Role Of Curcumin Research Articles

Curcumin protects against hypertension aggravated retinal ischemia/reperfusion in a rat stroke model

ABSTRACTThe pathogenesis of visual dysfunction in stroke remains unclear. The objective of this study was to explore retinal damage in stroke spontaneously hypertensive rats (SHR) and evaluate the role of curcumin in the retinal injury after stroke. Mature male SHR were used as the animal model for hypertension and age-matched male Wistar-Kyoto (WKY) rats as the normotensive controls. The rat model of stroke was made by bilateral vertebral artery electrocoagulation combined with transient bilateral common carotid artery ligation. The animals were randomly divided into sham group, ischemia/reperfusion group, solvent control group, and curcumin treatment group. Each group was subdivided into 2 h, 6 h, 24 h, 72 h, and 7 day after reperfusion. Blood pressure was measured in SHR and WKY rats. Eye fundus was examined in living animals, and then, tissue specimens were collected for histologic examination, terminal deoxynucleotidyl transferase-mediated 2’-deoxyuridine 5’-triphosphate nick end labeling, and immunohistochemistry. Retinopathy, induced by I/R, was more serious in rats with hypertension than that in normotensive rats (retinal thickness index, p = 0.004). The number of apoptosis in retinal capillary cells and neurons reduced significantly in the curcumin-treated groups. Curcumin treatment inhibited phosphorylated c-Jun N-terminal kinase (JNK) expression in SHR after retinal I/R injury. Thus, hypertension aggravated retinal I/R injury after stroke. Curcumin, a specific inhibitor of JNK, can prevent the development of hypertensive retinopathy after I/R injury by inhibiting apoptosis in retinal capillary cells and neurons.

Abstract 3060: Role of curcumin in targeting cancer-associated fibroblasts and modulation of tumor microenvironment in dendritic cell-based immunotherapy

Abstract INTRODUCTION: Cancer associated fibroblasts (CAFs), main component of tumor microenvironment (TME), modulate the recruitment and functions of tumor-associated immune cells by secreting various growth hormones, miRNAs and cytokines; thus having an important role in generation of immunosuppressive TME which is yet to be elucidated. Curcumin is known to have various properties including capability to modulate numerous target proteins including transcription factors, receptors, kinases, cytokines, enzymes and growth factors. Thus, aim of the study was to evaluate the effect of miRNAs and cytokines released by lung cancer patients’ derived CAFs and to assess immunomodulatory potential of curcumin on DC maturation by targeting these CAFs through modulating their TME. METHODOLOGY: CAFs were cultured from lung cancer patient derived tumor tissue biopsy and characterised using CAF-specific markers. Further, immature DCs (imDCs) were differentiated in presence of rGM-CSF and rIL-4 for 5-6 days. These imDCs were cultured in the presence of conditioned media derived from CAFs (CAFs-CM) as well as NFs (Normal Fibroblasts, NFs-CM) at day 6 for 48 hours to evaluate the effect of CAFs on DC maturation. Mature DCs (mDCs) were characterized by the presence of maturation markers CD80, CD83, CD86 and CTLA4 using qRT-PCR. Moreover, expression of miR-221, miR-222, miR-155, miR-142-3p and miR-146a was assessed to evaluate the role of epigenetic regulators on DC maturation. Cytokine profiling of CAFs-CM as well as CAFs-CM treated with curcumin was conducted. RESULTS: α-SMA+Vimentin+ cells were considered as CAFs. A significant upregulation of CD80, CD83 and CD86 was observed when cultured in the presence of NFs-CM while a remarkable downregulation of these markers was found when cultured in CAFs-CM. CTLA-4 was down regulated in NFs-CM as compared to CAFs-CM, suggesting the role of CAFs in generation of regulatory DCs. Amongst all miRNAs, miR-146a was shown to be up regulated dramatically in CAF-DCs (DCs cultured in CAFs-CM) as well as in CAFs-CM, suggesting the immunosuppressive role of miR-146a. Further, an increased expression of miR-146a was positively correlated with increased expression of anti-inflammatory cytokines like IL-6, IL-10, TGF-β and decreased expression of TNF-α (pro-inflammatory) in CM derived from CAF-DCs. Moreover, curcumin had the potential to convert regulatory DCs facilitated by CAFs into mDCs, which were characterized by high expression of co-stimulatory molecules, low expression of CTLA4, lower levels of immune suppressive cytokines production, lower levels of miR-146a. CONCLUSION: These findings provide insight into understanding the immunomodulatory role of curcumin in targeting CAFs and modulating the tumor microenvironment, thus enhancing antitumor immune response in DC based therapy. Citation Format: Sheefa Mirza, Nayan Jain, Rakesh Rawal. Role of curcumin in targeting cancer-associated fibroblasts and modulation of tumor microenvironment in dendritic cell-based immunotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3060. doi:10.1158/1538-7445.AM2017-3060

