Potential Role Of Curcumin Research Articles

Beneficial Effects of Curcumin in Polycystic Ovary Syndrome: A Review of Recent Literature and Underlying Mechanisms.

Polycystic Ovary Syndrome (PCOS) is a common endocrinological disorder that affects women of reproductive age and can lead to infertility. The prevalence of PCOS ranges from 5-21% depending on the diagnostic criteria and study population. Clinical manifestations include irregular or absent menstrual periods, obesity, and signs of hyperandrogenism. PCOS can also lead to long-term consequences such as metabolic syndrome, increased risk of cardiovascular diseases, endometrial cancer, diabetes mellitus, and hypertension. Metformin and oral contraceptive pills are the most commonly used drugs for PCOS management, but their efficiency is limited and they have some considerable side effects. Researchers are looking into alternative therapeutic options such as phytochemicals. Curcumin (CUR) is a polyphenolic compound found in the rhizome of Curcuma longa and has shown promising effects for females with PCOS. CUR exerts its anti-PCOS effects through different mechanisms such as reducing oxidative stress and inflammation, balancing hormone levels, and controlling the blood sugar and lipid profile. It can also reduce insulin resistance, regulate menstruation, and improve ovarian morphology and function. Despite its beneficial effects, CUR faces several challenges and limitations in clinical use, such as low bioavailability, instability, and rapid elimination. Therefore, researchers are investigating the potential of CUR nanoformulations and new drug delivery systems to overcome these barriers. With growing evidence regarding the potential role of CUR in PCOS treatment, we decided to provide an updated summary of the recent literature from clinical and preclinical studies on this topic.

The Role of Curcumin in Modulating Vascular Function and Structure during Menopause: A Systematic Review.

The risk of developing cardiovascular disease (CVD) escalates in women during menopause, which is associated with increased vascular endothelial dysfunction, arterial stiffness, and vascular remodeling. Meanwhile, curcumin has been demonstrated to enhance vascular function and structure in various studies. Therefore, this study systematically reviewed the recent literature regarding the potential role of curcumin in modulating vascular function and structure during menopause. The Ovid MEDLINE, PubMed, Scopus, and Web of Science electronic databases were searched to identify relevant articles. Clinical and preclinical studies involving menopausal women and postmenopausal animal models with outcomes related to vascular function or structure were included. After thorough screening, seven articles were selected for data extraction, comprising three animal studies and four clinical trials. The findings from this review suggested that curcumin has beneficial effects on vascular function and structure during menopause by addressing endothelial function, arterial compliance, hemodynamic parameters, and the formation of atherosclerotic lesions. Therefore, curcumin has the potential to be utilized as a supplement to enhance vascular health in menopausal women. However, larger-scale clinical trials employing gold-standard techniques to evaluate vascular health in menopausal women are necessary to validate the preliminary results obtained from small-scale randomized clinical trials involving curcumin supplementation (INPLASY, INPLASY202430043).

The Potential Role of Curcumin as a Regulator of microRNA in Colorectal Cancer: A Systematic Review.

Curcumin is known as a bioactive component that is found in the rhizomes of Curcuma longa. Curcumin is well known for its chemo-preventive and anticancer properties. However, its anticancer mechanism in colorectal cancer treatment is unclear, and some studies have shown that many microRNAs (miRs) could be potential targets for curcumin in colorectal cancer (CRC) treatment, so there is a need for their integration and clarification. We systematically searched international databases, including PubMed, Scopus, and Web of Science, until July 2021 by using some relevant keywords. The search resulted in 87 papers, among which there were 18 related articles. Curcumin was found to cause the upregulation of miR-497, miR-200c, miR-200b, miR-409-3p, miR-34, miR-126, miR-145, miR-206, miR-491, miR-141, miR-429, miR-101, and miR-15a and the downregulation of miR-21, miR-155, miR-221, miR-222, miR-17-5p, miR-130a, miR-27, and miR-20a. The present review study suggests that curcumin may be useful as a novel therapeutic agent for CRC by altering the expression level of miRs.

