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PubMed2002

Activations of ERK1/2 and JNK by transforming growth factor beta negatively regulate Smad3-induced alkaline phosphatase activity and mineralization in mouse osteoblastic cells.

Transforming growth factor (TGF) beta inhibits alkaline phosphatase (ALP) activity and mineralization in mouse osteoblastic MC3T3-E1 cells, whereas local administration of TGF-beta stimulates bone formation in vivo. We recently demonstrated that Smad3, a TGF-beta signaling molecule, promotes ALP activity and mineralization in MC3T3-E1 cells. Moreover, the target disruption of Smad3 in mouse is reported to cause a decrease in bone mineral density. These findings indicate that Smad3 plays an important role in the regulation of bone formation. However, why the effects of TGF-beta and Smad3 on ALP activity and mineralization are different remains unknown. The purpose of the present study is to clarify the role of mitogen-activated protein kinase (MAPK) in TGF-beta and Smad3 pathways in osteoblast. TGF-beta activated extracellular signal-regulated kinases/p42/p44 (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase (JNK) in mouse osteoblastic MC3T3-E1 cells. The expression of dominant negative type Smad3, Smad3DeltaC, affected neither TGF-beta-activated MAPKs nor TGF-beta-inhibited ALP activity. Specific inhibitors of ERK1/2 activation (PD98059 and U0126), as well as JNK inhibitors (curcumin and dicumarol) antagonized the inhibitory effects of TGF-beta on ALP activity and mineralization, whereas the specific inhibitor of p38 MAPK (SB203580) did not affect them. PD98059 and curcumin enhanced Smad3-induced ALP activity and mineralization, whereas SB203580 inhibited them. In the luciferase reporter assay using 3TP-lux with the specific Smad3-responsive element, PD98059, and curcumin enhanced TGF-beta- and Smad3-induced transcriptional activity in MC3T3-E1 cells. On the other hand, TGF-beta-induced production of type I collagen was antagonized by curcumin but not by PD98059. The present study indicated that TGF-beta-responsive ERK1/2 and JNK cascades negatively regulate Smad3-induced transcriptional activity as well as ALP activity and mineralization in osteoblasts.

Alkaline Phosphatase↗

PubMed2004

Modification of radiation-induced acute oral mucositis in the rat.

PURPOSE: A new non-toxic drug (compound A) consisting of curcumin, alpha-tocopherol and sunflower oil was developed and its efficacy tested in the treatment of radiation-induced oral mucositis in the rat. MATERIAL AND METHODS: Mature (12 weeks old, 200-225 g) female Sprague-Dawley rats were used. While under general anaesthesia, the tongues of the animals were slightly extended outside and a region of the underside of the tongue was irradiated in-situ with single doses of 2.27 MeV beta-rays from a 5-mm diameter 90Sr/90Y plaque. The dose-rate of the source was about 10 Gy min(-1) at the surface of the mucus membrane. Irradiations and subsequent assessment of the lesion were carried out under general anaesthesia maintained by a 1.5% halothane/oxygen mixture. Six groups of animals were irradiated with single doses of 13.5, 15.0, 16.5 or 18Gy. One subgroup (radiation only) received no further treatment, while the other five groups received 0.5 ml day(-1) of either compound A, sunflower oil, alpha-tocopherol, curcumin or water containing 10% ethanol by oral gavage until the end of experiments. Mucosal ulceration (erosion of mucosal epithelium) was considered as an end-point. From the day after irradiation until any acute radiation-induced oral mucosal lesion had healed, the tongues of the animals were assessed daily for the presence of radiation-induced mucositis (mucosal ulceration). Quantal data for the incidence of radiation-induced mucositis were analysed using logit analysis and a dose-modification factor was obtained. RESULTS: There was a modest increase in ED50, the dose expected to cause mucositis in 50% of the animals after both alpha-tocopherol and sunflower oil were administered. This resulted in dose-modification factors of 1.05. While curcumin treatment resulted in a dose-modification factor of 1.09. Compound A significantly reduced the incidence of radiation-induced mucositis with a statistically significant dose-modification factor of 1.2 +/- 0.1. CONCLUSIONS: Curcumin and other components of compound A appeared to be effective in the prevention of radiation-induced oral mucositis. However, the overall effect observed with the combination drug (compound A) appeared greater than additive.

Animals↗

PubMed2005

Effects of nuclear factor-kappaB inhibitors and its implication on natural killer T-cell lymphoma cells.

