curcumin and Pulmonary-Disease--Chronic-Obstructive

Chronic inflammation of the respiratory tract is one of the most concerning public health issues, as it can lead to chronic respiratory diseases (CRDs), some of which are more detrimental than others. Chronic respiratory diseases include chronic obstructive pulmonary disease (COPD), asthma, lung cancer, and pulmonary fibrosis. The conventional drug therapies for the management and treatment of CRDs only address the symptoms and fail to reverse or recover the chronic-inflammation-mediated structural and functional damage of the respiratory tract. In addition, the low efficacy and adverse effects of these drugs have directed the attention of researchers towards nutraceuticals in search of potential treatment strategies that can not only ameliorate CRD symptoms but also can repair and reverse inflammatory damage. Hence, there is a growing interest toward investigating the medicinal benefits of nutraceuticals, such as rutin, curcumin, zerumbone, and others. Nutraceuticals carry many nutritional and therapeutic properties, including anti-inflammatory, antioxidant, anticancer, antidiabetic, and anti-obesity properties, and usually do not have as many adverse effects, as they are naturally sourced. Recently, the use of nanoparticles has also been increasingly studied for the nano drug delivery of these nutraceuticals. The discrete size of nanoparticles holds great potential for the level of permeability that can be achieved when transporting these nutraceutical compounds. This review is aimed to provide an understanding of the use of nutraceuticals in combination with nanoparticles against CRDs and their mechanisms involved in slowing down or reversing the progression of CRDs by inhibiting pro-inflammatory signaling pathways.

Topics: Anti-Inflammatory Agents; Antioxidants; Curcumin; Functional Food; Humans; Hypoglycemic Agents; Inflammation; Pulmonary Disease, Chronic Obstructive; Rutin

　Hemodynamic stresses, including hypertension and myocardial infarction, activate neurohumoral factors such as the sympathetic nervous system and the renin-angiotensin system, and can lead to the progression of heart failure. Established pharmacological agents such as angiotensin II receptor blockers (ARBs), angiotensin-converting enzyme (ACE) inhibitors, and β-blockers target extra-cellular molecules and receptors on the cell membrane. These agents have shown some efficacy for the treatment of heart failure, but the long-term survival rate of patients with heart failure remains low. Additional effective pharmacological approaches are urgently required. Our previous studies have demonstrated that curcumin, a natural polyphenol derived from the root of Curcuma longa, prevented the development of heart failure in rat models of myocardial infarction and hypertensive heart disease. However, until recently curcumin's poor water solubility and extremely low bioavailability have presented serious challenges to its clinical applicability. In recent years, highly absorbable curcumin preparations have been developed using methods such as nanoparticle formation and micellization, and there are now high expectations for their wide clinical application. Our group has developed a highly absorbable curcumin formulation called Theracurmin using nanoparticulation and surface processing techniques. Our preliminary data indicated that Theracurmin may improve left ventricular diastolic function. Furthermore, we have already completed and are currently carrying out several clinical trials using Theracurmin against heart failure-related diseases. This paper summarizes and discusses the potential clinical applications of curcumin, focusing on our highly absorbable curcumin formulation, Theracurmin.

Topics: Administration, Oral; Animals; Biological Availability; Curcumin; Diabetes Mellitus, Type 2; Disease Models, Animal; Drug Compounding; Heart Failure; Humans; Life Style; Nanoparticles; Nanotechnology; Phytotherapy; Pulmonary Disease, Chronic Obstructive; Rats; Solubility

Vesicular systems like nanotechnology and liposomes are gaining tremendous attention lately in the field of respiratory diseases. These formulations enhance bioavailability of the drug candidate, which could be achieved through a novel drug delivery mechanism. Moreover, the therapeutic potential achieved through these systems is highly controllable over long durations of time providing better efficacy and patient compliance.. The objective of this paper is to review the recent literature on vesicular drug delivery systems containing curcumin.. We have collated and summarized various recent attempts made to develop different controlled release drug delivery systems containing curcumin which would be of great interest for herbal, formulation and biological scientists. There are several vesicular nanotechnological techniques involving curcumin which have been studied recently, targeting pulmonary diseases.. Different vesicular systems containing curcumin are being studied for their therapeutic potential in different respiratory diseases. There has been a renewed interest in formulations containing curcumin recently, primarily owing to the broad spectrum therapeutic potential of this miracle substance. Various types of formulations, containing curcumin, targeting different bodily systems have recently emerged and, nevertheless, the search for newer frontiers with this drug goes on.. This mini review, in this direction, tries to highlight the key research interventions employing vesicular systems of drug delivery with curcumin.

