Inhibitory effect of daphnetin on the C48/80-induced pseudo-allergic reaction.

Pseudo-allergic reaction is an allergic reaction mediated by nonimmunoglobulin E (IgE), which does not require prior contact with antigen sensitization and directly leads to mast cell degranulation. Daphnetin (DAP) is known for its anti-inflammatory effects, but there are few studies on the effect of DAP on pseudo-allergy and its mechanism. To investigate the effect of DAP on pseudo-allergy and its mechanism, we inflicted pseudo-allergy on RBL-2H3 cells using C48/80 in vitro. Moreover, to assess the antipseudo-allergy effect of C48/80 in vivo, mouse models of local anaphylaxis, systemic anaphylaxis, and itch were used. The in vitro results show that DAP inhibits degranulation and chemokine release; furthermore, DAP reduced the activation of the PLC-IP3R and MAPK signaling pathways induced by C48/80. Additionally, our in vivo results showed that DAP inhibited C48/80-induced local anaphylaxis and inhibited eosinophil aggregation, vasodilation and mast cell degranulation. In systemic anaphylaxis, DAP inhibits the decrease in body temperature and reduces the release of His, TNF-a and IL-8. In C48/80-induced itch, the number of scratches in mice was reduced. Our results demonstrate that DAP can play a suppressive role in the pseudo-allergy induced by C48/80, providing information for the cure of disorders linked to pseudo-allergic reactions.

Allantoin Inhibits Compound 48/80-Induced Pseudoallergic Reactions In Vitro and In Vivo.

Pseudoallergic reactions are hypersensitivity reactions mediated by an IgE-independent mechanism. Since allantoin (AT)-mediated pseudoallergy has not been studied, in this study, our objective is to investigate the anti-pseudoallergy effect of AT and its underlying mechanism. In vitro, ß-hexosaminidase (ß-Hex) and histamine (HIS) release assays, inflammatory cytokine assays, toluidine blue staining, and F-actin microfilament staining were used to evaluate the inhibitory effect of AT in RBL-2H3 cells stimulated with Compound 48/80 (C48/80). Western blot analysis is further performed to investigate intracellular calcium fluctuation-related signaling pathways. In vivo, Evans Blue extraction, paw swelling, and the diameter of Evans Blue extravasation were evaluated, and skin tissues are examined for histopathological examination in mice with passive cutaneous anaphylaxis (PCA) induced by C48/80. Body temperature is measured, and the levels of cytokines are further determined by ELISA kits in mice with active systemic anaphylaxis (ASA) induced by C48/80. The results show that AT dose-dependently inhibited degranulation in C48/80-stimulated RBL-2H3 cells by inhibiting ß-Hex and HIS release, reducing the levels of TNF-α, IL-8, and MCP-1, inhibiting shape changes due to degranulation and disassembling the F-actin cytoskeleton. Furthermore, AT dose-dependently inhibits the phosphorylation of PLCγ and IP3R. In vivo, AT decreased Evans Blue extravasation, paw swelling, and the diameter of Evans Blue extravasation and significantly ameliorate pathological changes and mast cell degranulation in C48/80-induced PCA. Furthermore, AT help the mice recover from the C48/80-induced decrease in body temperature and decreased the levels of cytokines in C48/80-treated ASA mice. Our results indicate that allantoin inhibits compound 48/80-induced pseudoallergic reactions. AT has the potential to be used in IgE-independent anti-allergic and anti-inflammatory therapies.

Bisdemethoxycurcumin attenuates OVA-induced food allergy by inhibiting the MAPK and NF-κB signaling pathways.