Natural killer/T-cell lymphoma (NKTL) is a highly aggressive disease. Despite the use of various treatment regimens, the prognosis of NKTL is poor, and new treatment strategies need to be determined. Because of the significant survival potential, nuclear factor (NF)-kappaB has become one of the major targets for drug development. In this study, we explored the effect and action mechanism of NF-kappaB inhibitors, BAY 11-7082 and curcumin, on NKTL cell lines (NKL, NK-92 and HANK1). Electrophoretic mobility shift assay showed that NF-kappaB was constitutively active in HANK1, a chemoresistant cell line. BAY 11-7082 and curcumin suppressed NF-kappaB activation in a time- and dose-dependent manner, which finally resulted in cell death. BAY 11-7082- and curcumin-induced cell death was associated with downregulation of Bcl-xL, cyclin D1, XIAP and c-FLIP, followed by caspase-8, poly(ADP-ribose) polymerase cleavage and activation. Given that the chemoresistant NK-92 cells respond to NF-kappaB inhibitors but not to conventional drugs, BAY 11-7082 and curcumin could be potentially useful for achieving improved outcome in chemotherapy-refractory NKTL.

CASP8 and FADD-Like Apoptosis Regulating Protein↗

PubMed2005

CSN5/Jab1 is involved in ligand-dependent degradation of estrogen receptor {alpha} by the proteasome.

Here, we show that estrogen receptor alpha (ERalpha) coimmunoprecipitates with CSN5/Jab1, a subunit of the COP9 signalosome (CSN), and that overexpression of CSN5/Jab1 causes an increase in ligand-induced ERalpha degradation. Inhibition of either the kinase activity associated with the CSN complex by curcumin or of nuclear export by leptomycin B (LMB) impaired estradiol-induced ERalpha degradation by the proteasome. Degradation of ERalpha induced by the pure antagonist ICI 182,780 (ICI) was blocked by curcumin but not by LMB, indicating that in the presence of ICI, ERalpha is degraded by a nuclear fraction of the proteasome. In addition, we observed that curcumin inhibited estradiol-induced phosphorylation of ERalpha. The use of three inhibitors of ERalpha degradation that target different steps of the estrogen response pathway (inhibition of the CSN-associated kinase, nuclear export, and proteasome) suggests that a phosphorylation event inhibited by curcumin is necessary for ERalpha binding to its cognate DNA target. Our results demonstrate that transcription per se is not required for ERalpha degradation and that assembly of the transcription-initiation complex is sufficient to target ERalpha for degradation by the proteasome.

Active Transport, Cell Nucleus↗

PubMed2000

SAPKs regulation of ischemic preconditioning.

The role of stress-activated protein kinases (SAPKs), c-Jun NH(2)-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase, in preconditioning (PC) was examined with the use of isolated rat hearts subjected to four cyclic episodes of 5-min ischemia and 10-min reperfusion followed by 30-min ischemia and 2-h reperfusion (I/R). A group of hearts was preperfused with 100 microM curcumin, a c-Jun and JNK1 inhibitor, or 5 microM SB 203580, a p38 MAP kinase inhibitor. Another group of hearts was preperfused with 20 microM anisomycin, a stimulator for both JNK and p38 MAP kinases. I/R increased the protein levels of JNK1, c-Jun, and p38 MAP kinase. PC also enhanced the induction of these kinases, but subsequent I/R-mediated increase was blocked by PC. Curcumin blocked I/R- and PC-mediated increase in JNK1 and c-Jun protein levels, whereas it had no effects on p38 MAP kinase. SB 203580, on the other hand, was equally effective in reducing the p38 MAP kinase activation but exerted no effects on JNK1 and c-Jun induction. I/R-mediated increased myocardial infarction was reduced by any of the following compounds: anisomycin, curcumin, and SB 203580. The cardioprotective effects of PC were abolished by either curcumin or SB 203580. The results demonstrate that PC is mediated by a signal-transduction pathway involving both JNK1 and p38 MAP kinase. Activation of SAPKs, although transient, is obligatory for PC.

Animals↗

PubMed2004

Phytoestrogens in common herbs regulate prostate cancer cell growth in vitro.