Curcumin Decreases Viability and Inhibits Proliferation of Imatinib-Sensitive and Imatinib-Resistant Chronic Myeloid Leukemia Cell Lines.

Chronic myeloid leukemia (CML) is a myeloproliferative haematological malignancy characterized by constitutive activation of BCR-ABL1 tyrosine kinase in the majority of patients. BCR-ABL1 expression activates signaling pathways involved in cell proliferation and survival. Current treatment options for CML include tyrosine kinase inhibitors (TKI) with resistance as a major issue. Various treatment options for overcoming resistance are being investigated. Among them, phytochemical curcumin could play an important role. Curcumin has been found to exhibit anti-cancerous effects in various models, including CML, through regulation of multiple molecular signaling pathways contributing to tumorigenesis. We have evaluated curcumin's effects on imatinib-sensitive LAMA84S and K562, as well as imatinib-resistant LAMA84R cell lines. Our results indicate a significant dose-dependent decrease in cell viability and proliferation of imatinib-sensitive and imatinib-resistant cell lines after curcumin treatment. Suppression of key signaling molecules regulating metabolic and proliferative events, such as Akt, P70S6K and NF-kB, was observed. Increased expression of caspase-3 suggests the potential pro-apoptotic effect of curcumin in the imatinib-resistant CML model. Additional in silico molecular docking studies revealed binding modes and affinities of curcumin with different targets and the results are in accordance with in vitro findings. Altogether, these results indicate the potential role of curcumin in the treatment of CML.

Curcumin supplementation improves oxidative stress and inflammation biomarkers in patients undergoing hemodialysis: a secondary analysis of a randomized controlled trial.

Recent studies have shed light on the potential role of curcumin in mitigating inflammation in patients with chronic kidney disease (CKD). This study aimed to evaluate the effects of curcumin supplementation on plasma levels of markers of inflammation and oxidative stress in patients with CKD undergoing hemodialysis (HD). These are secondary exploratory analyses from a previous double-blind, randomized controlled pilot study registered under ClinicalTrials.gov Identifier no. NCT00123456. It included 28 hemodialysis patients from a previous study divided into two groups: curcumin group (receiving juice with 2.5g of turmeric 3×/week for 12weeks) and a control group. The TNF-α, IL-6 and Ox-LDL plasma levels were measured by sandwich enzyme immunoassays ELISA; lipid peroxidation was measured by the reaction between malondialdehyde (MDA) and thiobarbituric acid. After 12weeks of supplementation with curcumin, the TNF-α plasma levels were significantly reduced [from 15.0 (8.23-73.3) to 6.17 (1.11-55.0) pg/mL, p = 0.01]. 12weeks of treatment with curcumin in HD patients resulted in a reduction in the biomarker of inflammation (TNF-α), confirming our previous hypothesis that curcumin has an anti-inflammatory effect.

The Potential Role of Curcumin in Modulating the Master Antioxidant Pathway in Diabetic Hypoxia-Induced Complications.

Oxidative stress is the leading player in the onset and development of various diseases. The Keap1-Nrf2 pathway is a pivotal antioxidant system that preserves the cells’ redox balance. It decreases inflammation in which the nuclear trans-localization of Nrf2 as a transcription factor promotes various antioxidant responses in cells. Through some other directions and regulatory proteins, this pathway plays a fundamental role in preventing several diseases and reducing their complications. Regulation of the Nrf2 pathway occurs on transcriptional and post-transcriptional levels, and these regulations play a significant role in its activity. There is a subtle correlation between the Nrf2 pathway and the pivotal signaling pathways, including PI3 kinase/AKT/mTOR, NF-κB and HIF-1 factors. This demonstrates its role in the development of various diseases. Curcumin is a yellow polyphenolic compound from Curcuma longa with multiple bioactivities, including antioxidant, anti-inflammatory, anti-tumor, and anti-viral activities. Since hyperglycemia and increased reactive oxygen species (ROS) are the leading causes of common diabetic complications, reducing the generation of ROS can be a fundamental approach to dealing with these complications. Curcumin can be considered a potential treatment option by creating an efficient therapeutic to counteract ROS and reduce its detrimental effects. This review discusses Nrf2 pathway regulation at different levels and its correlation with other important pathways and proteins in the cell involved in the progression of diabetic complications and targeting these pathways by curcumin.

