Anti-inflammatory Activity Of Curcumin Research Articles

Vascular anti-inflammatory effects of curcumin on HMGB1-mediated responses in vitro

High mobility group box 1 (HMGB1) protein up-regulates proinflammatory cytokines in several inflammatory diseases. Curcumin is a polyphenol responsible for the yellow color of the curry spice turmeric. It possesses diverse pharmacological properties such as anti-inflammatory, anti-oxidant, anti-proliferative and anti-angiogenic activities. However, the effects of curcumin on HMGB1-mediated proinflammatory responses have not been studied. The anti-inflammatory activities of curcumin were determined by measuring solute flux, leukocyte adhesion and migration and activation of proinflammatory proteins in HMGB1-activated human umbilical vein endothelial cells. Curcumin inhibited the release of HMGB1 by lipopolysaccharide (LPS)- and HMGB1-mediated barrier disruption, neutrophil adhesion and migration, and expression of cell adhesion molecules. Further studies revealed that curcumin down-regulated the cell surface receptor of HMGB1 in human endothelial cells. These findings suggest that curcumin exerts anti-inflammatory effects in HMGB1-mediated proinflammatory responses, endorsing its usefulness as therapy for vascular inflammatory diseases.

Anti-Inflammatory Activity of Curcumin in Macrophages Stimulated by Lipopolysaccharides from Porphyromonas gingivalis

Background:Porphyromonas gingivalis, a major periodontopathic bacterium, is necessary for periodontitis to take place. The lipopolysaccharide (LPS) of P. gingivalis stimulates cytokine secretion in immune cells, and thereby initiates the inflammation related to periodontitis. Macrophages are the important ones of the immune cells that are prominent at inflammatory periodontal sites. Curcumin, a major curcumanoid found in the spice turmeric, exhibits anti-inflammatory properties. The aim of this study was to investigate the anti-inflammatory effect and the mechanism of action of curcumin in macrophages stimulated by P. gingivalis LPS. Methods: RAW264.7 cells pre-treated with various concentrations of curcumin were stimulated by P. gingivalis LPS. TNF-α and IL-1β expressions were separately detected by RT-PCR and ELISA. Next, activation of NF-ĸB-dependent transcription was examined by luciferase assay. Results: Curcumin dose-dependently inhibited TNF-α and IL-1β gene expression and protein synthesis in RAW264.7 cells stimulated with P. gingivalis LPS. P. gingivalis LPS activated NF-ĸB-dependent transcription in RAW264.7 cells, which were down-regulated by pre-treatment with curcumin as well. Conclusion: Our data suggest that curcumin can inhibit P. gingivalis LPS-induced cytokine expression, and that this could be due to the inhibition of the NF-ĸB pathway.

Enhanced anti-inflammatory activity of curcumin, a naturally occurring pigment in turmeric via cyclodextrin complexation

Curcumin, a dietary pigment responsible for the yellow color of curry, has been used for the treatment of inflammatory diseases and exhibits a variety of pharmacological effects such as anti- inflammatory, anti-tumor, anti-oxidant, and anti-viral activity. In order to examine the potency of the curcumin in inflammation we used carrageenan induced rat hind paw odema model. As curcumin is practically water insoluble, it is hypothesized that pharmacological activity of curcumin could be improved by enhancing its water solubility. Water soluble complexes of curcumin with cyclodextrins were prepared and screened for greater solubility. Pure curcumin 100 mg/kg body weight along with curcumin complexes equivalent to 100 mg/kg body weight of pure curcumin were tested for the anti-inflammatory activity in Wister rats male rats using carrageenan induced hind paw edema model and compared with that of the reference compound diclofenac sodium at a dose level of 10 mg/kg body weight. Results were statistically analyzed using ANOVA. All the treatment groups showed statistically significant anti-inflammatory activity compared with that of vehicle control and positive control.