Prostate cancer is an important public health problem in the United States. Seven phytoestrogens found in common herbal products were screened for estrogen receptor binding and growth inhibition of androgen-insensitive (PC-3) and androgen-sensitive (LNCaP) human prostate tumor cells. In a competitive 3H-estradiol ligand binding assay using mouse uterine cytosol, 2.5 M quercetin, baicalein, genistein, epigallocatechin gallate (EGCG), and curcumin displaced > 85% of estradiol binding, whereas apigenin and resveratrol displaced > 40%. From growth inhibition studies in LNCaP cells, apigenin and curcumin were the most potent inhibitors of cell growth, and EGCG and baicalein were the least potent. In PC-3 cells, curcumin was the most potent inhibitor of cell growth, and EGCG was the least potent. In both cell lines, significant arrest of the cell cycle in S phase was induced by resveratrol and EGCG and in G2M phase by quercetin, baicalein, apigenin, genistein, and curcumin. Induction of apoptosis was induced by all of the 7 compounds in the 2 cell lines as shown by TUNEL and DNA fragmentation assays. Androgen responsiveness of the cell lines did not correlate with cellular response to the phytoestrogens. In conclusion, these 7 phytoestrogens, through different mechanisms, are effective inhibitors of prostate tumor cell growth.

Antineoplastic Agents, Hormonal↗

PubMedDate not supplied

Prevention of 1,2-dimethylhydrazine-induced circulatory oxidative stress by bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione during colon carcinogenesis.

We have performed this study to investigate the modulatory effect of bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione, a bisdemethoxy curcumin analog (BDMCA) on circulatory lipid peroxidation (LPO) and antioxidant status during 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Wistar rats. The effects were compared with that of the reference drug, curcumin. Increased tumor incidence as well as enhanced LPO in the circulation of tumor bearing rats was accompanied by a significant decrease in the level of reduced glutathione and activities of glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT). Intragastric administration of BDMCA or curcumin to DMH-treated rats significantly decreased colon tumor incidence and the circulatory LPO, with simultaneous enhancement of GSH content and GPx, GST, SOD and CAT activities. We report that BDMCA exert its chemopreventive effect by decreasing the colon tumor incidence as well as by modulating circulatory oxidative stress in DMH-treated rats through its influence on LPO and antioxidant status. The effects of BDMCA were comparable with that of the reference compound curcumin, a well known anticarcinogen and antioxidant. Thus, it would be suggested that the methoxy group is not responsible for the beneficial effects, however, the terminal phenolic moieties or the central 7-carbon chain may play a role.

1,2-Dimethylhydrazine↗

PubMed2006

Cumulative antioxidant defense against oxidative challenge in galactose-induced cataractogenesis in Wistar rats.

Natural dietary ingredients are known for their antioxidant activity. Of such, curcumin, the active principle of turmeric, at 0.01% in the diet proved as pro-oxidative in galactose-induced cataract in vivo. The purpose of this study was to investigate the effect of vitamin E (VE), a well-known antioxidant, in combination with curcumin on the onset and maturation of galactose induced cataract. Periodic slit-lamp microscope examination indicated that in combination with vitamin-E, 0.01% curcumin (G-IV) delayed the onset and maturation of galactose-induced cataract. Biochemical analyses revealed that combined treatment of 0.01% curcumin and vitamin-E diet exhibited an efficient antioxidant effect, as it inhibited lipid peroxidation and contributed to a distinct rise in reduced glutathione content. The results indicate that natural dietary ingredients are effective in combination rather than the individual administration as they are complementing each other in reducing the risk of galactose induced cataract.

Animals↗

PubMed2000

Influence of dietary spices and their active principles on pancreatic digestive enzymes in albino rats.

A few common spices or their active principles were examined for their possible influence on digestive enzymes of pancreas in experimental rat. Groups of animals were maintained for 8 weeks on the following spice diets: curcumin (0.5%), capsaicin (15 mg%), piperine (20 mg%), ginger (50 mg%), cumin (1.25%), fenugreek (2%), mustard (250 mg%) and asafoetida (250 mg%). Dietary curcumin, capsaicin, piperine, ginger, fenugreek and asafoetida prominently enhanced pancreatic lipase activity. Curcumin, capsaicin, piperine, ginger, cumin and asafoetida also stimulated pancreatic amylase. Trypsin was significantly stimulated by curcumin, capsaicin, piperine, ginger and cumin, while chymotrypsin was stimulated by all the spices tested except mustard. This stimulatory influence of test spices on the pancreatic digestive enzymes was however not observed when their intake was restricted to a single oral dose. The positive influences on the pancreatic digestive enzymes exerted by a good number of spices consumed in diet could be a factor contributing to the well recognised digestive stimulant action of spices.