Potential Role of Curcumin and Its Nanoformulations to Treat Various Types of Cancers.

Cancer is a major burden of disease globally. Each year, tens of millions of people are diagnosed with cancer worldwide, and more than half of the patients eventually die from it. Significant advances have been noticed in cancer treatment, but the mortality and incidence rates of cancers are still high. Thus, there is a growing research interest in developing more effective and less toxic cancer treatment approaches. Curcumin (CUR), the major active component of turmeric (Curcuma longa L.), has gained great research interest as an antioxidant, anticancer, and anti-inflammatory agent. This natural compound shows its anticancer effect through several pathways including interfering with multiple cellular mechanisms and inhibiting/inducing the generation of multiple cytokines, enzymes, or growth factors including IκB kinase β (IκKβ), tumor necrosis factor-alpha (TNF-α), signal transducer, and activator of transcription 3 (STAT3), cyclooxygenase II (COX-2), protein kinase D1 (PKD1), nuclear factor-kappa B (NF-κB), epidermal growth factor, and mitogen-activated protein kinase (MAPK). Interestingly, the anticancer activity of CUR has been limited primarily due to its poor water solubility, which can lead to low chemical stability, low oral bioavailability, and low cellular uptake. Delivering drugs at a controlled rate, slow delivery, and targeted delivery are other very attractive methods and have been pursued vigorously. Multiple CUR nanoformulations have also been developed so far to ameliorate solubility and bioavailability of CUR and to provide protection to CUR against hydrolysis inactivation. In this review, we have summarized the anticancer activity of CUR against several cancers, for example, gastrointestinal, head and neck, brain, pancreatic, colorectal, breast, and prostate cancers. In addition, we have also focused on the findings obtained from multiple experimental and clinical studies regarding the anticancer effect of CUR in animal models, human subjects, and cancer cell lines.

Does Curcumin Have an Anticaries Effect? A Systematic Review of In Vitro Studies.

Dental caries is one of the most important oral health problems and a common infectious microbial disease. Streptococcus mutans (S. mutans) has been regarded as the primary etiologic factor in the formation of dental caries. Curcumin (CUR) has an antibacterial action and could be used in the eradication of S. mutans to control dental caries. This systematic review was undertaken with the aim of evaluating the anticaries effect of CUR. A comprehensive search was conducted in the PubMed/Medline, Cochrane - CENTRAL, and Scopus databases. Based on the PICO model, studies which evaluated the anticaries effects of CUR up until 24 February 2020 with language restrictions were selected for this systematic review. From 753 papers found, 13 met the eligibility criteria and were included. In 12 out of 13 included studies, CUR had significant antibacterial and anticaries effects. CUR had inhibitory effects on S. mutans growth, acid production, ATPase and sortase A activity, biomass, viability and metabolism reduction of biofilm, reduced exopolysaccharide production of biofilms, changes in biofilm structure, and had anti-adhesion effects against S. mutans. This systematic review suggests promising antibacterial and anticaries effects of CUR including inhibition of S. mutans growth, acid production, ATPase and sortase A activity. This review provides unique information regarding the potential role of CUR in the prevention and treatment of dental carries as a natural, accessible, safe, and inexpensive agent to increase oral and dental health. However, clinical randomized controlled trials are needed to confirm these results.