Abstract 1478: Curcumin inhibits epithelial-mesenchymal transition and invasion in breast cancer cells by controlling miR-34a expression

Abstract Breast cancer in advanced stages tends to develop metastases and / or chemoresistance, in both cases therapeutic options are limited and have low probability of success, which represents the biggest obstacle in reducing mortality from this disease. There is a close connection between the Epithelial-Mesenchymal Transition (EMT) process of cancer cells and the acquisition of invasive and metastatic ability. Numerous EMT mediators have been described in cancer and among them miRNAs play a fundamental role in regulating such process, suggesting that it could be a therapeutic target to address this phenotype. Curcumin (diferuloylmethane) is a derivative compound of Curcuma longa that has therapeutic properties in various cancers as blocking initiation and tumor progression through its anti-inflammatory, antioxidant, proapoptotic, antiangiogenic and antimetastatic effects. The role of curcumin on EMT in non-cancerous breast cells MCF-10F and in breast cancer cell lines MCF-7 and MDA-MB-231 was evaluated. This work shows that in all these cell lines curcumin induced the expression of tumor suppressor microRNA miR-34a and repressed the expression of several genes involved in EMT and metastasis as Axl, Slug, Twist, N-cadherin, vimentin, fibronectin, among others. Consequently, curcumin inhibited the migration and invasiveness in these cells, irrespective of the expression of estrogen and progesterone receptors and p53 mutational status. Blockade of miR-34a by transfection with antagomiR-34a inhibited the effect of curcumin on EMT genes and on the migratory/invasive potential of cells indicating that miR-34a plays a central role in the Curcumin-mediated suppression of EMT and invasion. Therefore, results confirm the suppressive effect of curcumin on EMT and invasion in breast cancer cells, showing that such substance exerts this effect by inducing expression of miRNA miR-34a and consequently the repression of several of its target genes. Supported by Tarapacá University, Arica, Chile (GMC). Citation Format: Marcela Gallardo, Richard Ponce-Cusi, Gloria M. Calaf. Curcumin inhibits epithelial-mesenchymal transition and invasion in breast cancer cells by controlling miR-34a expression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1478. doi:10.1158/1538-7445.AM2017-1478

Efficacy of nanocurcumin supplementation on insulin resistance, lipids, inflammatory factors and nesfatin among obese patients with non-alcoholic fatty liver disease (NAFLD): a trial protocol

ObjectivesDifferent studies have been conducted on the role of curcumin in health since having multiple properties, including antioxidant and anti-inflammatory effects. Due to the lack of studies regarding curcumin effects...

Efficacy of Curcumin in the Modulation of Anxiety Provoked by Sulfite, a Food Preservative, in Rats.

