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PubMed2005

Synthesis of novel curcumin mimics with asymmetrical units and their anti-angiogenic activity.

Novel curcumin mimics with asymmetrical units phenyl group with alkyl amide, chloro-substituted benzamide, or heteroaromatic amide moieties were synthesized and their anti-angiogenic activity was evaluated with the proliferation and tube formation inhibitory activity on the human umbilical vein endothelial cells. Compounds 5, 14, 17, and 18 showed potent growth inhibitory activity and tube formation inhibitory activity.

Angiogenesis Inhibitors↗
PubMed2004

A new curcumin derivative, HBC, interferes with the cell cycle progression of colon cancer cells via antagonization of the Ca2+/calmodulin function.

HBC (4-[3,5-Bis-[2-(4-hydroxy-3-methoxy-phenyl)-ethyl]-4,5-dihydro-pyrazol-1-yl]-benzoic acid) is a recently developed curcumin derivative which exhibits potent inhibitory activities against the proliferation of several tumor cell lines. In the present study, we identified Ca2+/calmodulin (Ca2+/CaM) as a direct target protein of HBC using phage display biopanning. Ca2+/CaM-expressing phages specifically bound to the immobilized HBC, and the binding was Ca2+ dependent. Moreover, flexible docking modeling demonstrated that HBC is compatible with the binding cavity for a known inhibitor, W7, in the C-terminal hydrophobic pocket of Ca2+/CaM. In biological systems, HBC induced prolonged phosphorylation of ERK1/2 and activated p21(WAF1) expression, resulting in the induction of G0/G1 cell cycle arrest in HCT15 colon cancer cells. These results suggest that HBC inhibits the cell cycle progression of colon cancer cells via antagonizing of Ca2+/CaM functions.

Amino Acid Sequence↗
PubMed2004

Fluoride curcumin derivatives: new mitochondrial uncoupling agents.

The mitochondrial effects of two fluoride curcumin derivatives were studied. They induced the collapse of mitochondrial membrane potential (DeltaPsi), increased mitochondrial respiration, and decreased O(2)*- production and promoted Ca(2+) release. These effects were reversed by the recoupling agent 6-Ketocholestanol, but not by cyclosporin A, an inhibitor of the permeability transition pore (PTP), suggesting that these compounds act as uncoupling agents. This idea was reinforced by the analysis of the physico-chemical properties of the compounds indicating, that they are mainly in the anionic form in the mitochondrial membrane. Moreover, they are able to induce PTP opening by promoting the oxidation of thiol groups and the release of cytochrome c, making these two molecules potential candidates for induction of apoptosis.

Animals↗
PubMed2005

Mixed ligand copper(II) complexes of phenanthroline/bipyridyl and curcumin diketimines as DNA intercalators and their electrochemical behavior under Nafion and clay modified electrodes.

The mode of binding of copper(II) mixed ligand complexes of phen/bpy and Knoevenagel condensate of curcumin (4-salicylidene-1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione) and 4-X-anilines with herring sperm DNA has been investigated using spectral and electrochemical techniques in Tris-HCl buffer pH 7.1. On titration with DNA, usual hypochromism and unusual (large) red shift (30-35 nm) for some of these complexes were observed in their absorption spectra of intense intraligand (IL) pi-pi* transition around 420 nm. Variations in the absorbance due to their interaction with DNA on time scale were also investigated, under fixed concentrations of complex and DNA. On interaction with DNA, the quasi-reversible CuII/I redox couple slightly improves its reversibility with considerable decrease in current intensity. The intercalation of these copper complexes into the DNA base pairs was also investigated by gel retardation assay method. All the experimental results indicate that the phen mixed copper(II) complexes intercalate more effectively into the DNA base pairs than their bpy counterparts. Significant differences in the redox behavior of these copper(II) complexes under electrochemically modified GC electrodes with Nafion and K10 Montmorillonite clay have also been investigated and discussed.