Topics: Asthma; Curcumin; Delayed-Action Preparations; Drug Compounding; Drug Delivery Systems; Humans; Liposomes; Nanomedicine; Nanoparticles; Pulmonary Disease, Chronic Obstructive; Respiration Disorders

The expression of NF-kappaB (NF-kappaB)-dependent pro-inflammatory genes in response to oxidative stress is regulated by the acetylation-deacetylation status of histones bound to the DNA. It has been suggested that in severe asthma and in chronic obstructive pulmonary disease (COPD) patients, oxidative stress not only activates the NF-kappaB pathway but also alters the histone acetylation and deacetylation balance via post-translational modification of histone deacetylases (HDACs). Corticosteroids have been one of the major modes of therapy against various chronic respiratory diseases such as asthma and COPD. Failure of corticosteroids to ameliorate such disease conditions has been attributed to their inability to either recruit HDAC2 or to the presence of an oxidatively modified HDAC2 in asthmatics and COPD subjects. Naturally occurring polyphenols such as curcumin and resveratrol have been increasingly considered as safer nutraceuticals. Curcumin is a polyphenol present in the spice turmeric, which can directly scavenge free radicals such as superoxide anion and nitric oxide and modulate important signaling pathways mediated via NF-kappaB and mitogen-activated protein kinase pathways. Polyphenols also down-regulate expression of pro-inflammatory mediators, matrix metalloproteinases, adhesion molecules, and growth factor receptor genes and they up-regulate HDAC2 in the lung. Thus, curcumin may be a potential antioxidant and anti-inflammatory therapeutic agent against chronic inflammatory lung diseases.

Topics: Anti-Inflammatory Agents; Antioxidants; Asthma; Curcumin; Gene Expression; Glucocorticoids; Humans; Inflammation; NF-kappa B; Pulmonary Disease, Chronic Obstructive; Signal Transduction; Steroids

Oxidative stress plays a key role in the development of chronic pulmonary complications of sulfur mustard (SM). Curcuminoids are polyphenols with documented safety and antioxidant activity. The present study aimed to investigate the efficacy of short-term supplementation with curcuminoids (co-administered with piperine to enhance the bioavailability of curcuminoids) in alleviating systemic oxidative stress and clinical symptoms, and improvement of health-related quality of life (HRQoL) in subjects suffering from chronic pulmonary complications due to SM exposure who are receiving standard respiratory treatments. Eighty-nine subjects were recruited to this randomized double-blind placebo-controlled trial, being randomly allocated to either curcuminoids (1500 mg/day) + piperine (15 mg/day) combination (n = 45) or placebo (n = 44) for a period of 4 weeks. High-resolution computed tomography suggested the diagnosis of bronchiolitis obliterans in all subjects. Efficacy measures were changes in serum levels of reduced glutathione (GSH) and malonedialdehyde (MDA). The severity and frequency of respiratory symptoms and HRQoL were also assessed using St. George respiratory Questionnaire (SGRQ) and COPD Assessment Test (CAT) indices. Serum levels of GSH were increased whilst those of MDA decreased by the end of trial in both groups. Likewise, there were significant improvements in the total as well as subscale (symptoms, activity and impact) SGRQ and CAT scores in both groups. However, comparison of magnitude of changes revealed a greater effect of curcuminoids-piperine combination compared to placebo in elevating GSH, reducing MDA and improving CAT and SGRQ (total and subscale) scores (p < 0.001). Regarding the promising effects of curcuminoids on the measures of systemic oxidative stress, clinical symptoms and HRQoL, these phytochemicals may be used as safe adjuvants in patients suffering from chronic SM-induced pulmonary complications who are receiving standard treatments.