Bisdemethoxycurcumin (BDMC) is an important ingredient derived from turmeric in addition to curcumin. It has been reported that BDMC can be used to treat mast cell-mediated allergic diseases. In the present study, a food allergy (FA) murine model sensitized by intraperitoneal injection followed by oral challenge with ovalbumin (OVA) was established. BDMC was orally administered at 100 and 200 mg/kg for 11 days in the challenge phase to treat OVA-induced FA mice. FA symptoms such as diarrhea score, anaphylactic symptom score and rectal temperature were recorded. Intestinal tissue was also observed by hematoxylin and eosin staining. In addition, other allergic indicators were also analyzed by ELISA and western blot analysis. The present study demonstrated that BDMC could suppress the decreases in rectal temperature, diarrhea and anaphylactic symptoms in FA mice. BDMC could also ameliorate the inflammation of intestinal tissues in FA mice. BDMC not only decreased the production of OVA-specific immunoglobulin (OVA-sIg)E, IgG1, histamine, mouse mast cell protease-1, diamine oxidase, cytokines (IL-4, IL-5 and IL-13) but increased cytokines interferon-γ production. The protein expression results showed that the levels of Gata-3 were decreased but T-bet levels were increased. Furthermore, compared with the OVA group, phosphorylated (p)-p38, p-JNK, p-ERK and p-NF-κBp65 levels were decreased and p-IκBα level was increased. In conclusion, the results showed that BDMC possessed a protective effect on FA. Furthermore, BDMC was able to regulate the T-helper cells (Th)1/Th2 immune balance and inhibit the activation of MAPK and NF-κB pathways in FA mice.

Inhibitory Effect of Bisdemethoxycurcumin on DNCB-Induced Atopic Dermatitis in Mice.

Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Bisdemethoxycurcumin (BDMC) is an ingredient from the rhizome of the traditional Chinese herbal medicine turmeric. BDMC has been reported to have important pharmacological properties, such as anti-inflammatory, antioxidant, antitumor and antiproliferative activities. However, its effect on atopic dermatitis has not been reported. The purpose of our study was to demonstrate the effectiveness of BDMC on TNF-α/IFNγ-stimulated HaCaT cells and on 2,4-dinitrochlorobenzene (DNCB)-induced AD mice. Our studies showed in vitro that BDMC was able to significantly inhibit the mRNA expression of chemokines and cytokines in TNF-α/IFN-γ-stimulated HaCaT cells and alleviate their inflammatory response. Our studies found in vivo that BDMC was able to significantly improve the symptoms of DNCB-induced AD skin lesions, decrease the number of scratches, ear thickness, and spleen index, improve inflammatory cells and mast cell infiltration and decrease skin thickness. Moreover, it was also able to inhibit the mRNA expression levels of chemokines and inflammatory cytokines and the activation of the MAPK and NF-κB signaling pathways. Thus, the results indicated that BDMC can improve atopic dermatitis in mice and that further clinical studies are warranted on its treatment of AD.

Berberine and Cisplatin Exhibit Synergistic Anticancer Effects on Osteosarcoma MG-63 Cells by Inhibiting the MAPK Pathway.

Berberine (BBR) has been reported to have potent anticancer activity and can increase the anticancer effects of chemotherapy drugs. The present study aims to investigate whether BBR and cisplatin (DDP) exert synergistic effects on the osteosarcoma (OS) MG-63 cell line. In the present study, MG-63 cells were treated with BBR and DDP alone or in combination. The effects of these therapeutics on cell viability, colony formation, migration, invasion, nuclear morphology, apoptosis, and the cell cycle, as well as their role in regulating the expression of proteins related to apoptosis, the cell cycle, and the mitogen-activated protein kinase (MAPK) pathway, were determined. The results demonstrated that BBR or DDP significantly inhibited the proliferation of MG-63 cells in a dose- and time-dependent manner. The combination treatment of BBR and DDP exerted a prominent inhibitory effect on proliferation and colony formation. Furthermore, the results showed that the combination treatment of BBR and DDP enhanced the inhibition of cell migration and invasion and reversed the changes in nuclear morphology. The results showed that the combination treatment of BBR and DDP induced apoptosis and cell cycle arrest in the G0/G1 phase. Mechanistically, the combination treatment of BBR and DDP inhibited the expression of MMP-2/9, Bcl-2, CyclinD1, and CDK4, enhanced the expression of Bax and regulated the activity of the MAPK pathway. Collectively, our data suggest that the combination therapy of BBR and DDP markedly enhanced OS cell death.

Characterization of free and glycosidically bound volatile compounds, fatty acids, and amino acids in Vitis davidii Foex grape species native to China.