Sulfites are used as food preservatives and excessive sulfite might disturb the body systems including the brain. Curcumin shows protective effects on the nervous system toxicity. The present study aimed to evaluate the protective role of curcumin in sulfite-induced anxiety in rats. Male rats were divided into five groups. The rats in groups I to V received distilled water (vehicle of sulfite, 1 mL/d), olive oil (vehicle of curcumin, 1 mL/d), curcumin (100 mg/kg/d), sulfite (25 mg/kg/d), and sulfite+curcumin, respectively, by daily gastric gavage for 8 weeks. At the end of 8 weeks the rats were tested in the elevated plus-maze for anxiety. The results showed that concomitant treatment of curcumin during sulfite consumption prevented the reduction of the time spent in the open arm and entrance to the open arm (the indexes of anxiety). Besides, an increase was found in motor activity of the rats in the sulfite+curcumin group compared to the sulfite-treated animals. Exposure of sulfite in rats can induce anxiety, and curcumin can act as an anti-anxiety agent.

Curcumin Suppresses the Activity of Inhibitor-κB Kinase in an in vitro Inflamed Human Intestinal Mucosa Model by S -nitrosylation

In previous study, we found curcumin to possess anti-inflammatory properties in lipopolysaccharide (LPS)-induced macrophage cells due to the involvement of curcumin and S-nitrosylation in the NF-κB pathway. However, the role of curcumin on regulation of NF-κB signaling pathway through S-nitrosylation in an in vitro inflamed human intestinal mucosa model has not yet been elucidated. This study aimed to concern inhibitory effects of curcumin on NF-κB pathway in two type of inflamed human intestinal cells, Caco-2 and HT-29. Western blot presented the protein expression of iNOS can be reduced by treated curcumin with 30 μM for 12h. Consistently, pro-inflammatory cytokines, such as IL-1β, IL-6, TNFα and IFN-γ was also repressed. The results also shows curcumin reduced the amount of nitrite and nitrate in inflamed human intestinal cells, Caco-2 and HT-29, maintained total S-nitrosylation level on proteins. Furthermore, the protection of S-nitrosylation on IKKβ in inflamed Caco-2 and HT-29 cells 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 an in vitro inflamed human intestinal mucosa model.

Propoxur-induced oxidative DNA damage in human peripheral blood mononuclear cells: protective effects of curcumin and α-tocopherol

The present study enumerates the attenuating effects of curcumin and α-tocopherol against propoxur induced oxidative DNA damage in human peripheral blood mononuclear cells (PBMC). Cultured cells were isolated from peripheral blood of healthy volunteers, and were exposed to varying concentrations of propoxur (0–21 μg/ml) for 6, 12, and 24 h, and in combination with curcumin (9.2 μg/ml) or α-tocopherol (4.3 μg/ml) or both. Cytotoxic effect of propoxur was examined by MTT assay. The role of oxidative stress beneath the cytotoxicity of propoxur was evaluated by the measurement of reduced glutathione (GSH), malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) levels in cell lysate. A concentration-dependent cell death, depletion of GSH, an increase in the level of both MDA and 8-OH-dG were observed. Co-treatment with curcumin or α-tocopherol significantly attenuates depleted GSH, decrease in MDA and 8-OH-dG levels in propoxur exposed cells (p < 0.05). The results of the present study provide experimental evidence of involvement of oxidative stress in propoxur-mediated genotoxicity in human PBMC and highlight the antioxidant role of curcumin and α-tocopherol following propoxur exposure.