2,2'-Dipyridyl↗
PubMed2006

Curcumin activated both receptor-mediated and mitochondria-mediated proteolytic pathways for apoptosis in human glioblastoma T98G cells.

The therapeutic effect of curcumin (CCM), a polyphenolic compound from the rhizome of Curcuma longa, has not yet been examined in glioblastoma. We used human glioblastoma T98G cells to explore the efficacy of CCM for inducing apoptosis and identifying proteolytic mechanisms involved in this process. Trypan blue dye exclusion test showed decrease in cell viability with increasing dose of CCM. Wright staining and ApopTag assay showed, respectively, morphological and biochemical features of apoptosis in T98G cells exposed to 25 microM and 50 microM of CCM for 24 h. Treatment with CCM activated receptor-mediated pathway of apoptosis as Western blotting showed activation of caspase-8 and cleavage of Bid to tBid. Besides, CCM caused an increase in Bax:Bcl-2 ratio, and mitochondrial release of cytochrome c, Second mitochondrial activator of caspases/Direct IAP binding protein with low pI (Smac/Diablo), and apoptosis-inducing-factor (AIF) indicating involvement of mitochondria-mediated pathway as well. Down regulation of the nuclear factor kappa B (NFkappaB), increased expression of inhibitor of nuclear factor kappa B alpha (IkappaB alpha), and decreased expression of inhibitor-of-apoptosis proteins (IAPs) such as c-IAP1 and c-IAP2 in T98G cells following CCM treatment suggested suppression of survival signal. Activation of caspase-9 and caspase-3 was detected in generation of 35 kD and 20 kD active fragments, respectively. Calpain and caspase-3 activities cleaved 270 kD alpha-spectrin at specific sites to generate 145 kD spectrin break down product (SBDP) and 120 kD SBDP, respectively. Our results strongly suggest that CCM induced both receptor-mediated and mitochondria-mediated proteolytic mechanisms for induction of apoptosis in T98G cells.

Antineoplastic Agents↗
PubMed2004

Study of the interaction of proteins with curcumin and SDS and its analytical application.

It is found that protein and sodium dodecyl sulphonate (SDS) can enhance resonance light scattering (RLS) of curcumin (CU). Based on this phenomenon, a new quantitative method for protein in aqueous solution has been developed. In the BR (pH 3.5) buffer, the RLS intensity of CU-SDS system is greatly enhanced by protein. The enhanced RLS is proportional to the concentration of protein in the range of 0.00020-20.0 microgml(-1) for bovine serum albumin (BSA) and 0.00040-1.0 microgml(-1) for human serum albumin (HSA) and their detection limits are 0.16 and 0.041 ngml(-1), respectively. An actual sample is satisfactorily determined. In addition, the interaction mechanism between protein and CU-SDS is also studied by using multi-techniques such as RLS, absorption spectroscopy and fluorescence, zeta potential assay measurement.

Animals↗
PubMed2006

Investigation of the interaction between curcumin and nucleic acids in the presence of CTAB.

It is found that nucleic acid can enhance the resonance light scattering (RLS) enhancement effect of curcumin (CU) in the presence of cationic surfactant cetyltrimethylammonium bromide (CTAB). The investigation indicates that in BR (pH 4.3) buffer, both the positive CTAB and negative yeast RNA (yRNA) combine and form a positive large association, then which is bound on the two carbon atoms of the carbonyls of CU through hydrogen bond and hydrophobic force and form CU-CTAB-yRNA ternary complex, resulting in the RLS enhancement of this system. Based on it, a sensitive method for determination of nucleic acids at ngml(-1) is established.

Cetrimonium↗
PubMed2002

Basal levels and patterns of anticancer drug-induced activation of nuclear factor-kappaB (NF-kappaB), and its attenuation by tamoxifen, dexamethasone, and curcumin in carcinoma cells.