Withdrawn: Potential Role of Curcumin in amelioration of Skin Diseases: A Comprehensive Review

The article has been withdrawn at the request of the editor of the journal Current Traditional Medicine due to incoherent content. Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused. The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php Bentham Science Disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Protective effects of Curcumin against development of atherosclerosis

Atherosclerosis is characterized by oxidative damage, which affects lipoproteins, the walls of blood vessels, and subcellular membranes. The oxidation of low-density lipoproteins (LDLs) plays an important role in the development of atherosclerosis. Curcumin is a component of turmeric, a spice used in many types of cooking and gives the yellow color to turmeric, was first isolated almost two centuries ago, and its structure as diferuloylmethane was determined in 1910. Since the time of Ayurveda (1900 Bc) numerous therapeutic activities have been assigned to turmeric for a wide variety of diseases and conditions, including those of the skin, pulmonary, and gastrointestinal systems, aches, pains, wounds, sprains, and liver disorders. Curcumin has been known that turmeric exhibits anti-inflammatory activity, this activity of turmeric is due to curcumin, a diferuloylmethane, and has been shown to regulate numerous transcription factors, cytokines, protein kinases, adhesion molecules, redox status and enzymes that have been linked to inflammation. The process of inflammation has been shown to play a major role in most chronic illnesses, like atherosclerosis. The researchers showed that curcumin exhibited protective effects as indicated by inhibition of lipoperoxidation of subcellular membranes. Oral curcumin inhibits LDL oxidation and has hypocholesterolemic effects in rabbits with experimental atherosclerosis. In the current review, we provide evidence for the potential role of curcumin in the prevention and treatment of atherosclerosis and pharmacological safety and negligible cost.

Curcumin Ameliorates Cisplatin-Induced Nephrotoxicity and Potentiates Its Anticancer Activity in SD Rats: Potential Role of Curcumin in Breast Cancer Chemotherapy.

Breast malignant neoplastic disease is one of the most complex diseases, as it is a multifactorial disease in which virtually all the targets are instantly or indirectly inter-reliant on each other. Cisplatin (CIS), an inorganic antineoplastic agent is widely utilized in the treatment of various solid tumors including breast cancer. Despite everything, its clinical use is limited, due to ototoxicity, peripheral neuropathy, and nephrotoxicity. The present work was directed to assess the combined result of curcumin (CUR) and CIS in 7, 12-dimethyl benz[a]anthracene (DMBA) induced breast cancer in rats and the prevention of nephrotoxicity induced by the latter. CIS-induced nephrotoxicity was assessed by change in body weight, kidney weight, altered levels of BUN, creatinine, TNF-α, IL-6, IL-8, IL-10, and histopathology of the kidney. Anticancer activity was assessed by measurement of tumor weight, tumor volume, % tumor inhibition, levels of PPAR-γ, and BDNF in mammary tumors and histopathology of mammary tumors. CUR pre-treatment mitigated nephrotoxicity by reducing the inflammatory markers (TNF-α, IL-6, and IL-8; p < 0.001). Further, it reduced mammary cancer via increasing the expression of PPAR-γ (p < 0.001) and decreasing the expression of BDNF (p < 0.001) in mammary tumors. It also reduced tumor volume, further postulating that CUR might adjunct the anticancer activity of the CIS. To the best of our knowledge, this is the first report, which showed that CUR ameliorated CIS-induced nephrotoxicity and improved its anticancer activity in DMBA induced breast cancer in female Sprague-Dawley rats.

The potential role of curcumin in prostate cancer: the importance of optimizing pharmacokinetics in clinical studies.

Curcumin, a commercially available nutritional supplement, has been studied for use as a chemopreventive agent and an anti-cancer therapy in prostate cancer (1). The anti-tumor activity of curcumin and its analogues are well-documented from preclinical studies using prostate cancer models, including its effects on androgen receptor (AR) signaling and numerous downstream targets (e.g., VEGF, PTEN, NF-κB) (2-7). Curcumin was shown to down-regulate AR expression, limit AR binding to the androgen response element of the prostate specific antigen (PSA) gene, and reduce the expression of PSA in LNCaP cells (2). Pyridine analogues of curcumin were shown to have an inhibitory effect on CWR-22Rv1 AR activity and cell growth (5).