Berries of six Vitis davidii Foex (spine grape) cultivars ('Baiputao', 'Gaoshan 1', 'Gaoshan 2', 'Seputao', 'Miputao', and 'Tianputao') were harvested from a commercial vineyard in Hunan Province in China. Free and bound volatile compounds and fatty acids were analyzed by GC-MS, and amino acids were analyzed by HPLC. 'Tianputao' and 'Miputao' were characterized by relatively higher concentrations of aromatic amino acids and lower concentrations of branched-chain amino acids. The major free volatile compounds of spine grapes were hexanal, (E)-2-hexenal, 1-hexanol, (E)-2-hexenol, (E)-ß-damascenone, and benzeneacetaldehyde. The major glycosidically bound volatile compounds identified were 1-hexanol, menthol, nerol, 1-butanol, 3-methyl-3-butenol, benzenemethanol, ß-phenylethanol, eugenol, and guaiacol. (E)-ß-damascenone, benzeneacetaldehyde, guaiacol, and eugenol had odor activity values (OAVs) > 1 in all cultivar grapes. Partial least squares discriminant analysis (PLS-DA) revealed 'Tianputao' to be distinct from the other cultivars due to its relatively higher concentrations of major terpenoids, norisoprenoids, higher alcohols, and aromatic amino acids.

A new ocotillol-type ginsenoside from stems and leaves of Panax quinquefolium L. and its anti-oxidative effect on hydrogen peroxide exposed A549 cells.

A new ocotillol-type ginsenoside, namely 12-one-pseudoginsenoside F11 (12-one-PF11), was isolated from stems and leaves of Panax quinquefolium, whose structure was elucidated 6-O-[α-L-rhamnopyranosyl-(1-2)-ß-D-glucopyranosyl]-dammar-12-one-20S,24R-epoxy-3ß,6α,25-triol. 12-one-PF11 significantly suppressed hydrogen peroxide induced oxidative stress in human lung carcinoma A549 cells. As compared with model group, 12-one-PF11 improved cell viability of A549 cells in a dose-dependent manner, and significantly decreased the generation of malondialdehyde (MDA) and increased production of superoxide dismutase (SOD) and glutathione (GSH) and protein expression levels of nuclear related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in A549 cells.

Berberine suppresses mast cell-mediated allergic responses via regulating FcɛRI-mediated and MAPK signaling.

The anti-allergic effect of berberine was evaluated in cellular and animal models of allergic responses. In this study, the results of the in vitro model of immunoglobulin (Ig) E-mediated mast cell degranulation showed that berberine significantly inhibited the release of ß-hexosaminidase (ß-HEX), histamine, IL-4 and TNF-α in rat basophilic leukemia cells (RBL-2H3 cells). Pretreatment with berberine prevented morphological changes in IgE-stimulated RBL-2H3 cells such as the recovery of an elongated shape. Pretreatment with berberine also suppressed the phosphorylation of antigen-induced Lyn, Syk, and Gab2, thus suppressing the downstream MAPK pathways. In the in vivo model of allergic responses, administration of berberine inhibited passive cutaneous anaphylaxis (PCA) in mice. The above results indicate berberine could suppress mast cell activation and allergic responses.

Coptisine Suppresses Mast Cell Degranulation and Ovalbumin-Induced Allergic Rhinitis.

Coptisine is one of the main components of isoquinoline alkaloids in the coptidis rhizome. The effect of coptisine on allergic rhinitis has not been investigated. In this study, we report the effects and mechanisms of coptisine using monoclonal anti-2,4,6-dinitrophenyl-immunoglobulin (Ig) E/human serum albumin (DNP-IgE/HSA)-stimulated rat basophilic leukemia cells (RBL-2H3 cells) in vitro and an ovalbumin (OVA)-induced allergic rhinitis (AR) in mice. The results showed that coptisine markedly decreased the levels of ß-hexosaminidase, histamine, interleukin (IL)-4, and tumor necrosis factor (TNF)-α. Coptisine also prevented morphological changes, such as restoring an elongated shape, inhibiting granule release on toluidine blue staining, and reorganizing inhibited filamentous actins (F-actin). Additionally, coptisine blocked the phosphorylation of phosphoinositide3-kinase (PI3K)/Akt (as known as protein kinase B(PKB)) in RBL-2H3 cell. Furthermore, the results showed that coptisine suppressed OVA-induced allergic rhinitis symptoms, such as nasal rubbing and OVA-specific IgE, and histamine, IL-4 and TNF-α levels in the serum of AR mice. These data suggested that coptisine should have inhibitory effects on the inflammatory responses of mast cells, and may be beneficial for the development of coptisine as a potential anti-allergic drug.

Inhibitory effects of bisdemethoxycurcumin on mast cell-mediated allergic diseases.