Curcumin increases the sensitivity of Paclitaxel-resistant NSCLC cells to Paclitaxel through microRNA-30c-mediated MTA1 reduction

Non-small-cell lung cancer is one of the most lethal cancers in the worldwide. Although Paclitaxel-based combinational therapies have long been used as a standard treatment in aggressive non-small-cell lung cancers, Paclitaxel resistance emerges as a major clinical problem. It has been demonstrated that Curcumin from Curcuma longa as a traditional Chinese medicine can inhibit cancer cell proliferation. However, the role of Curcumin in Paclitaxel-resistant non-small-cell lung cancer cells is not clear. In this study, we investigated the effect of Curcumin on the Paclitaxel-resistant non-small-cell lung cancer cells and found that Curcumin treatment markedly increased the sensitivity of Paclitaxel-resistant non-small-cell lung cancer cells to Paclitaxel. Mechanically, the study revealed that Curcumin could reduce the expression of metastasis-associated gene 1 (MTA1) gene through upregulation of microRNA-30c in Paclitaxel-resistant non-small-cell lung cancer cells. During the course, MTA1 reduction sensitized Paclitaxel-resistant non-small-cell lung cancer cells and enhanced the effect of Paclitaxel. Taken together, our studies indicate that Curcumin increases the sensitivity of Paclitaxel-resistant non-small-cell lung cancer cells to Paclitaxel through microRNA-30c-mediated MTA1 reduction. Curcumin might be a potential adjuvant for non-small-cell lung cancer patients during Paclitaxel treatment.

The role of curcumin in disruption of HIF-1α accumulation to alleviate adipose fibrosis via AMPK-mediated mTOR pathway in high-fat diet fed mice

Adipose hypoxia and hypoxia-inducible factor 1α (HIF-1α) accumulation are tightly associated with adipose dysfunction. Curcumin is a polyphenol with positive effects on inflammation and fibrosis. This study aims to investigate the effects of curcumin on HIF-1α and fibrosis in hypoxic adipose tissue. Curcumin attenuated high-fat diet (HFD) induced adipose hypoxia and HIF-1α overexpression. Moreover, curcumin effectively reduced inflammatory cytokine and extracellular matrix deposition in adipose tissue, demonstrating its inhibitory effects on adipose inflammation and fibrosis. Curcumin increased AMP-activated protein kinase (AMPK) phosphorylation and suppressed mammalian target of rapamycin (mTOR) activation, while knockdown of AMPK diminished the suppressive effects on mTOR activation and HIF-1α induction, further indicating that curcumin blocked mTOR/HIF-1α signaling via regulation of AMPK. In conclusion, curcumin prevented adipose hypoxia and decreased HIF-1α-associated adipose fibrosis via suppression of AMPK-mediated mTOR pathway, suggesting that HIF-1α might be a therapeutical target for the prevention of fibrosis in adipose tissue.

The aryl hydrocarbon receptor as an antitumor target of synthetic curcuminoids in colorectal cancer

BackgroundCurcumin has proven to be a potent antitumor agent in both preclinical and clinical models of colorectal cancer (CRC). It has also been identified as a ligand of the transcription factor known as the aryl hydrocarbon receptor (AHR). Our laboratory has identified the AHR as a mechanism which contributes to both tumorigenesis in a mouse model of inflammatory CRC as well an apoptotic target in vitro. Curcumin's role as an AHR ligand may modulate its effects to induce colon cancer cell death, and this role may be enhanced via structural modification of the curcumin backbone. We sought to determine if the two piperidone analogs of curcumin, RL66 and RL118, exhibit more robust antitumor actions than their parent compound in the context of colorectal cancer in vitro. Moreover, to ascertain the ability of curcumin, RL66 and RL118 to activate the AHR and evaluate if this activation has any effect on CRC cell death. Materials and methodsDLD1, HCT116, LS513, and RKO colon cell lines were propagated in vitro. Natural curcumin was obtained commercially, whereas RL66 and RL118 were synthesized and characterized de novo. Multiwell fluorescent/luminescent signal detection was used to simultaneously ascertain cell viability, cell cytonecrosis, and relative amounts of apoptotic activity. AHR activity was measured with a dual luciferase reporter gene system. Stable expression of small interfering RNA interference was established in the HCT116 cell lines to create AHR “knock down” cell lines. ResultsBoth RL66 and RL118 proved to be more potent antitumor agents than their parent compound curcumin in all cell lines tested. The majority of this cell death was due to induction of apoptosis, which occurred earlier and to a greater degree following RL66 and RL118 treatment as opposed to curcumin. Also, RL66 and RL118 were found to be activators of AHR, and a portion of their ability to cause cell death was dependent on this induction. Curcumin was found unable to activate the AHR, and levels of AHR messenger RNA did not change their effects on cell death. ConclusionsPiperidone analogs of curcumin exhibited enhanced antitumor effects in vitro as opposed to their parent compound. Even more, this enhanced cell death profile may be partially attributed to the ability of these compounds to activate the AHR. Further study of synthetic curcumin analogs as chemopreventives and chemoadjuncts in CRC is warranted. Also, more generally, the AHR may represent a potential putative target for novel anticancer agents for CRC.