S-nitrosylation of Inhibitor-κB kinase: Identifying Novel Targets of Curcumin

In this study, we investigated the preventive effects of curcumin using LPS (Lipopolysaccharides)-induced Raw264.7 cells and the potential role of curcumin in regulation of anti-inflammation through S-nitrosylation. Western blot presented the protein expression of iNOS can be reduced by treated curcumin with 5, 10 and 15 μM separately for 12 and 24h. Consistently, pro-inflammatory cytokines, such as IL-1β, IL-6, TNFα and IFN-γ was also repressed. Moreover, 5, 10 and 15 μM curcumin reduced the amount of nitrite and nitrate in LPS-induced Raw264.7 cells maintained total S-nitrosylation level on proteins at 12h, the similar results was also observed at 24h that indicating curcumin inhibited NO oxidation. Furthermore, the protection of S-nitrosylation on IKKβ in LPS-induced Raw264.7 cells at 12h by curcumin caused the repression of IκB phosphorylation and NF-κB activation. In conclusion, this study verified that curcumin-mediated S-nitrosylation may be as an important regulator for anti-inflammation in LPS-induced Raw264.7 cells.

Curcumin represses the activity of inhibitor-κB kinase in dextran sulfate sodium-induced colitis by S-nitrosylation

In this study, we investigated the preventive effects of curcumin using dextran sulfate sodium (DSS)-induced colitis and the potential role of curcumin in regulation of anti-inflammation through S-nitrosylation. After curcumin treatment for 6days, the body weight and disease activity index of DSS-induced mice was alleviated and the colonic length was also rescued. Western blot presented that the protein expression of iNOS can be reduced by curcumin. Consistently, mRNA level of iNOS and pro-inflammatory cytokines, such as TNFα, IL-1β, and IL-6, was also repressed. Moreover, Curcumin reduced the amount of nitrite in DSS-induced colitis but not affected total S-nitrosylation level on proteins on day 6, indicating that curcumin inhibited NO oxidation. Furthermore, the protection of S-nitrosylation on IKKβ in DSS-induced colitis for 6days by curcumin caused the repression of IκB phosphorylation and NF-κB activation. In conclusion, this study verified that curcumin-mediated S-nitrosylation may be as an important regulator for anti-inflammation in DSS-induced colitis of mice.

The inhibition of PI3K and NFκB promoted curcumin-induced cell cycle arrest at G2/M via altering polyamine metabolism in Bcl-2 overexpressing MCF-7 breast cancer cells.

Bcl-2 protein has been contributed with number of genes which are involved in oncogenesis. Among the many targets of Bcl-2, NFκB have potential role in induction of cell cycle arrest. Curcumin has potential therapeutic effects against breast cancer through multiple signaling pathways. In this study, we investigated the role of curcumin in induction of cell cycle arrest via regulating of NFκB and polyamine biosynthesis in wt and Bcl-2+ MCF-7 cells. To examine the effect of curcumin on cell cycle regulatory proteins, PI3K/Akt, NFκB pathways and polyamine catabolism, we performed immunoblotting assay. In addition, cell cycle analysis was performed by flow cytometry. The results indicated that curcumin induced cell cycle arrest at G2/M phase by downregulation of cyclin B1 and Cdc2 and inhibited colony formation in MCF-7wt cells. However, Bcl-2 overexpression prevented the inhibition of cell cycle associated proteins after curcumin treatment. The combination of LY294002, PI3K inhibitor, and curcumin induced cell cycle arrest by decreasing CDK4, CDK2 and cyclin E2 in Bcl-2+ MCF-7 cells. Moreover, LY294002 further inhibited the phosphorylation of Akt in Bcl-2+ MCF-7 cells. Curcumin could suppress the nuclear transport of NFκB through decreasing the interaction of P-IκB-NFκB. The combination of wedelolactone, NFκB inhibitor, and curcumin acted different on SSAT expression in wt MCF-7 and Bcl-2+ MCF-7 cells. NFκB inhibition increased the SSAT after curcumin treatment in Bcl-2 overexpressed MCF-7 cells. Inhibition of NFκB activity as well as suppression of ROS generation with NAC resulted in the partial relief of cells from G2/M checkpoint after curcumin treatment in wt MCF-7 cells. In conclusion, the potential role of curcumin in induction of cell cycle arrest is related with NFκB-regulated polyamine biosynthesis.

