Stability of curcumin in buffer solutions and characterization of its degradation products

Wang, Ying Jan; Pan, Min‐Hsiung; Cheng, Ann‐Lii; Lin, Liang-In; Ho, Yuan‐Soon; Hsieh, Chang‐Yao; Lin, Jen‐Kun

doi:10.1016/s0731-7085(96)02024-9

Cited by 1,445 publications

(1,001 citation statements)

References 16 publications

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“…These authors have thoroughly studied the stability of curcumin in aqueous solvents in the presence of thiols. We used cell culture medium containing 10% FBS; and these conditions have been shown also to stabilize curcumin [54]. Curcumin has been shown to induce mitochondrial membrane-permeability transition pores through thiol oxidation [55].…”

Section: Discussionmentioning

confidence: 99%

Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)

Sandur

Ichikawa

Pandey

et al. 2007

Free Radical Biology and Medicine

264

172

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Extensive research within last half a century has indicated that curcumin (diferuloylmethane), a yellow pigment in curry powder, exhibits antioxidant, anti-inflammatory and proapoptotic activities. Whether anti-inflammatory and proapoptotic activities assigned to curcumin, are mediated through its antioxidant mechanism was investigated. We found that TNF-mediated NF-κB activation was inhibited by curcumin; and glutathione reversed the inhibition. Similarly, suppression of TNFinduced AKT activation by curcumin, was also abrogated by glutathione. The reducing agent also counteracted the inhibitory effect of curcumin on TNF-induced NF-κB regulated antiapoptotic (Bcl-2, Bcl-xL, IAP1), proliferative (cyclin D1) and proinflammatory (COX-2, iNOS and MMP-9) gene products. The suppression of TNF-induced AP-1 activation by curcumin was also reversed by glutathione. Also, the direct proapoptotic effects of curcumin were inhibited by glutathione and potentiated by depletion of intracellular glutathione by buthionine sulfoximine. Moreover, curcumin induced the production of reactive oxygen species (ROS) and modulated the intracellular GSH levels. Quenchers of hydroxyl radicals, however, were ineffective in inhibiting curcumin mediated NF-κB suppression. Further, N-acetylcysteine partially reversed the effect of curcumin. Based on these results we conclude that curcumin mediate its apoptotic and anti-inflammatory activities through modulation of the redox status of the cell.

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Section: Discussionmentioning

confidence: 99%

Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)

Sandur

Ichikawa

Pandey

et al. 2007

Free Radical Biology and Medicine

264

172

View full text Add to dashboard Cite

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“…containing 10% fetal calf serum and in human blood, <20% of curcumin being degraded within 1 h and approximately 50% by 8 h [15]. trans-6-(4 0 -Hydroxy-3 0 -methoxyphenyl)-2,4-dioxo-5-hexenal is a major degradation product; vanillin, ferulic acid, feruloylmethane are minor degradation products…”

Section: U N C O R R E C T E D P R O O Fmentioning

confidence: 99%

Curcumin as “Curecumin”: From kitchen to clinic

Goel

Kunnumakkara

Aggarwal

2008

Biochemical Pharmacology

1,864

1,290

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“…Stability in cell culture medium containing 10% FBS or in human blood is greater than in phosphate buffer, but 50% of the molecule has still decomposed after 8 hours [23,24].…”

Section: Introductionmentioning

confidence: 99%

Curcumin derivatives: Molecular basis of their anti-cancer activity

Basile

Ferrari

Lazzari

et al. 2009

Biochemical Pharmacology

161

129

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Curcumin, a phenolic compound from the plant Curcuma longa L., has shown a wide-spectrum of chemopreventive, anti-oxidant and anti-tumor properties. Although its promising chemotherapeutic activity, preclinical and clinical studies highlight Curcumin limited therapeutic application due to its instability in physiological conditions. To improve its stability and activity, many derivatives have been synthesized and studied, among which bis-DemethoxyCurcumin (bDMC) and diAcetylCurcumin (DAC). In this report, we show that both bDMC and DAC are more stable than Curcumin in physiological medium. To explore the mechanism of their chemotherapeutic effect, we studied their role in proliferation in the HCT116 human colon cancer cells. We correlated kinetic stability and cellular uptake data to their biological effects. Both bDMC and DAC impair correct spindles formation and induce a p53-and p21 CIP1/WAF1 -independent mitotic arrest, which is more stable and long-lasting for bDMC. A subsequent p53/p21 CIP1/WAF1 -dependent inhibition of G1 to S transition is triggered by Curcumin and DAC as a consequence of the mitotic slippage, preventing postmitotic cells from re-entering the cell cycle. Conversely, the G1/S arrest induced by bDMC is a direct effect of the drug and concomitant to the mitotic block. Finally, we demonstrate that bDMC induces rapid DNA double-strand breaks, moving for its possible development in anti-cancer clinical applications.

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Stability of curcumin in buffer solutions and characterization of its degradation products

Cited by 1,445 publications

References 16 publications

Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)

Role of pro-oxidants and antioxidants in the anti-inflammatory and apoptotic effects of curcumin (diferuloylmethane)

Curcumin as “Curecumin”: From kitchen to clinic

Curcumin derivatives: Molecular basis of their anti-cancer activity

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