Amylases↗

PubMed2004

Spice phenolics inhibit human PMNL 5-lipoxygenase.

A wide variety of phenolic compounds and flavonoids present in spices possess potent antioxidant, antimutagenic and anticarcinogenic activities. We examined whether 5-lipoxygenase (5-LO), the key enzyme involved in biosynthesis of leukotrienes is a possible target for the spices. Effect of aqueous extracts of turmeric, cloves, pepper, chili, cinnamon, onion and also their respective active principles viz., curcumin, eugenol, piperine, capsaicin, cinnamaldehyde, quercetin, and allyl sulfide were tested on human PMNL 5-LO activity by spectrophotomeric and HPLC methods. The formation of 5-LO product 5-HETE was significantly inhibited in a concentration-dependent manner with IC(50) values of 0.122-1.44 mg for aqueous extracts of spices and 25-83 microM for active principles, respectively. The order of inhibitory activity was of quercetin>eugenol>curcumin>cinnamaldehyde>piperine>capsaicin>allyl sulfide. Quercetin, eugenol and curcumin with one or more phenolic ring and methoxy groups in their structure showed high inhibitory effect, while the non-phenolic spice principle allyl sulfide showed least inhibitory effect on 5-LO. The inhibitory effect of quercetin, curcumin and eugenol was similar to that of synthetic 5-LO inhibitors-phenidone and NDGA. Moreover, the inhibitory potency of aqueous extracts of spice correlated with the active principles of their respective spices. The synergistic or antagonistic effect of mixtures of spice active principles and spice extracts were investigated and all the combinations of spice active principles/extracts exerted synergistic effect in inhibiting 5-LO activity. These findings clearly suggest that phenolic compounds present in spices might have physiological role in modulating 5-LO pathway.

Arachidonate 5-Lipoxygenase↗

PubMed1991

The effect of spices on cholesterol 7 alpha-hydroxylase activity and on serum and hepatic cholesterol levels in the rat.

The effect of feeding curcumin, capsaicin, ginger, mustard, black pepper and cumin on cholesterol and bile acid metabolism was studied in rats. The activity of hepatic cholesterol-7 alpha-hydroxylase, the rate-limiting enzyme of bile acid biosynthesis, was significantly elevated in curcumin (turmeric), capsaicin (red pepper), ginger and mustard treated animals. The enzyme activity was comparable to controls in black pepper and cumin fed rats. Serum and liver microsomal cholesterol contents were significantly higher in the curcumin and capsaicin treated animals. Thus, this study has suggested that the spices--turmeric, red pepper, ginger and mustard can stimulate the conversion of cholesterol to bile acids, an important pathway of elimination of cholesterol from the body. However, simultaneous stimulation of cholesterol synthesis by the spice principles--curcumin and capsaicin suggests that there may not be any significant contribution of stimulation of bile acid biosynthesis to the hypocholesterolemic action of these spices, and the latter action may solely be due to interference with exogenous cholesterol absorption.

Animals↗

PubMed1995

TGF-beta induces expression of monocyte chemoattractant JE/monocyte chemoattractant protein 1 via transcriptional factor AP-1 induced by protein kinase in osteoblastic cells.

In this work, we demonstrate the signal-transducing mechanism of TGF-beta 1 for gene expression of monocyte chemoattractant JE/monocyte chemoattractant protein 1 (MCP-1) in clonal osteoblastic MC3T3-E1 cells. TGF-beta 1-induced JE/MCP-1 gene expression in the cells was inhibited markedly by H-7 (1-(5-isoguinolinesulfonyl)-2-O-methylpiperazine-dihydrochloride) and staurosporine, potent inhibitors of protein kinase. TGF-beta 1-induced expression of both early proto-oncogenes c-fos and c-jun in the cells was also inhibited by H-7 and staurosporine. Antisense oligonucleotides to c-fos and c-jun genes inhibited significantly the cytokine-induced JE/MCP-1 gene expression. Curcumin, a specific inhibitor of c-jun/AP-1, inhibited the cytokine-induced c-jun gene expression in a dose-dependent manner, though the c-fos gene expression was not affected. TGF-beta 1 stimulated transcriptionally the JE/MCP-1 gene expression, and this stimulation was inhibited significantly by curcumin. Curcumin-induced inhibition of the JE/MCP-1 gene product was also evidenced by both an assay involving immunoprecipitation with antiserum specific for JE/MCP-1 and an assay for monocyte chemotaxis. Curcumin markedly inhibited AP-1 binding activity to 12-tetradecanoyl phorbol-13-acetate-responsive element (TRE) in the cytokine-treated cells. Furthermore, H-7 and staurosporine also inhibited the binding activity to TRE in the cells treated by the cytokine. These results demonstrate that TGF-beta 1 induces expression of monocyte chemoattractant JE/MCP-1 via the transcriptional factor AP-1 induced by protein kinase in the osteoblastic cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1995

[Substituted methoxyphenol with antioxidative activity: correlation between physicochemical and biological results].