Abstract 3207: Curcumin induces pancreatic cancer cell death by targeting IAPs

Abstract Background Pancreatic cancer has among the highest mortality rates compared to other cancer types, with 94% of patients dying within five years of diagnosis. Contributing to the high mortality rate, patients with pancreatic cancer do not present significant symptoms until the disease is advanced. Moreover, treatment strategies have not improved substantially over the last decade. For this reason, a recent trend has led toward focusing on the use of herb-derived compounds, such as curcumin (turmeric derivative), to explore alternative treatments that will improve current pancreatic cancer therapy. Objective The objectives of this study were (1) to determine the effects of curcumin on pancreatic cancer cell metabolism, viability, cell cycle and morphology, and (2) to determine the mechanism by which curcumin induces cell death in pancreatic cancer cells by analyzing intracellular expression levels of inhibitor of apoptosis proteins (IAPs). Design/method Pancreatic adenocarcinoma cell lines (Panc-1 and MiaPaCa-2) were used to assess the effects of curcumin in pancreatic cancer. Effects on metabolism, viability and cell cycle were assayed by Alamar Blue, Trypan Blue and Propidium Iodide (PI) staining/flow cytometry (FACSCalibur). Morphological imaging was performed using Hoffman Modulation microscopy. Apoptosis was detected by Annexin V/PI flow cytometry (MACSQuant) and the expression of IAPs was assessed by Western blot. Results These data show that curcumin decreases pancreatic cancer cell metabolism and viability. Cell cycle stages were arrested in pancreatic cancer cells treated with curcumin compared to the non-treated controls. Apoptotic cells were detected by microscopy and confirmed by Annexin V/PI staining with subsequent flow cytometry analysis. IAPs levels are reduced in pancreatic cancer cell lines treated with curcumin compared to non-treated controls. Conclusion These results demonstrate that pancreatic adenocarcinoma cell lines are sensitive to curcumin treatment. Moreover, curcumin's possible mechanism of action is inducing apoptosis by targeting IAPs. Collectively, these data suggest a potential role for curcumin in pancreatic cancer therapy. Citation Format: Carlos J. Diaz Osterman, Malyn May Asuncion Valenzuela, Heather R. Ferguson Bennit, Salma Khan, Nathan R. Wall. Curcumin induces pancreatic cancer cell death by targeting IAPs. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3207. doi:10.1158/1538-7445.AM2014-3207

Potential role of curcumin and taurine combination therapy on human myeloid leukemic cells propagated in vitro

Curcumin and taurine are natural products that have been used in this study evaluating their therapeutic effect on myeloid leukemic cells propagated in vitro. Sixty patients with myeloid leukemia and 30 healthy volunteers were enrolled in the study. All patient groups were admitted to the Medical Oncology Department of the National Cancer Institute, Cairo University. There were statistically significant differences between treated leukemic cells compared to normal mononuclear leukocytes in cell density, interferon-γ and immunophenotypic profile, mainly CD4+, CD8 + and CD25+. This work highlights the possibility of using curcumin and taurine as a potential useful therapy in the management of patients suffering from chronic and acute myeloid leukemias.