Nuclear factor-kappaB (NF-kappaB) has been implicated in the development of drug resistance in cancer cells. We systematically examined the baseline levels of NF-kappaB activity of representative carcinoma cell lines, and the change of NF-kappaB activity in response to a challenge with four major anticancer drugs (doxorubicin, 5-fluorouracil, cisplatin, and paclitaxel). We found that the basal level of NF-kappaB activity was heterogeneous and roughly correlated with drug resistance. When challenged with various drugs, all the cell lines examined responded with a transient activation of NF-kappaB which then declined to basal level despite variation in the concentration of the agent and the timing of the treatment. In contrast to tumor necrosis factor-alpha (TNF-alpha), which activates NF-kappaB in minutes, NF-kappaB activation induced by anticancer drugs usually occurred more than 1hr after stimulation. A gradual increase of total NF-kappaB and its nuclear translocation, and cytoplasmic translocation of nuclear IkappaBalpha and its degradation were involved in this process. In particular, when cells were pretreated with common biologic modulators such as tamoxifen, dexamethasone, and curcumin, the doxorubicin-induced NF-kappaB activation was attenuated significantly. This inhibition may play a role in sensitizing cancer cells to chemotherapeutic drugs. This study has demonstrated that activation of NF-kappaB is a general cellular response to anticancer drugs, and the mechanism of activation appears to be distinct from that induced by TNF-alpha. These observations may have implications for improving the efficacy of systemic chemotherapy for cancer patients.

Active Transport, Cell Nucleus↗
PubMed1998

Glutathione-independent mechanism of apoptosis inhibition by curcumin in rat thymocytes.

Curcumin (CUR) is a natural yellow dye with antioxidant and scavenging properties present in Curcuma species. It is widely used as an anti-inflammatory, anti-mutagenic and chemopreventive agent. In addition to its inhibitory effect on proliferation, CUR has recently been shown to block dexamethasone-induced programmed cell death (apoptosis) of rat thymocytes. Because cellular thiols seem to play a role in redox regulation of apoptosis, the mechanism of the anti-apoptotic effect of CUR was studied by examining the levels of glutathione and acid-soluble sulfhydryl groups. CUR was shown to prevent the glutathione loss occurring in dexamethasone-treated thymocytes, enhancing intracellular glutathione content at 8 hr to 192% of that of nontreated cells. A 60% increase in acid-soluble sulfhydryl groups was also observed. In the presence of L-buthionine S,R-sulfoximine (BSO, an inhibitor of glutathione synthesis), intracellular glutathione content of thymocytes treated with dexamethasone and CUR fell to 31% and that of the acid-soluble sulfhydryl groups to 23% of control after 8 hr. Unexpectedly, the electrophoretic and flow cytometric studies of DNA fragmentation demonstrated that apoptosis did not occur even after 20 hr of incubation with buthionine S,R-sulfoximine and dexamethasone, while control thymocytes and the cells treated only with buthionine S,R-sulfoximine showed DNA fragmentation at a level corresponding to spontaneous apoptosis. These results show that CUR treatment elevated the concentrations of glutathione and nonprotein sulfhydryl groups, thus preventing their decrease in apoptotic thymocytes. Coadministration of L-buthionine S,R-sulfoximine and CUR did not affect the anti-apoptotic effect of CUR suggesting a glutathione-independent mechanism of cell protection.

Animals↗
PubMed2003

Pro-inflammatory agents accumulate during donor liver cold preservation: a study on increased adhesion molecule expression and abrogation by curcumin in cultured endothelial cells.