Curcumin Inhibits Chondrocyte Hypertrophy of Mesenchymal Stem Cells through IHH and Notch Signaling Pathways.

Using tissue engineering technique to repair cartilage damage caused by osteoarthritis is a promising strategy. However, the regenerated tissue usually is fibrous cartilage, which has poor mechanical characteristics compared to hyaline cartilage. Chondrocyte hypertrophy plays an important role in this process. Thus, it is very important to find out a suitable way to maintain the phenotype of chondrocytes and inhibit chondrocyte hypertrophy. Curcumin deriving from turmeric was reported with anti-inflammatory and anti-tumor pharmacological effects. However, the role of curcumin in metabolism of chondrocytes, especially in the chondrocyte hypertrophy remains unclear. Mesenchymal stem cells (MSCs) are widely used in cartilage tissue engineering as seed cells. So we investigated the effect of curcumin on chondrogenesis and chondrocyte hypertrophy in MSCs through examination of cell viability, glycosaminoglycan synthesis and specific gene expression. We found curcumin had no effect on expression of chondrogenic markers including Sox9 and Col2a1 while hypertrophic markers including Runx2 and Col10a1 were down-regulated. Further exploration showed that curcumin inhibited chondrocyte hypertrophy through Indian hedgehog homolog (IHH) and Notch signalings. Our results indicated curcumin was a potential agent in modulating cartilage homeostasis and maintaining chondrocyte phenotype.

Role of Curcumin in Treatment of Alzheimer Disease

A lot of research findings support that curcumin (diferuloyl methane) has antioxidant, anti-inflammatory and antitumor activity. In India, curcumin has a widespread use as food additive and herbal medicine for human diseases without any side effect. Though curcumin is well established as an anticancer agent but there are a few reports about its promising role against amyloid diseases. According to recent finding curcumin play a crucial inhibitory role in pathophysiology of Alzheimer’s disease (AD). Oral administration of curcumin or its metabolites has shown the inhibition of Aβ deposition, Aβ oligomerization and tau phosphorylation in the brain of AD animal model including behavioural improvement. But still it is unknown whether the curcumin is directly involved in those processes or enhance those mechanisms. Thus in this review we want to focus on overall mechanism of curcumin in AD. Some strategies to overcome the problem of low absorption and fast clearance of curcumin nanoparticles have also been proposed.

Effects of 744ins20 – ter240 &lt;I&gt;BRCA1&lt;/I&gt; mutation on breast/ovarian carcinogenesis and the role of curcumin in telomerase inhibition