Most allergic reactions are induced by mast cell activation. Mast cells play vital roles in the pathogenesis of allergic diseases. Bisdemethoxycurcumin (BDMC), a natural curcuminoid, has potential anti-allergic effects. Hence, we explored the effect of BDMC on mast cell-mediated allergic diseases. The study proved that BDMC suppresses ß-hexosaminidase release, granule release, and membrane ruffling in monoclonal anti-2,4,6-dinitrophenyl-immunoglobulin (Ig) E/human serum albumin (DNP-IgE/HSA)-stimulated rat basophilic leukaemia cells (RBL-2H3 cells), and BDMC suppressed ovalbumin (OVA)-induced allergic rhinitis (AR) symptoms and OVA-specific IgE levels in AR mice. Furthermore, BDMC increased the survival of compound 48/80 anaphylaxis shock mice and elevated the decreased rectal temperature in OVA-induced active systemic anaphylaxis mice. These findings indicate that BDMC regulates the degranulation of mast cells, demonstrating its potential in the treatment of mast cell-induced allergic reactions.

Anti-inflammatory effect of epigallocatechin gallate in a mouse model of ovalbumin-induced allergic rhinitis.

Currently, a variety of studies have demonstrated that green tea has anti-allergic properties, and the major polyphenolic compound, epigallocatechin gallate (EGCG), plays a significant role. Some research indicates that EGCG reduces the production and expression of allergy-related substances. Therefore, EGCG has a potential effect of reducing allergic rhinitis (AR). In this study, the effect of EGCG on allergic rhinitis in an ovalbumin (OVA)-induced mouse model was investigated. After administration of EGCG, the number of sneezes and the occurrence of nasal rubbing were significantly decreased, the concentrations of immunoglobulin E (IgE) and histamine were suppressed in AR mouse serum, the levels of interleukin (IL)-1ß, IL-4, and IL-6 were reduced in AR mice nasal lavage fluid (NLF), and the nasal mucosa mRNA and protein expression of cyclooxygenase 2 (COX-2), IL-1ß, IL-4, and IL-6 were inhibited. The data indicate that EGCG has a beneficial effect of reducing allergic rhinitis.

Hepatoprotective effect of the flavonoid fraction isolated from the flower of Inula britannica against D-Galactosamine-induced hepatic injury.

The aim of this study was to investigate the mechanism and nature of the protective effect of Inula britannica flower flavonoids (IBFF) on antioxidants and the inhibition of inflammation in liver injury. Liver injury was induced in a mouse model by intraperitoneal injection of D-Galactosamine (D-Gal; 850 mg/kg) and IBFF was administered orally at 125, 250 or 500 mg/kg once a day for 7 days. The results revealed that IBFF reversed the increases in serum aminotransferase levels and lipid peroxidation and also reversed the decreases in hepatic glutathione content. IBFF attenuated the D-Gal-induced increases in tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA and protein levels in the liver. Our data suggest that IBFF ameliorates D-Gal-induced acute liver injury and that this protection may be due to its antioxidative and anti-inflammatory activities.

Protective effect of myricetin in dextran sulphate sodium-induced murine ulcerative colitis.

In the present study, the protective effect of myricetin administered orally at 200, 100 or 50 mg/kg for 10 days was evaluated in a murine model of acute experimental colitis induced by dextran sulphate sodium (DSS). Macroscopic analysis was carried out to determine the effect of myricetin on pro-inflammatory cytokines, inflammatory markers and oxidative damage in biopsies of colonic tissues. The results showed that treatment with myricetin ameliorated body weight loss in a dose-dependent manner and significantly reduced histology scores. Myricetin decreased the production of nitric oxide (NO), myeloperoxidase (MPO) and malondialdehyde (MDA), while increasing the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Furthermore, the levels of the cytokines interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) were significantly decreased. Taken together, the results suggest that the anticolitis effects of myricetin may be attributed to anti-inflammatory and antioxidant actions. Additional investigation is required to determine the detailed mechanisms of action.

Composition and bioactivity of polysaccharides from Inula britannica flower.