Cold hypoxia and re-oxygenation during organ preservation leads to a variety of stresses, including expression of adhesion molecules, which can promote inflammatory responses and compromised function. These studies were undertaken to investigate the pro-inflammatory activities of factors present in the vascular bed at the end of cold storage in livers during clinical hepatic transplantation. Effluent perfusate (termed pro-inflammatory vascular effluent-PVE) washed out at the end of cold storage, was collected from 10 donor livers, and used in a bio-assay with cultured endothelial cells exposed to cold hypoxia and re-oxygenation. Adhesion molecule expressions for intercellular adhesion molecule 1 (ICAM-1) and E-selectin were measured using molecular techniques and Northern blot analyses. Cells exposed to PVE during warming showed up-regulation of both ICAM-1 and E-selectin (p<0.05 in both cases) in all 10 preparations. Addition of curcumin (an inhibitor of nuclear transcription for the inflammatory cascade) abrogated expression of adhesion molecules at a statistically significant level for ICAM-1 in 8/10 PVE, and for E-selectin in all 10 PVE. We conclude that pro-inflammatory agents accumulate in livers during clinical liver transplantation and on rewarming may add to graft injury.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

Curcumin enhances the immunosuppressive activity of cyclosporine in rat cardiac allografts and in mixed lymphocyte reactions.

Curcumin (CCM; diferuoylmethane) is a dietary pigment in curry with known antineoplastic and anti-inflammatory effects. The immunosuppressive effects of CCM were studied in (1) rat heterotopic cardiac transplant models, using Brown-Norway (BN, RT1(n)) hearts to WKY (RT1(u)) hosts or Buffalo (BUF, RT1(b)) hearts to Wistar-Furth (WF, RT1(u)) hosts, (2) reverse transcriptase-polymerase chain reaction analysis of cytokines from transplanted specimens, and (3) mixed lymphocyte reactions (MLR). In the BN-to-WKY model, CCM alone significantly increased the mean survival time (MST) to 20.5 to 24.5 days, as compared to 9.1 days among nontreated controls. The combination of CCM and subtherapeutic doses of CsA produced further prolongation of the MST to 28.5 to 35.6 days, better than that of CCM or CsA alone (P <.05). In a BUF-to-WF model, CCM alone did not increased the MST, unless it was combined with subtherapeutic doses of CsA, wherein two thirds of the grafts survived for more than 60 days (P <.05 as compared to either treatment group). Cytokine analysis revealed significantly reduced expression of interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and granzyme B in the day 3 specimens of the CCM and CCM CsA-treated allografts compared with the nontreated allograft controls. MLRs using the two MHC-incompatible rat strains (BNxWKY) showed an effect of increasing concentrations of CCM and/or CsA, which by combination index (CI) analysis showed a synergistic effect (CI = 0.22 to 0.81). This study for the first time demonstrates the effectiveness of CCM as a novel adjuvant immunosuppressant with cyclosporine both in vivo and in vitro.

Animals↗
PubMed2000

Inhibition by curcumin of diethylnitrosamine-induced hepatic hyperplasia, inflammation, cellular gene products and cell-cycle-related proteins in rats.

Curcumin (CCM), a major yellow pigment of turmeric obtained from powdered rhizomes of the plant Curcuma longa Linn, is commonly used as coloring agent in foods, drugs and cosmetics. In this study we report that gavage administration of 200 mg/kg or 600 mg/kg CCM effectively suppressed diethylnitrosamine (DEN)-induced liver inflammation and hyperplasia in rats, as evidenced by histopathological examination. Immunoblotting analysis showed that CCM strongly inhibited DEN-mediated the increased expression of oncogenic p21(ras) and p53 proteins in liver tissues of rats. In cell-cycle-related proteins, CCM selectively reduced the expression of proliferating cell nuclear antigen (PCNA), cyclin E and p34(cdc2), but not Cdk2 or cyclin D1. Moreover, CCM also inhibited the DEN-induced increase of transcriptional factor NF-kappa B. However, CCM failed to affect DEN-induced c-Jun and c-Fos expression. It has become widely recognized that the development of human hepatocellular carcinoma (HCC) is predominantly due to the chronic inflammation by virus, bacteria or chemical. Our results suggest a potential role for CCM in the prevention of HCC.

Animals↗
PubMed1997

Effects of n-tritriacontane-16,18-dione, curcumin, chlorphyllin, dihydroguaiaretic acid, tannic acid and phytic acid on the initiation stage in a rat multi-organ carcinogenesis model.