&lt;b&gt;Introduction&lt;/b&gt;: Breast cancer is cancer which develops from breast tissue. It can also begin in the cells of the lobules and in other tissues in the breast. Invasive breast cancer is breast cancer that has spread from where it began in the ducts or lobules to surrounding tissue. Breast cancer risk is correlated with high estrogen level. &lt;I&gt;BRCA1&lt;/I&gt; gene mutation increases the risk of hereditary breast/ovarian carcinogenesis. Telomerase can protect telomere shortening. It plays a key role in cancer development. Curcumin is a yellow component in Curcuma longa Linn. and has antioxidant properties. It has a potential role in inhibition of cellular migration or invasion and even metastasis.&lt;br /&gt; &lt;b&gt;Material and methods&lt;/b&gt;: A study on the effect of 744ins20 – ter240 &lt;I&gt;BRCA1&lt;/I&gt; mutation at exon 10 on DNA repair function by MTT dye reduction and a study on telomerase inhibition caused by curcumin with the telomerase activity assay and trypan blue exclusion assay were conducted. &lt;br /&gt; &lt;b&gt;Results&lt;/b&gt;: The percentages of cell viability in mutant cells were lower than the percentages of cell viability in wild type cells at various H2O2 concentrations (p &lt; 0.05). This mutation caused a DNA repair defect and curcumin could inhibit telomerase function and affected cancer cell progression.&lt;br /&gt; &lt;b&gt;Conclusions&lt;/b&gt;: 744ins20 – ter240 &lt;I&gt;BRCA1&lt;/I&gt; mutation is involved in a DNA repair defect. It drives oxidative stress. Cancer development prevention by enhancing antioxidant defenses may be affected by this mutation, and it causes breast/ovarian carcinogenesis. Curcumin can inhibit telomerase function. Antioxidants need to be explored for the prophylaxis and treatment of hereditary and basal-like breast cancers.

Anti-aging Role of Curcumin by Modulating the Inflammatory Markers in Albino Wistar Rats

PurposeAdvanced age is associated with an accumulation of free radical damage, which leads to physiological and clinical modifications. Numerous pharmaceutical and nutraceuticals are considered to influence longevity and prompting healthy ageing. Therefore, the current study attempted to investigate Curcumin's role in the inflammatory indices as anti-ageing marker in albino Wistar rats. MethodsTwelve months old rats were used in the study, grouped as Normal control (NC), Sham control (SC), Curcumin-1, Curcumin-2 and Curcumin-3. Last three groups received Curcumin at the dosages of 100 mg, 200 mg and 400 mg/kg body weight respectively. After six months of intervention, blood was collected for the estimation of C-reactive protein (CRP), Serum Albumin, Globulin, Lymphocyte percentage, Total Antioxidant Capacity (TAC), Malondialdehyde (MDA), Superoxide Dismutase (SOD) and Nitric Oxide (NO) level using standard procedures. ResultsThere was a significant decline in the CRP level (p < 0.05) in rats treated with 200 mg and 400 mg of Curcumin/kg body weight. The MDA level was found to be significantly increased (p < 0.05) in animals fed with 400 mg of Curcumin/kg body weight as compared to NC. The NO level was increased significantly (p < 0.05) in rats treated with 200 and 400 mg of Curcumin/kg body weight. ConclusionFinding of the study suggests that Curcumin exhibits favorable influence in slowing down of ageing process by suppressing age-related changes in inflammatory indices.

THE POTENTIAL AMELIORATIVE EFFECT OF CURCUMIN IN SCHISTOSOMA MANSONI INFECTED MICE: AN ULTRSTRUCTURAL STUDY ON THE TESTES

This investigation has been designed to evaluate the antibilharzial efficiency and the possible ameliorative role of curcumin on adult male Swiss albino mice testes. Thirty animals were used in this experiment, divided equally into 3 groups control, infected with S. mansoni and infected then treated with curcumin. Histological examination was performed on the testes using transmission electron microscopy (TEM). Results indicated that the testes in the infected group showed thickening and irregularity in the surrounding basal lamina, cytoplasmic vacuolation of atrophied Sertoli cells, shrinkage and pyknotic nuclei of spermatogonia as well as primary spermatocytes, especially in front of the sex vesicles. Furthermore, Sertoli cells contained various forms of mitochondrial degeneration and wide intercellular spaces of adherent junction among the Sertoli as well as spermatogenic cells. Besides, most of sperms were markedly affected. Supplementation of curcumin minimized the degenerative changes in the nuclear envelope and sex vesicles of the primary spermatocyte nuclei besides narrowing the adherent junction among Sertoli cells and germ cells. In conclusion, curcumin proved to have a potential role in minimizing the deleterious effect of S. mansoni in testes of the infected mice.