Guaiacol moiety has been found in antiinflammatory compounds present in traditional african or chinese medicine. As the activity of these products could be due to reactions with the reactive oxygen species (ROS) or enzymes involved in the inflammatory reaction, a comparative study has been done between biological and physico-chemical investigations. Antioxidant properties of six guaiacol derivatives were measured in vitro by the inhibition of cyclooxygenase activities in human platelets and of the release of ROS by human polymorphonuclear leucocytes (PMNs). PMNs were stimulated by the bacterial peptide N-fMetLeuPhe (FMLP) and the protein kinase C activator phorbol myristate acetate (PMA) using luminol as chemiluminescent probe. Electron Spin Resonance (ESR) and the technique of spin-trapping with 5,5-dimethyl-pyrroline-N-oxide (DMPO) have been used to quantify hydroxyl and superoxide scavenging activities. Hydroxyl radicals were generated by the Fenton's reaction (Fe2+/H2O2) and the superoxide anion by the acetaldehyde/xanthine oxydase system (AC/XOD). The PMNs tests revealed that curcumin and methyl ferulate appeared as the most active compounds. Platelet cycloxygenase activity was inhibited by curcumin and cyclovalone. ESR studies showed a better ROS scavenging activity for vanillin, methyl ferulate and curcumin. Whatever test we used, curcumin and methylferulate appeared as the most interesting antioxidative compounds.

Antioxidants↗

PubMed2003

In vitro peroxynitrite scavenging activity of diarylheptanoids from Curcuma longa.

Peroxynitrite is a cytotoxic intermediate produced by the reaction between the superoxide anion (O(2)) and nitric oxide (NO). The aim of this study was to investigate the scavenging effects of Curcuma longa L. on authentic peroxynitrite, and further studies are planned that will attempt to identify the active principles from the active fractions. The methanolic extract of C. longa showed 50% scavenging activity (IC(50)) at concentration of 1.7 +/- 0.08 micro g/ml, and was thus fractionated with several solvents. The peroxynitrite scavenging activity potential of the individual fraction was in the order of ethyl acetate > dichloromethane > water fraction. The ethyl acetate soluble fraction exhibiting strong scavenging activity was further purified by repeated silica gel column chromatography. Peroxynitrite scavenging diarylheptanoids, curcumin I (1), curcumin II (2), and curcumin III (3) were isolated as active principles. Compounds 1-3 showed the peroxynitrite scavenging activities with IC(50) values of 4.0 +/- 0.04, 6.4 +/- 0.30, and 29.7 +/- 1.29 micro M, respectively. Penicillamine as positive control exhibited IC(50) value of 2.38 +/- 0.34 micro M. The structure-activity relationship of diarylheptanoids on peroxynitrite was also discussed.

Curcuma↗

PubMed1990

Fuel smoke condensate induced DNA damage in human lymphocytes and protection by turmeric (Curcuma longa).

Twigs-dry leaves smoke condensate (TDS) was investigated for its DNA damaging activity in human peripheral lymphocytes, by using a sensitive method, fluorescence analysis of DNA unwinding (FADU). An aqueous turmeric component (Aq.T) was studied as a protective agent. TDS at one to 100 folds dilution induced 55% DNA damage at 20 min, while 12-O-tetradecanoylphorbol-13-acetate (TPA) at 10 ng/ml induced only 25% damage. Aq.T at 300 ng/microliter afforded 90% protection to DNA against TDS and 65% against TPA. The mechanism of Aq.T protection was investigated by using (i) inhibitors of arachidonate cascade, viz., indomethacin (28 microM), NDGA (10 microM), DBAP (36 microM), (ii) antioxidant enzymes viz., CAT (0.2 U/microliter), SOD (0.6 U/microliter), (iii) antioxidants--BHA, curcumin (40 microM), mixed gangliosides (20 nM) and protease inhibitor TLCK (100 microM). These compounds offered the following extents of protection to DNA against TDS: indomethacin--40%, NDGA--83%, DBAP--70%, SOD--38%, CAT--40%, BHA--38%, curcumin--60%, mixed gangliosides--88%, TLCK--85%. Against TPA as clastogenic agent, the extents of protection were: indomethacin--73%, NDGA--32%, DBAP--72%, SOD--60%, CAT, BHA-negligible, curcumin--23%, mixed gangliosides--60%, TLCK--59%. These results indicate that (i) TDS and TPA induce DNA damage possibly by different mechanisms, (ii) Aq.T is a more effective protectant against TDS whereas it is on par with other inhibitors against TPA.