Topics: Adult; Alkaloids; Antioxidants; Benzodioxoles; Bronchiolitis; Chronic Disease; Curcuma; Curcumin; Double-Blind Method; Glutathione; Humans; Male; Malondialdehyde; Middle Aged; Mustard Gas; Oxidative Stress; Phytotherapy; Piper; Piperidines; Plant Extracts; Polyphenols; Polyunsaturated Alkamides; Pulmonary Disease, Chronic Obstructive; Quality of Life; Respiratory Function Tests

COPD is mainly caused by tobacco smoking and is associated with a high frequency of coronary artery disease. There is growing recognition that the inflammation in COPD is not only confined to the lungs but also involves the systemic circulation and can impact nonpulmonary organs, including blood vessels. α1-antitrypsin-low-density lipoprotein (AT-LDL) complex is an oxidatively modified LDL that accelerates atherosclerosis. Curcumin, one of the best-investigated natural products, is a powerful antioxidant. However, the effects of curcumin on AT-LDL remain unknown. We hypothesized that Theracurmin(®), a highly absorptive curcumin with improved bioavailability using a drug delivery system, ameliorates the inflammatory status in subjects with mild COPD.. This is a randomized, double-blind, parallel-group study. Subjects with stages I-II COPD according to the Japanese Respiratory Society criteria were randomly assigned to receive 90 mg Theracurmin(®) or placebo twice a day for 24 weeks, and changes in inflammatory parameters were evaluated.. There were no differences between the Theracurmin(®) and placebo groups in terms of age, male/female ratio, or body mass index in 39 evaluable subjects. The percent changes in blood pressure and hemoglobin A1c and LDL-cholesterol, triglyceride, or high-density lipoprotein-cholesterol levels after treatment were similar for the two groups. However, the percent change in the AT-LDL level was significantly (P=0.020) lower in the Theracurmin(®) group compared with the placebo group.. Theracurmin(®) reduced levels of atherosclerotic AT-LDL, which may lead to the prevention of future cardiovascular events in mild COPD subjects.

Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; alpha 1-Antitrypsin; Anti-Inflammatory Agents; Atherosclerosis; Biological Availability; Biomarkers; Curcumin; Double-Blind Method; Down-Regulation; Drug Administration Schedule; Drug Compounding; Female; Gastrointestinal Absorption; Humans; Japan; Lipoproteins, LDL; Male; Middle Aged; Pulmonary Disease, Chronic Obstructive; Time Factors; Treatment Outcome; Young Adult

Epidemiological studies have reported an association between exposures to ambient air pollution and respiratory diseases, including chronic obstructive pulmonary disease (COPD). Pneumonitis is a critical driving factor of COPD and exposure to air pollutants (e.g., acrolein) is associated with increased incidence of pneumonitis.. Currently available anti-inflammatory therapies provide little benefit against respiratory diseases. To this end, we investigated the preventive role of curcumin against air pollutant-associated pneumonitis and its underlying mechanism.. A total of 40 subjects was recruited from Chengdu, China which is among the top three cities in terms of respiratory mortality related to air pollution. The participants were randomly provided either placebo or curcumin supplements for 2 weeks and blood samples were collected at the baseline and at the end of the intervention to monitor systemic markers. In our follow up mechanistic study, C57BL/6 mice (n = 40) were randomly allocated into 4 groups: Control group (saline + no acrolein), Curcumin only group (curcumin + no acrolein), Acrolein only group (saline + acrolein), and Acrolein + Curcumin group (curcumin + acrolein). Curcumin was orally administered at 100 mg/kg body weight once a day for 10 days, and then the mice were subjected to nasal instillation of acrolein (5 mg/kg body weight). Twelve hours after single acrolein exposure, all mice were euthanized.. Curcumin supplementation, with no noticeable adverse responses, reduced circulating pro-inflammatory cytokines in association with clinical pneumonitis as positive predictive while improving those of anti-inflammatory cytokines. In the pre-clinical study, curcumin reduced pneumonitis manifestations by suppression of intrinsic and extrinsic apoptotic signaling, which is attributed to enhanced redox sensing of Nrf2 and thus sensitized synthesis and restoration of GSH, at least in part, through curcumin-Keap1 conjugation.. Our study collectively suggests that curcumin could provide an effective preventive measure against air pollutant-enhanced pneumonitis and thus COPD.

