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Anticancer potential of curcumin: preclinical and clinical studies.

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TLDR
Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis, and Pharmacologically,Curcumin has been found to be safe.
Abstract
Curcumin (diferuloylmethane) is a polyphenol derived from the plant Curcuma longa, commonly called turmeric. Extensive research over the last 50 years has indicated this polyphenol can both prevent and treat cancer. The anticancer potential of curcumin stems from its ability to suppress proliferation of a wide variety of tumor cells, down-regulate transcription factors NF- κB, AP-1 and Egr-1; down-regulate the expression of COX2, LOX, NOS, MMP-9, uPA, TNF, chemokines, cell surface adhesion molecules and cyclin D1; down-regulate growth factor receptors (such as EGFR and HER2); and inhibit the activity of c-Jun N-terminal kinase, protein tyrosine kinases and protein serine/threonine kinases. In several systems, curcumin has been described as a potent antioxidant and anti-inflammatory agent. Evidence has also been presented to suggest that curcumin can suppress tumor initiation, promotion and metastasis. Pharmacologically, curcumin has been found to be safe. Human clinical trials indicated no dose-limiting toxicity when administered at doses up to 10 g/day. All of these studies suggest that curcumin has enormous potential in the prevention and therapy of cancer. The current review describes in detail the data supporting these studies. Curcumin, derived from turmeric (vernacular name: Haldi), is a rhizome of the plant Curcuma longa. The medicinal use of this plant has been documented in Ayurveda (the Indian

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Inhibitory effect of curcumin on nitric oxide production from lipopolysaccharide-activated primary microglia

TL;DR: The current results suggest that curcumin is a promising agent for the prevention and treatment of both NO and microglial cell-mediated neurodegenerative disorders.
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Curcumin potentiates the apoptotic effects of chemotherapeutic agents and cytokines through down-regulation of nuclear factor-κB and nuclear factor-κB–regulated gene products in IFN-α–sensitive and IFN-α–resistant human bladder cancer cells

TL;DR: It is found that curcumin inhibited the proliferation, induced cell cycle arrest, and DNA fragmentation in both IFN-α–sensitive (RT4V6) and IFN–resistant (KU-7) bladder cancer cells.
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Protein-stabilized Pickering emulsions: Formation, stability, properties, and applications in foods

TL;DR: A review of protein-stabilized Pickering emulsions can be found in this article, focusing on protein nanoparticles, microgels, and fibrils, and the challenges of utilizing protein-based pickering emulsion in the food industry are also discussed.
Journal ArticleDOI

Curcumin and synthetic analogs induce reactive oxygen species and decreases specificity protein (Sp) transcription factors by targeting microRNAs

TL;DR: These results identify a new and highly potentCurcumin derivative and demonstrate that in cells where curcumin and RL197 induce ROS, an important underlying mechanism of action involves perturbation of miR-ZBTB10/ZBTb4, resulting in the induction of these repressors which downregulate Sp transcription factors and Sp-regulated genes.
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Curcumin treatment alleviates the effects of glutathione depletion in vitro and in vivo: therapeutic implications for Parkinson's disease explained via in silico studies.

TL;DR: Treatment of dopaminergic neuronal cells and mice with curcumin restores depletion of GSH levels, protects against protein oxidation, and preserves mitochondrial complex I activity which normally is impaired due to GSH loss.
References
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TL;DR: The inhibition of NF-kappa B activation by antioxidants and specific protease inhibitors may provide a pharmacological basis for interfering with these acute processes in suppressing toxic/septic shock, graft-vs-host reactions, acute inflammatory reactions, severe phase response, and radiation damage.
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AP-1 as a regulator of cell life and death

TL;DR: Interestingly, the growth-promoting activity of c-Jun is mediated by repression of tumour suppressors, as well as upregulation of positive cell cycle regulators, whereas JunB has the converse effect.
Journal Article

Phase I clinical trial of curcumin, a chemopreventive agent, in patients with high-risk or pre-malignant lesions.

TL;DR: It is demonstrated that curcumin is not toxic to humans up to 8,000 mg/day when taken by mouth for 3 months and a biologic effect ofCurcumin in the chemoprevention of cancer is suggested.
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Transcriptional regulation of endothelial cell adhesion molecules: NF-kappa B and cytokine-inducible enhancers.

TL;DR: A model has been proposed for the cytokine‐induced E‐selectin enhancer that is similar to the stereospecific complex proposed forThe inter‐ feron‐β gene promoter, in which multiple DNA bending proteins facilitate the assembly of higher order complexes of transcriptional activators that interact as a unit with the basal transcriptional machinery.
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Influence of Piperine on the Pharmacokinetics of Curcumin in Animals and Human Volunteers

TL;DR: The study shows that in the dosages used, piperine enhances the serum concentration, extent of absorption and bioavailability of curcumin in both rats and humans with no adverse effects.
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