In this paper, the composition and biological activities of polysaccharides from Inula britannica flower IBP obtained by water extraction were investigated. The properties and chemical compositions of IBP were analyzed with HPLC and IR methods. The results showed that IBP consisted of two kinds of polysaccharides with the molecular weight of 3500 Da, 700 Da. IBP consisted of mannose, glucuronic acid, rhamnose, galacturonic acid, glucose, galactose, arabinose with a molar ratio of 4.1:1:1.4:2.7:14.6:6.3:7.9. The IR spectrum of IBP revealed the typical characteristics of polysaccharides and protein. IBP was administered orally at three doses [100, 200 and 400 mg/kg body weight] for 14 days to the diabetic mice induced by alloxan. The body weight, plasma glucose, serum triglyceride (TG), total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and liver glycogen were evaluated in normal and alloxan-induced diabetic mice. IBP could dose-dependently significantly increase the body weight of diabetic mice, and reverse the decrease of plasma glucose, glycogen and the decrease of blood lipid of diabetic mice as compared to those in control group. These results indicated that IBP could be developed to a potential anti-diabetic drug in the future.

Suppressive effect of berberine on experimental dextran sulfate sodium-induced colitis.

The anti-inflammatory effect of berberine was evaluated in murine model of acute experimental colitis induced by dextran sulfate sodium (DSS). Berberine, given orally at 40, 20, 10 mg/kg for 10 days, ameliorated all the supposed inflammatory symptoms of the induced colitis, such as body weightloss, blood hemoglobin reduction, high myeloperoxidase levels, and malondialdehyde content-inflamed mucosa. Furthermore, the cytokine production of splenic lymphocytes was analyzed. The results showed the IFN-γ and IL-12 were increased, but IL-4 and IL-10 were decreased in DSS-induced colitis,when those were compared with the normal control. But the administration of berberine to DSS-induced colitis mice showed lower production of IFN-γ and IL-12 and higher production of IL-4 and IL-10 than the DSS-induced colitis mice. The results suggest that the protective effects of berberine against the DSS-induced colitis may be associated with the regulation of cytokine production.

Effect of Quercetin in the 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-Induced Mouse Model of Parkinson's Disease.

In this paper, the protective effect of the bioflavonoid quercetin on behaviors, antioxidases, and neurotransmitters in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-(MPTP-) induced Parkinson's disease (PD) was investigated. Quercetin treatment (50 mg/kg, 100 mg/kg and 200 mg/kg body weight) was orally administered for 14 consecutive days. The results show that quercetin treatment markedly improves the motor balance and coordination of MPTP-treated mice. Significant increases were observed in the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and Na(+), K(+)-ATPase, AchE, the content of dopamine (DA) in the quercetin plus MPTP groups compared to those in the MPTP group. Significant reduction the 4-hydroxy-2-nonenal (4-HNE) immunoreactivity in striatum of brains was observed in the quercetin plus MPTP groups in comparison to the MPTP group. Taken together, we propose that quercetin has shown antiparkinsonian properties in our studies. More work is needed to explore detailed mechanisms of action.

[Reversal effect of Fe3O4-magnetic nanoparticles on multi-drug resistance of ovarian carcinoma cells and its correlation with apoptosis-associated genes].

BACKGROUND AND OBJECTIVE: Resistance to cisplatin (DDP) remains a major obstacle for the successful treatment of ovarian cancer. This study was to determine the reversal effect of Fe3O4-magnetic nanoparticles (MNPs) on DDP-resistance of ovarian carcinoma cell line SKOV3/DDP, and to explore its correlation with apoptosis-associated genes. METHODS: SKOV3/DDP cells were divided into the DDP group, the Fe3O4-MNPs group, the combination (DDP plus Fe3O4-MNPs) group, and the control group. Cell proliferation was determined by MTT assay. Cell apoptosis was analyzed by flow cytometry (FCM). Intracellular DDP level was detected by inductively coupled plasma atomic emission spectrometry (ICP-AES). The expressions of apoptosis-associated genes, bcl-2, and survivin were detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Fe3O4-MNPs reversed DDP-resistance of SKOV3/DDP cells by 2.259 folds. The cell apotosis rate and the intracellular DDP level were significantly higher in the combination group than in the DDP group (P<0.05). Moreover, the mRNA levels of bcl-2 and survivin were significantly lower in the combination group than in the DDP group(P<0.05). CONCLUSIONS: Fe3O4-MNPs can reverse the DDP resistance of ovarian carcinoma SKOV3/DDP cells, and the effect may be ascribed to the down-regulation of bcl-2 and survivin expression.

