(2alpha), and oxytocin)-, high K(+)-, and Ca(2+) channel activator (Bay K 8644)-induced uterine contractions in a concentration-dependent manner. The inhibition rate of honokiol on spontaneous contractions appeared to be slower than that of magnolol-induced response. The time periods that were required for honokiol and magnolol, at 100 micromol/l, to abolish 50% spontaneous contractions were approximately 6 min. Furthermore, honokiol and magnolol at 10 micromol/l also blocked the Ca(2+)-dependent oscillatory contractions. Consistently, the increases in intracellular Ca(2+) concentrations ([Ca(2+)](i)) induced by PGF(2alpha) and high K(+) were suppressed by both honokiol and magnolol at 10 micromol/l. After washout of these treatments, the rise in [Ca(2+)](i) induced by PGF(2alpha) and high K(+) was still partially abolished. In conclusion, the inhibitory effects of honokiol and magnolol on uterine contraction may be mediated by blockade of external Ca(2+) influx, leading to a decrease in [Ca(2+)](i). Honokiol and magnolol may be considered as putative Ca(2+) channel blockers and be of potential value in the treatment of gynecological dysfunctions associated with uterine muscular spasm and dysmenorrhea.

Animals↗