Catechols↗

PubMed2003

Sulindac sulfide and caffeic acid phenethyl ester suppress the motility of lung adenocarcinoma cells promoted by transforming growth factor-beta through Akt inhibition.

Cell migration is essential for invasive and metastatic phenotypes of cancer cells. Potential chemopreventive agents of cancer-sulindac sulfide, caffeic acid phenethyl ester (CAPE), curcumin, and (+)-catechin-have been reported to interfere with several types of intracellular signaling. In this study, we examined the effects of these agents on transforming growth factor-beta(TGF-beta)-induced motility and Akt phosphorylation in A549 cells. Judged by gold particle phagokinesis assay, sulindac sulfide, CAPE, and curcumin suppressed the motility of A549 cells promoted by TGF-beta. LY294002, a specific inhibitor of phosphatidylinositol 3-kinase(PI3K)/Akt signaling, also suppressed TGF-beta-induced motility and Akt phosphorylation. Sulindac sulfide and CAPE, but not curcumin, suppressed TGF-beta-induced Akt phosphorylation. We conclude that sulindac sulfide and CAPE suppress the motility promoted by TGF-beta in lung adenocarcinoma cells through the suppression of Akt. Our observations raise the possibility that these agents, except for (+)-catechin, can be applied not only as chemopreventive agents but also as anti-metastatic therapy.

Adenocarcinoma↗

PubMed2007

Changes in glycoprotein components in streptozotocin--nicotinamide induced type 2 diabetes: influence of tetrahydrocurcumin from Curcuma longa.

Curcuma longa (Zingiberaceae) has been used traditionally as antidiabetic, and has been proven scientifically to possess high antioxidant activity and anticancer properties. The active components of Curcuma longa such as curcumin and tetrahydrocurcumin (THC), a major colourless metabolite of curcumin also possesses antidiabetic, antiinflammatory and antioxidant activity. The ethnopharmacological value of this plant, the effect of THC on glycoproteins was carried out in normal and streptozotocin-nicotiniamide induced type 2 hyperglycaemic rats for 45 days. Glucose, plasma insulin and glycoprotein components in plasma and tissues (hexose, hexosamine, fucose and sialic acid) were determined. Oral administration of THC to diabetic rats showed a decrease in the level of blood glucose and plasma glycoproteins. The levels of plasma insulin and tissue sialic acid were increased where as the levels of tissue hexose, hexosamine and fucose were near normal in diabetic rats treated with THC. The present study indicates that the THC possesses a significant beneficial effect on glycoprotein moiety in addition to its antidiabetic effect. The effect of THC is more prominent than curcumin.

Animals↗

PubMed1996

Anti-genotoxic effects in mice after the interaction between coffee and dietary constituents.

The interaction between coffee (100 mg freeze-dried home brew/kg body weight) and dietary constituents was assessed for anti-genotoxic effects against cyclophosphamide, N-methyl-N-nitro-N- nitrosoguanidine (MNNG), N-nitroso-N-ethylurea, mitomycin C and urethane (URE) in the mouse bone marrow micronucleus test. Combinations of dietary constituents consisting of (1) chlorogenic acid, caffeic acid, ellagic acid and ferulic acid, (2) beta-carotene, curcumin and alpha-tocopherol, (3) chlorogenic acid, curcumin, alpha-tocopherol, anethole and eugenol, and (4) beta-carotene, curcumin, ellagic acid and chlorogenic acid were used in this study. Before the genotoxin was injected i.p., identical groups of mice were orally administered either vehicle control, coffee, dietary constituents, or coffee plus dietary constituents. Co-administration of coffee with the dietary constituents enhanced the anti-genotoxic effect compared with that of either coffee or the dietary constituents alone. Two-factor analysis of variance of the data suggests that there is a significant synergistic interaction between coffee and the dietary constituents for anti-genotoxic effects against MNNG (combination 1 and 2) and URE (combination 4).

Allylbenzene Derivatives↗