Curcumin Enhances Performance Recovery After Exerciseinduced Muscle Damage

Unaccustomed exercise with a large eccentric component produces the greatest muscle fiber damage, inflammation, delayed-onset muscle soreness (DOMS) and functional deficits. Curcumin (extract of the Indian spice, turmeric) has potent anti-inflammatory activity in a variety of inflammation models, but has not been evaluated with respect to exercise-induced muscle damage. It is possible that the anti-inflammatory activity of curcumin could hasten recovery of performance due to an attenuation of the primary and especially secondary inflammation associated with delayed regeneration of muscle fibers, soreness, and CNS fatigue. PURPOSE 1) to develop a mouse model of performance recovery following exercise-induced muscle damage and 2) to determine the effects of curcumin on performance recovery in this model. METHODS In EXP 1, treadmill run times to fatigue (36m/min, 8% grade) were performed at 24, 48, 72 & 96 h after an uphill (UP) or downhill (DWN) run in male mice. DWN running was 150 min starting at 16m/min, −5% grade with increments every 5 min to 22m/min, −14% grade. UP running was the same, but grade was increased from 5% to 14%. Separate groups of mice were sacrificed at 24, 48 and 96 h after UP and DWN for collection of blood, muscle (soleus), and selected brain regions. Creatine kinase (CK) was measured in blood and inflammatory cytokines (IL-1β, IL-6, and TNF-α) were measured in muscle and brain. Exp 2 evaluated the effect of curcumin on performance recovery at 48 and 72 h after UP and DWN. Mice were fed curcumin (10 mg) once daily in a highly palatable food pellet (410 mg; bacon flavor) for 3 d prior to UP or DWN running. RESULTS In EXP 1, treadmill run time to fatigue was suppressed in DWN vs Up by over 50% for up to 72 h following the initial run. DWN was also associated with an increase in plasma CK at 24 and 48 h, and inflammatory cytokines in muscle (IL-6 & IL-1β) and brain (IL-1β only in cortex & cerebellum) at 24h. In EXP 2, curcumin feedings attenuated the reduction in run time to fatigue at 48 and 72 h in DWN, with no effect in UP. CONCLUSIONS In this model, recovery of endurance capacity takes up to 72 h following downhill running, which is associated with an increase in plasma CK, and muscle and brain inflammatory cytokines. Ingestion of Curcumin (anti-inflammatory herbal supplement) for 3 d prior to muscle-damaging exercise hastens recovery of endurance performance, but the extent to which this is due to a reduction in the inflammatory response (in muscle and/or CNS) awaits further research. Funded by the DOD, Natick Soldier Center, Grant # DAAD 16-02-C-0015.

CURCUMIN INHIBITION OF INFLAMMATORY CYTOKINE PRODUCTION BY HUMAN PERIPHERAL BLOOD MONOCYTES AND ALVEOLAR MACROPHAGES

Curcumin, a dietary pigment responsible for the yellow colour of curry, has been used for the treatment of inflammatory diseases and exhibits a variety of pharmacological effects such as anti-inflammatory activity. The mechanism in anti-inflammatory activity of curcumin has been investigated; however, little is known about the effect of curcumin on cytokine production by human peripheral blood monocytes and alveolar macrophages. In the present study, we shed light on the effect of curcumin on inflammatory cytokine production by human peripheral blood monocytes and alveolar macrophages. To this end, we determined the concentrations of interleukin-8 (IL-8), monocyte inflammatory protein-1 (MIP-1α), monocyte chemotactic protein-1 (MCP-1), interleukin-1β (IL-1β), and tumour necrosis factor-α (TNF-α) in the culture supernatants from phorbor ester, 4β phorbor 12β-myristate-13α acetate (PMA)- or lipo-polysaccharide (LPS)-stimulated monocytes and alveolar macrophages in the presence or absence of curcumin. Curcumin inhibited the production of IL-8, MIP-1α, MCP-1, IL-1β, and TNF-α by PMA- or LPS-stimulated monocytes and alveolar macrophages in a concentration- and a time-dependent manner. These results show that curcumin exhibits an inhibitory effect on the production of IL-8, MIP-1α, MCP-1, IL-1β, and TNF-α by PMA- or LPS-stimulated monocytes and alveolar macrophages.

Anti-inflammatory and irritant activities of curcumin analogues in rats.

The anti-inflammatory activity of curcumin (C), sodium curcuminate (NaC), diacetyl curcumin (DAC), triethyl curcumin (TEC), tetrahydro curcumin (THC) and ferulic acid (FA) was compared with that of phenylbutazone (PB) using the carrageenin-induced rat paw edema and cotton pellet granuloma tests. The rank order of potencies of curcumin analogues and PB in carrageenin-induced inflammation were NaC greater than THC greater than C greater than PB greater than TEC. The curcumin analogues de decreased carrageenin-induced paw edema at low doses, however, at higher doses this effect was partially reversed. FA and DAC were devoid of anti-inflammatory activity. Curcumin analogues were less effective in inhibiting the granulomatous tissue formation. Maximum activity was observed with TEC whereas C, NaC and PB were almost half as effective as TEC. C and NaC possess both anti-inflammatory and irritant properties as was evident from experiments in which drugs were incorporated into carrageenin and the cotton pellets for inducing inflammation. The anti-inflammatory action of NaC is not mediated through release of steroids from the adrenal cortex or inhibition of the biosynthesis of prostaglandins from arachidonic acid. The results of the present study support the rationale for the use of powdered rhizome of tumeric (contains 0.6% of curcumin) for conditions of sprain and inflammation.