Topics: Acrolein; Air Pollutants; Animals; Apoptosis; Body Weight; Curcumin; Cysteine; Cytokines; Kelch-Like ECH-Associated Protein 1; Mice; Mice, Inbred C57BL; Models, Animal; NF-E2-Related Factor 2; Pneumonia; Pulmonary Disease, Chronic Obstructive

Chronic obstructive pulmonary disease (COPD) is a common respiratory disease characterized by symptoms of shortness of breath and chronic inflammation. Curcuma zedoaria (Christm.) Roscoe is a well-documented traditional medical herb that is frequently used in the treatment of COPD. Previously, we identified a diarylheptanoid compound (1-(4-hydroxy-5-methoxyphenyl)-7-(4,5-dihydroxyphenyl)-3,5-dihydroxyheptane; abbreviated as HMDD) from this herb that exhibited potent agonistic activity on β2-adrenergic receptors (β2 adrenoreceptor) that are present on airway smooth muscle cells. In this work, we used chemically synthesized HMDD compound, and confirmed its bioactivity on β2 adrenoreceptors. Then by a proteomics study and anti-inflammatory evaluation detections, we found that HMDD downregulated the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) signaling pathway and suppressed the NLRP3 receptor expression in RAW264.7 macrophages and in a COPD model in A549 lung carcinoma cells. HMDD also decreased nitric oxide production levels, and impacted other interleukins and the phosphorylation of NF-κB and ERK pathways. We performed molecular docking of HMDD on β2 adrenoreceptor and NLRP3 protein models. This work reports the anti-inflammatory effects of HMDD and suggests a dual-targeting mechanism of β2-adrenoreceptor agonism and NLRP3 inhibition. Such a mechanism scientifically supports the clinical uses of Curcuma zedoaria (Christm.) Roscoe in treating COPD, as it can simultaneously relieve persistent breathlessness and inflammation. HMDD can be considered as a potential non-steroidal anti-inflammatory drug in novel therapy design for the treatment of COPD and other inflammatory diseases.

Topics: Anti-Inflammatory Agents; Curcuma; Diarylheptanoids; Humans; Inflammation; Molecular Docking Simulation; NF-kappa B; NLR Family, Pyrin Domain-Containing 3 Protein; Pulmonary Disease, Chronic Obstructive; Signal Transduction

Topics: Animals; Apoptosis; Autophagy; Curcumin; Disease Models, Animal; Endoplasmic Reticulum Stress; Lung; Male; Pulmonary Disease, Chronic Obstructive; Rats, Sprague-Dawley; Sirtuin 1; Up-Regulation

Peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated nuclear hormone receptor, is considered to be a potential target for the anti-inflammatory treatment of COPD, and its anti-inflammatory efficacy is likely related to the inhibition of transcriptional regulation of nuclear factor (NF)-κB. Curcumin, a dietary polyphenol isolated from the rhizome of turmeric, has been found to have therapeutic benefits in chronic obstructive pulmonary disease (COPD) via inhibiting NF-κB. However, whether the anti-inflammatory efficacy of curcumin in COPD is associated with PPARγ has scarcely been investigated before. The purpose of this study was to validate the relationship between PPARγ and NF-κB in cigarette smoke (CS)-induced COPD models, and then to investigate whether the therapeutic effect of curcumin on COPD is achieved through modulating the PPARγ-NF-κB signaling pathway. Our experiments in vitro illustrated that PPARγ might be upstream of NF-κB in cigarette smoke extract (CSE)-treated Beas-2B cells, and that curcumin could significantly ameliorate CSE-induced cell viability reduction and inflammation though up-regulating PPARγ and inhibiting NF-κB activation. Importantly, we found that the inhibitory effect on NF-κB by curcumin was dependent on PPARγ in T0070907-treated or PPARγ shRNA-transfected Beas-2B cells, indicating that curcumin inhibited CSE-induced inflammation partially through modulating the PPARγ-NF-κB pathway. Furthermore, we also observed that the effect of curcumin on PPARγ protein expression and NF-κB activation in CS-exposed rats was consistent with the results from experiments in vitro, and curcumin effectively attenuated pulmonary function decline and inflammatory responses in CS-exposed rats. In conclusion, all the results revealed that curcumin attenuated CS-induced inflammation both in vivo and in vitro, presumably by modulating the PPARγ-NF-κB pathway.