Efflux Pump Inhibition Effect of Curcumin and Phenylalanine Arginyl β- Naphthylamide (PAβN) against Multidrug Resistant Pseudomonas Aeruginosa Isolated from Burn Infections in Tanta University Hospitals

Introduction : Multidrug resistant (MDR) Pseudomonas aeuroginosa strains are very important pathogens causing hospital acquired infections especially in intensive care units. One of the mechanisms of developing drug resistance is efflux pump through which bacteria extrude antibiotics. If these efflux channels are blocked or inhibited, increased drug concentration can be obtained inside a bacterial cell with optimal drug dose. This study was aimed to investigate the role of curcumin and phenylalanine arginyl β-naphthylamide(PAβN) as efflux pump inhibitors (EPIs). Materials and Methods : A total of 40 Pseudomonas aeruginosa isolates were taken from burn wounds. Antibiotic susceptibility was performed using disc diffusion test, then minimum inhibitory concentration (MIC) against selected antibiotics before and after adding PAβN (20mg/L, 50mg/L) and curcumin (from 5 to 50μg/ml) was tested. Results : MDR isolates showed significant reduction in MIC after adding curcumin (50μg/ml) and PAβN (20mg/L) with selected antibiotics, while no change in MIC was observed when were used alone, indicating their efflux pump inhibitor activity. Conclusion : curcumin and PAβN potentiated the effect of antibiotics and thus change their susceptibility pattern which can be attributed to efflux pumps inhibition. Further genotypic studies may be needed to confirm.

Curcumin: The miraculous golden ingredient of Indian saffron

&#x0D; &#x0D; &#x0D; Abstract&#x0D; Background: Indian Saffron (Curcuma longa) also called turmeric; has been consumed for centuries by people as a dietary component and used in the traditional medicine as a household remedy for various diseases in India, China and South East Asia. Curcumin (diferuloyl methane), the main yellow bioactive pigment in turmeric has been shown to have a broad spectrum of biological activities. Purpose of study: The present review was performed to evaluate the molecular mechanism of action and role of Curcumin in health and disease. Sources of evidence: The literature search was conducted using Sciencedirect, Medline, Scopus data bases, 26 studies were included in this review. Main arguement: Animal studies with curcumin exhibited its digestive and anti- ulcer role through its excess production of mucin, bile, and digestive enzymes. Curcumin is effective in preventing cognitive impairment in Alzheimer Disease, Parkinson Disease and other oxidative stress related pathologies due to its antioxidative, anti-inflammatory roles. It has been suggested that the ability of curcumin to quench free radicals and reactive oxygen species (ROS) results in its protective role towards neuronal tissues against toxic chemicals as Manganese. Anticancer effect is mainly mediated through apoptosis of cancer cell lines. Clinically curcumin is used to reduce post-operative inflammation. Conclusions: Safety evaluation studies indicate that both turmeric and curcumin are well tolerated at a high dose without any toxic effects and therefore, have the potential for the development of modern medicine in the treatment of various diseases.&#x0D; Key words: Curcumin, antioxidant, anticancer, anti-inflammatory.&#x0D; &#x0D; &#x0D;

Nrf2 Knockdown Disrupts the Protective Effect of Curcumin on Alcohol-Induced Hepatocyte Necroptosis.