The modifying effects of the naturally occurring antioxidants n-tritriacontane-16,18-dione (TTAD), curcumin, dihydroguaiaretic acid (DHGA), chlorophyllin, tannic acid and phytic acid on the initiation stage in a rat multi-organ carcinogenesis model were examined in male F344 rats. Animals were initiated with two i.p. injections of 2,2'-dihydroxy-di-n-propylnitrosamine (DHPN), followed by two i.g. administrations of N-ethyl-N-hydroxyethylnitrosamine (EHEN), and then three s.c. injections of 3,2'-methyl-4-aminobiphenyl (DMAB) during the first 3 weeks. Starting 1 day before the first carcinogen application, groups of rats received diet containing one of the antioxidants (0.2% TTAD, the others at 1% each) until 1 week after the last carcinogen exposure. Surviving animals were killed and complete autopsies were performed at the end of week 36. Histological examination revealed no inhibitory effects in terms of the multiplicities and/or incidences of neoplastic lesions in any of the organs examined, other than a significant increase in seminal vesicle atypical hyperplasia observed in rats treated with tannic acid. Thus, the antioxidants, with the exception of tannic acid, did not show any modifying effects on the initiation stage in the present multi-organ carcinogenesis model and at the present dose levels applied.

Aminobiphenyl Compounds↗
PubMed1998

Chemopreventive efficacy of curcumin-free aqueous turmeric extract in 7,12-dimethylbenz[a]anthracene-induced rat mammary tumorigenesis.

The modulating effects of turmeric (T), ethanolic turmeric extract (ETE) and curcumin-free aqueous turmeric extract (CFATE) on the initiation or post-initiation phases of DMBA-induced mammary tumorigenesis were investigated in female Sprague-Dawley rats. Dietary administration of 1% T/0.05% ETE 2 weeks before, on the day of DMBA treatment (day 55) and 2 weeks after the single dose (15 mg/animal) of DMBA (during the initiation period) resulted in significant suppression of DMBA-induced mammary tumorigenesis as seen by a reduction in tumor multiplicity, tumor burden and tumor incidence. However, simultaneous administration of 1% T-derived CFATE as the sole source of drinking water during the initiation phase did not suppress DMBA-induced mammary tumorigenesis. Dietary administration of 1% T/0.05% ETE or 1% T-derived CFATE as the sole source of drinking water starting 48 h after DMBA treatment and continuing until the end of the experiment (during the post-initiation period) resulted in significant suppression of DMBA-induced mammary tumorigenesis as seen by reduction in the tumor multiplicity and/or tumor burden although tumor incidence was unaffected. The present data clearly indicate that dietary administration of T/ETE showed strong chemopreventive activity during initiation as well as post-initiation phases of DMBA-induced rat mammary tumorigenesis while CFATE was found to be weakly active only when it was administered during the post-initiation phase.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2002

Protective effects of curcumin against ischaemia/reperfusion insult in rat forebrain.

Oxidative stress is believed to be implicated in the pathogenesis of postischaemic cerebral injury. Many antioxidants were shown to be neuroprotective in experimental models of cerebral ischaemia/reperfusion (I/R). The present study was designed to investigate the potential protective effects of curcumin (CUR) against I/R insult in rat forebrain. The model adopted was that of surgically-induced forebrain ischaemia, performed by means of bilateral common carotid artery occlusion (BCCAO) for 1 h, followed by reperfusion for another 1h. The effects of a single i.p. dose of CUR (50, 100 or 200 mg kg(-1)), administered 0.5 h after the onset of ischaemia, were investigated by assessing oxidative stress-related biochemical parameters in rat forebrain. CUR, at the highest dose level (200 mg kg(-1)), decreased the I/R-induced elevated xanthine oxidase (XO) activity, superoxide anion (O(2)*(-)) production, malondialdehyde (MDA) level and glutathione peroxidase (GPx), superoxide dismutase (SOD), and lactate dehydrogenase (LDH) activities. On the other hand, CUR did not affect the declined reduced glutathione (GSH) content due to I/R insult. Worth mentioning is that the activity of catalase (CAT) did not change in response to either I/R insult or drug treatment. In conclusion, CUR was found to protect rat forebrain against I/R insult. These protective effects may be attributed to its antioxidant properties and/or its inhibitory effects on xanthine dehydrogenase/xanthine oxidase (XD/XO) conversion and resultant O(2)*(-) production.