The reversal effect of magnetic Fe3O4 nanoparticles loaded with cisplatin on SKOV3/DDP ovarian carcinoma cells.

To explore whether the magnetic nanoparticles of Fe3O4 (MNPs-Fe3O4) loaded with cisplatin can reverse the diaminedichloro platinum (DDP) resistance to multidrug resistance of ovarian carcinoma cells and to investigate its mechanisms. The SKOV3/DDP cells were divided into DDP treatment (DDP group), MNPs-Fe3O4 treatment (MNPs-Fe3O4 group), DDP + MNPs-Fe3O4 treatment (DDP + MNPs-Fe3O4 group), and control group. After incubation with those conjugates for 48 h, the cytotoxic effects were measured by MTT assay. Apoptosis and the intracellular DDP concentration were investigated by flow cytometry and inductively coupled plasma atomic emission spectroscopy, respectively. The expression of apoptosis associated gene Bcl-2 mRNA was detected by reverse transcription polymerase chain reaction and the expressions of MDR1, lung resistance-related protein (LRP), and P-glycoprotein (P-gp) genes were studied by Western blot. Our results indicated that the 50% inhibition concentration (IC50) of the MNPs-Fe3O4 loaded with DDP was 17.4 micromol/l, while the IC50 was 39.31 micromol/l in DDP groups (p < 0.05); Apoptosis rates of SKOV3/DDP cells increased more than those of DDP groups. Accumulation of intracellular cisplatin in DDP + MNPs-Fe3O4 groups was higher than those in DDP groups (p < 0.05). Moreover, the expression of Bcl-2 mRNA and the protein expressions of MDR1, LRP, and P-gp were decreased when compared with those of DDP groups, respectively. Our results suggest that MNPs-Fe3O4 can reverse the DDP resistance to the ovarian carcinoma cell. The effects may be associated with over-expression of MDR1, LRP, P-gp, and Bcl-2, which can increase the intracellular platinum accumulation and induce the cell apoptosis.

[Inhibition effect of gambogic acid on MUTZ-1 cell line and its possible mechanism].

This study was aimed to investigate the effects of gambogic acid on the cells of high-risk patients with myelodysplastic syndrome (MDS) in vitro and its mechanism. The inhibition effect of gambogic acid on growth of MUTZ-1 cell line of MDS-RAEB was detected by MTT method. Apoptosis and cell cycle were detected by morphological observation and flow cytometry respectively. The expressions of bax/bcl-2 gene at mRNA level were detected by RT-PCR. The results indicated that the Gambogic acid inhibited the growth of MUTZ-1 cells, the inhibitory rate of gambogic acid with the range of 0.2 - 0.8 microg/ml was enhanced along with increasing of drug concentration. Flow cytometric assay showed that the apoptotic rate of MUTZ-1 cells treated by gambogic acid also was enhanced along with increasing of drug concentration, the apoptotic rates resulting from gambogic acid (0, 0.4, 0.6, 0.8 microg/ml) were (5 +/- 0.5)%, (13 +/- 0.5)%, (37 +/- 0.7)% and (56 +/- 0.6)% respectively. The characteristic changes of apoptosis emerged in MUTZ-1 cells after being exposed to gambogic acid. Gambogic acid could significantly down-regulate the expressions of bcl-2 gene in a dose dependent manner, however, it had no effects on bax gene. It is concluded that within the range of concentration from 0.4 to 0. 8 microg/ml, gambogic acid can inhibit the growth of MUTZ-1 cells by inducing their apoptosis and down-regulating the expression of bcl-2 gene, which may be one of the main mechanisms underlying its antitumor effects.

Evaluation of immunological effects of hochu-ekki-to (TJ-41) prophylactic administration in mice.

We evaluated the immunological effects of a Kampo (Chinese) prescription Hochuekki-to (TJ-41) for 32 weeks and 1 week prophylactically in mice, The splenic natural killer cells (NK) of C57BL/6N mice prophylactically treated with TJ-41 for 32 weeks showed little enhanced cytotoxicity against NK-sensitive YAC-1 targets, but mice treated for 1 week showed significantly enhanced cytotoxicity. TJ-41 administration for 32 weeks increased the splenic NK cell population and CD4/CD8 significantly, but TJ-41 for 1 week was not affected. Further, there were no adverse effects of TJ-41 administration for 32 weeks. Whether or not that duration of administration can have the same beneficial effects on humans await further studies.