It has emerged that hepatocyte necroptosis plays a critical role in chronic alcoholic liver disease (ALD). Our previous study has identified that the beneficial therapeutic effect of curcumin on alcohol-caused liver injury might be attributed to activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), whereas the role of curcumin in regulating necroptosis and the underlying mechanism remain to be determined. We first found that chronic alcohol consumption triggered obvious hepatocyte necroptosis, leading to increased expression of receptor-interacting protein 1, receptor-interacting protein 3, high-mobility group box 1, and phosphorylated mixed lineage kinase domain-like in murine livers. Curcumin dose-dependently ameliorated hepatocyte necroptosis and alleviated alcohol-caused decrease in hepatic Nrf2 expression in alcoholic mice. Then Nrf2 shRNA lentivirus was introduced to generate Nrf2-knockdown mice. Our results indicated that Nrf2 knockdown aggravated the effects of alcohol on liver injury and necroptosis and even abrogated the inhibitory effect of curcumin on necroptosis. Further, activated Nrf2 by curcumin inhibited p53 expression in both livers and cultured hepatocytes under alcohol stimulation. The next in vitro experiments, similar to in vivo ones, revealed that although Nrf2 knockdown abolished the suppression of curcumin on necroptosis of hepatocytes exposed to ethanol, p53 siRNA could clearly rescued the relative effect of curcumin. In summary, for the first time, we concluded that curcumin attenuated alcohol-induced hepatocyte necroptosis in a Nrf2/p53-dependent mechanism. These findings make curcumin an excellent candidate for ALD treatment and advance the understanding of ALD mechanisms associated with hepatocyte necroptosis.

Systematic Review and Meta-Analysis of Randomized Trials: Curcumin Treatment for Clinical Remission Induction in Patients with Mild to Moderate Ulcerative Colitis

Introduction: Curcumin is a phytochemical compound with anti-inflammatory properties. There is limited data regarding the utility of such alternative medicines in treatment of Ulcerative colitis (UC). A few recent randomized trials looked at the role of curcumin in achieving remission induction in patients with mild - moderate UC. This has never been systematically reviewed. Aims: Primary outcome was to evaluate the efficacy of curcumin in achieving clinical remission induction [SCCAI (simple clinical colitis activity index) score 3) and safety profile. Methods: Study Selection Criteria: Randomized controlled trials comparing the efficacy of curcumin (2-3gms oral capsules daily or 140mg rectal enema daily) plus mesalamine (1600-4000mg daily) (CM group) versus placebo plus mesalamine (PM group) in patients with mild to moderate UC. Data collection & extraction: Articles were searched in Medline, Pubmed, and Ovid journals. Two authors independently searched and extracted data. Any differences were resolved by mutual agreement. Statistical Methods: Pooled proportions were calculated using both fixed and random effects model. The heterogeneity among studies was tested using Cochran's Q test based upon inverse variance weights. Results: Initial search identified 142 reference articles, of which 24 were selected and reviewed. Three studies (N=184) that met the inclusion criteria were included in this analysis. Median age of the patients was 41 years, predominantly male population (62.5%). The p for chi-squared heterogeneity for all the pooled accuracy estimates was > 0.10. At a mean follow up period of 6 weeks (ranged 4-8 weeks), the pooled odds ratio for clinical remission induction in CM group versus PM group was 6.78 (95% CI = 2.39 to 19.23) after a mean treatment period of 6 weeks. Odds ratio for clinical improvement in CM group versus PM group was 4.83 (95% CI = 2.00 to 11.65). Adverse events (mild nausea, transient increase in stool frequency, and abdominal bloating) in both the group were similar, with an odds ratio of 1.13 (95% CI = 0.34 to 3.70) in CM group versus PM group. Conclusion: In patients with mild to moderate UC, 4-8 weeks of curcumin treatment along with mesalamine is superior to placebo plus mesalamine. It is a safe and promising agent for the treatment of ulcerative colitis.

Roles of Curcumin and Monochromatic Light in Optimizing Liver Function to Support Egg Yolk Biosynthesis in Magelang Ducks

Roles of Curcumin and Monochromatic Light in Optimizing Liver Function to Support Egg Yolk Biosynthesis in Magelang Ducks