Topics: Animals; Anti-Inflammatory Agents; Curcumin; Humans; Lung; Male; NF-kappa B; PPAR gamma; Pulmonary Disease, Chronic Obstructive; Rats; Rats, Sprague-Dawley; Signal Transduction; Smoking

The purpose of this study is to evaluate the therapeutic effects of curcumin on airway inflammation using LPS and cigarette smoke (LC)-induced COPD murine models and LPS-stimulated human bronchial epithelial (BEAS-2B) cells. In this research, COPD murine models were established after challenged with LPS for 2 days and exposed to cigarette smoke for 35 days. Treatment with curcumin for 10 days distinctly alleviated airway inflammation and airway remolding in LC-induced COPD mice according to the lung H&E histopathological examination. The number of neutrophils and lymphocytes in broncho alveolar lavage fluid (BALF) was significantly decreased in curcumin+LC-treated group compared with the LC-induced mice. Additionally, curcumin inhibited BEAS-2B cells proliferation, which suggested the preventive effect of curcumin on progressive airway remolding and inflammatory response mediated by bronchial epithelial cells. Further investigation demonstrated an underlying molecular mechanism for the therapeutic effects of curcumin may rely on the inhibition of the degradation of IκBα and COX-2 expression in curcumin+LC-treated COPD mice and LPS-stimulated BEAS-2B cells. Overall, curcumin alleviates the airway inflammation and airway remolding, which is closely related to inhibit the BEAS-2B cells proliferation and suppress the activation of NF-κB and COX-2 expression. These findings indicate that curcumin may be a potential agent for the therapy of COPD.

Topics: Airway Remodeling; Animals; Bronchi; Cell Line; Curcumin; Cyclooxygenase 2; Epithelial Cells; Humans; Inflammation; Mice; NF-kappa B; NF-KappaB Inhibitor alpha; Pulmonary Disease, Chronic Obstructive; Smoke; Tobacco Products

To investigate the effects of curcumin on alveolar epithelial injury in a rat model of chronic obstructive pulmonary disease (COPD) and its potential mechanism.. The rat COPD model was established by cigarette smoke exposure combined with intratracheal administration of lipopolysaccharide. Thirty-eight male Sprague-Dawley rats were randomly divided into four groups: control, COPD model, COPD with curcumin and COPD with solvent groups. Neutrophil and macrophage infiltration in bronchoalveolar lavage fluid (BALF) was evaluated, and the levels of IL-6, IL-8 and TNF-α in BALF and serum were determined by ELISA. Histopathological examination and TUNEL staining were used to assess the alveolar epithelial injury. The protein expression of p66Shc and p-p66Shc in the lung tissues was determined by immunohistochemistry and western blot.. Curcumin significantly decreased the numbers of total cells, neutrophils and macrophages in BALF from COPD rats. In addition, the levels of IL-6, IL-8 and TNF-α in BALF and serum of COPD rats were significantly decreased after treatment with curcumin. Moreover, curcumin ameliorated emphysema and ultrastructural damage of alveolar epithelial cells in COPD rats. The apoptosis index of alveolar epithelial cells in the COPD with curcumin group was significantly lower than that in the COPD model group. Furthermore, the protein expression of p66Shc and p-p66Shc in alveolar epithelia was significantly decreased in the COPD with curcumin group compared with COPD model group.. Curcumin attenuates alveolar epithelial injury in COPD rats, which may be partially due to the down-regulation of p66Shc.

Topics: Adenocarcinoma, Bronchiolo-Alveolar; Alveolar Epithelial Cells; Animals; Apoptosis; Curcumin; Cytokines; Disease Models, Animal; Gene Expression Regulation; Lipopolysaccharides; Male; Pulmonary Disease, Chronic Obstructive; Random Allocation; Rats; Rats, Sprague-Dawley; Src Homology 2 Domain-Containing, Transforming Protein 1; Tobacco Smoke Pollution

To assess the efficacy of a combination of Boswellia serrata, licorice root (Glycyrrhiza glabra) and Tumeric root (Curcuma longa) as natural leukotriene inhibitor, antiinflammatory and antioxidant products respectively in controlling bronchial asthma.. The study comprised 63 patients with bronchial asthma that are further subdivided into two groups .Group 1 receiving oral capsule (combined herb) in a soft-gelatin capsule 3 times daily for 4weeks and group 2 receiving placebo. Plasma leukotriene C(4) (LTC(4))(,) nitric oxide (NO) and malondialdehyde (MDA) levels were measured and pulmonary function was also assessed in all patients enrolled in the study.. There was a statistically significant decrease in the plasma levels of LTC(4), (MDA), and NO in target therapy group when compared with placebo group.. The used extract contained Boswellia serrata, Curcuma longa and Glycyrrhiza has a pronounced effect in the management of bronchial asthma.