Curcumin Modulates Nuclear Factor κB (NF-κB)-mediated Inflammation in Human Tenocytes in Vitro: ROLE OF THE PHOSPHATIDYLINOSITOL 3-KINASE/Akt PATHWAY

Inflammatory processes play essential roles in the pathogenesis of tendinitis and tendinopathy. These events are accompanied by catabolic processes initiated by pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Pharmacological treatments for tendinitis are restricted to the use of non-steroidal anti-inflammatory drugs. Recent studies in various cell models have demonstrated that curcumin targets the NF-κB signaling pathway. However, its potential for the treatment of tendinitis has not been explored. Herein, we used an in vitro model of human tenocytes to study the mechanism of curcumin action on IL-1β-mediated inflammatory signaling. Curcumin at concentrations of 5–20 μm inhibited IL-1β-induced inflammation and apoptosis in cultures of human tenocytes. The anti-inflammatory effects of curcumin included down-regulation of gene products that mediate matrix degradation (matrix metalloproteinase-1, -9, and -13), prostanoid production (cyclooxygenase-2), apoptosis (Bax and activated caspase-3), and stimulation of cell survival (Bcl-2), all known to be regulated by NF-κB. Furthermore, curcumin suppressed IL-1β-induced NF-κB activation via inhibition of phosphorylation and degradation of inhibitor of κBα, inhibition of inhibitor of κB-kinase activity, and inhibition of nuclear translocation of NF-κB. Furthermore, the effects of IL-1β were abrogated by wortmannin, suggesting a role for the phosphatidylinositol 3-kinase (PI-3K) pathway in IL-1β signaling. Curcumin suppressed IL-1β-induced PI-3K p85/Akt activation and its association with IKK. These results demonstrate, for the first time, a potential role for curcumin in treating tendon inflammation through modulation of NF-κB signaling, which involves PI-3K/Akt and the tendon-specific transcription factor scleraxis in tenocytes.

The nontoxic natural compound Curcumin exerts anti-proliferative, anti-migratory, and anti-invasive properties against malignant gliomas

BackgroundNew drugs are constantly sought after to improve the survival of patients with malignant gliomas. The ideal substance would selectively target tumor cells without eliciting toxic side effects. Here, we report on the anti-proliferative, anti-migratory, and anti-invasive properties of the natural, nontoxic compound Curcumin observed in five human glioblastoma (GBM) cell lines in vitro.MethodsWe used monolayer wound healing assays, modified Boyden chamber trans-well assays, and cell growth assays to quantify cell migration, invasion, and proliferation in the absence or presence of Curcumin at various concentrations. Levels of the transcription factor phospho-STAT3, a potential target of Curcumin, were determined by sandwich-ELISA. Subsequent effects on transcription of genes regulating the cell cycle were analyzed by quantitative real-time PCR. Effects on apoptosis were determined by caspase assays.ResultsCurcumin potently inhibited GBM cell proliferation as well as migration and invasion in all cell lines contingent on dose. Simultaneously, levels of the biologically active phospho-STAT3 were decreased and correlated with reduced transcription of the cell cycle regulating gene c-Myc and proliferation marking Ki-67, pointing to a potential mechanism by which Curcumin slows tumor growth.ConclusionsCurcumin is part of the diet of millions of people every day and is without known toxic side effects. Our data show that Curcumin bears anti-proliferative, anti-migratory, and anti-invasive properties against GBM cells in vitro. These results warrant further in vivo analyses and indicate a potential role of Curcumin in the treatment of malignant gliomas.

Is Curcumin for Monoclonal Gammopathy of Undetermined Significance without Risk? – Letter

Comment on: The potential role of curcumin in patients with monoclonal gammopathy of undefined significance--its effect on paraproteinemia and the urinary N-telopeptide of type I collagen bone turnover marker. [Clin Cancer Res. 2009]