Animals↗
PubMed1999

Anti-tumor promoting potential of naturally occurring diarylheptanoids structurally related to curcumin.

In recent years, there have been considerable efforts to search for naturally occurring substances for intervention of carcinogenesis. Many components from medicinal or dietary plants have been identified to possess potential chemopreventive properties. For instance, curcumin, a yellow colouring agent from turmeric (Curcuma longa Linn., Zingiberaceae) has been shown to inhibit tumor formation in diverse animal models. Alpinia oxyphylla Miquel that also belongs to ginger family has been used in oriental herbal medicine. In the present work, we have evaluated the anti-tumor promoting potential of yakuchinone A (1-[4'-hydroxy-3'-methoxyphenyl]-7-phenyl-3-heptanone) and yakuchinone B (1-[4'-hydroxy-3'-methoxyphenyl]-7-phenylhept-1-en-3-one), major pungent ingredients of A. oxyphylla. Thus, topical application of yakuchinone A or B significantly suppressed TPA-induced epidermal ornithine decarboxylase activity. They also reduced TPA-stimulated production of tumor necrosis factor-alpha in cultured human promyelocytic leukemia (HL-60) cells. Both compounds blunted the TPA-induced superoxide generation in differentiated HL-60 cells in a concentration-related manner and also inhibited lipid peroxidation in rat brain homogenates. Furthermore, yakuchinone A and yakuchinone B nullified the activation of the activator protein-1 (AP-1) in immortalized mouse fibroblast cells in culture. These findings indicate that pungent diarylheptanoids from A. oxyphylla have anti-tumor promotional properties that can contribute to their chemopreventive potential.

3T3 Cells↗
PubMedDate not supplied

4-Hydroxy-3-methoxybenzoic acid methyl ester: a curcumin derivative targets Akt/NF kappa B cell survival signaling pathway: potential for prostate cancer management.

Transcription factor NFkappaB and the serine/threonine kinase Akt play critical roles in mammalian cell survival signaling and have been shown to be activated in various malignancies including prostate cancer (PCA). We have developed an analogue of curcumin called 4-hydroxy-3-methoxybenzoic acid methyl ester (HMBME) that targets the Akt/NFkappaB signaling pathway. Here, we demonstrate the ability of this novel compound to inhibit the proliferation of human and mouse PCA cells. HMBME-induced apoptosis in these cells was tested by using multiple biochemical approaches, in addition to morphologic analysis. Overexpression of constitutively active Akt reversed the HMBME-induced growth inhibition and apoptosis, illustrating the direct role of Akt signaling in HMBME-mediated growth inhibition and apoptosis. Further, investigation of the molecular events associated with its action in LNCaP cells shows that: 1) HMBME reduces the level of activated form of Akt (phosphorylated Akt); and 2) inhibits the Akt kinase activity. Further, the transcriptional activity of NFkappaB, the DNA-binding activity of NFkappaB, and levels of p65 were all significantly reduced following treatment with HMBME. Overexpression of constitutively active Akt, but not the kinase dead mutant of Akt, activated the basal NFkappaB transcriptional activity. HMBME treatment had no influence on this constitutively active Akt-augmented NFkappaB transcriptional activity. These data indicate that HMBME-mediated inhibition of Akt kinase activity may have a potential in suppressing/decreasing the activity of major survival/antiapoptotic pathways. The potential use of HMBME as an agent that targets survival mechanisms in PCA cells is discussed.

Animals↗