Topics: Adolescent; Adult; Anti-Inflammatory Agents; Asthma; Biological Products; Complementary Therapies; Curcuma; Drugs, Chinese Herbal; Glycyrrhiza; Humans; Inflammation Mediators; Leukotriene Antagonists; Leukotriene C4; Malondialdehyde; Middle Aged; Nitric Oxide; Plant Extracts; Plant Roots; Pulmonary Disease, Chronic Obstructive; Young Adult

Recent studies have demonstrated that K-ras mutations in lung epithelial cells elicit inflammation that promotes carcinogenesis in mice (intrinsic inflammation). The finding that patients with chronic obstructive pulmonary disease (COPD), an inflammatory disease of the lung, have an increased risk of lung cancer after controlling for smoking suggests a further link between lung cancer and extrinsic inflammation. Besides exposure to cigarette smoke, it is thought that airway inflammation in COPD is caused by bacterial colonization, particularly with non-typeable Hemophilus influenzae (NTHi). Previously, we have shown that NTHi-induced COPD-like airway inflammation promotes lung cancer in an airway conditional K-ras-induced mouse model. To further test the role of inflammation in cancer promotion, we administered the natural anti-inflammatory agent, curcumin, 1% in diet before and during weekly NTHi exposure. This significantly reduced the number of visible lung tumors in the absence of NTHi exposure by 85% and in the presence of NTHi exposures by 53%. Mechanistically, curcumin markedly suppressed NTHi-induced increased levels of the neutrophil chemoattractant keratinocyte-derived chemokine by 80% and neutrophils by 87% in bronchoalveolar lavage fluid. In vitro studies of murine K-ras-induced lung adenocarcinoma cell lines (LKR-10 and LKR-13) indicated direct anti-tumoral effects of curcumin by reducing cell viability, colony formation and inducing apoptosis. We conclude that curcumin suppresses the progression of K-ras-induced lung cancer in mice by inhibiting intrinsic and extrinsic inflammation and by direct anti-tumoral effects. These findings suggest that curcumin could be used to protract the premalignant phase and inhibit lung cancer progression in high-risk COPD patients.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Cell Survival; Chemokines; Curcumin; Female; Genes, ras; Haemophilus Infections; Haemophilus influenzae; Inflammation; Lung Neoplasms; Male; Mice; Neutrophils; Pulmonary Disease, Chronic Obstructive

Oxidative stress as a result of cigarette smoking is an important etiologic factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic steroid-insensitive inflammatory disease of the airways. Histone deacetylase-2 (HDAC2), a critical component of the corticosteroid anti-inflammatory action, is impaired in lungs of patients with COPD and correlates with disease severity. We demonstrate here that curcumin (diferuloylmethane), a dietary polyphenol, at nanomolar concentrations specifically restores cigarette smoke extract (CSE)- or oxidative stress-impaired HDAC2 activity and corticosteroid efficacy in vitro with an EC(50) of approximately 30 nM and 200 nM, respectively. CSE caused a reduction in HDAC2 protein expression that was restored by curcumin. This decrease in HDAC2 protein expression was reversed by curcumin even in the presence of cycloheximide, a protein synthesis inhibitor. The proteasomal inhibitor, MG132, also blocked CSE-induced HDAC2 degradation, increasing the levels of ubiquitinated HDAC2. Biochemical and gene chip analysis indicated that curcumin at concentrations up to 1 muM propagates its effect via antioxidant-independent mechanisms associated with the phosphorylation-ubiquitin-proteasome pathway. Thus curcumin acts at a post-translational level by maintaining both HDAC2 activity and expression, thereby reversing steroid insensitivity induced by either CSE or oxidative stress in monocytes. Curcumin may therefore have potential to reverse steroid resistance, which is common in patients with COPD and asthma.

Topics: Adrenal Cortex Hormones; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Curcumin; Cycloheximide; Electron Spin Resonance Spectroscopy; Histone Deacetylase 2; Histone Deacetylase Inhibitors; Histone Deacetylases; Humans; Monocytes; Nicotiana; Oligonucleotide Array Sequence Analysis; Oxidants; Oxidative Stress; Protein Synthesis Inhibitors; Pulmonary Disease, Chronic Obstructive; Repressor Proteins; Smoke; Smoking; U937 Cells