• Nutrition Research and Practice
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• v.9 no.2
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• pp.117-122
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• 2015

BACKGROUND/OBJECTIVES: Curcumin, a major component of the Curcuma species, contains antioxidant and anti-inflammatory properties. Although it was found to induce apoptosis in cancer cells, the functional role of curcumin as well as its molecular mechanism in anti-inflammatory response, particularly in intestinal cells, has been less investigated. The intestine epithelial barrier is the first barrier and the most important location for the substrate coming from the lumen of the gut. SUBJECTS/METHODS: We administered curcumin treatment in the human intestinal epithelial cell lines, T84 and Caco-2. We examined endoplasmic reticulum (ER) stress response by thapsigargin, qPCR of XBP1 and BiP, electrophysiology by wild-type cholera toxin in the cells. RESULTS: In this study, we showed that curcumin treatment reduces ER stress and thereby decreases inflammatory response in human intestinal epithelial cells. In addition, curcumin confers protection without damaging the membrane tight junction or actin skeleton change in intestine epithelial cells. Therefore, curcumin treatment protects the gut from bacterial invasion via reduction of ER stress and anti-inflammatory response in intestinal epithelial cells. CONCLUSIONS: Taken together, our data demonstrate the important role of curcumin in protecting the intestine by modulating ER stress and inflammatory response post intoxication.

• Journal of Periodontal and Implant Science
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• v.41 no.3
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• pp.157-163
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• 2011

Purpose: Curcumin is known to exert numerous biological effects including anti-inflammatory activity. In this study, we investigated the effects of curcumin on the production of interleukin-6 (IL-6) by murine macrophage-like RAW 264.7 cells stimulated with lipopolysaccharide (LPS) from Prevotella intermedia, a major cause of inflammatory periodontal disease, and sought to determine the underlying mechanisms of action. Methods: LPS was prepared from lyophilized P. intermedia ATCC 25611 cells by the standard hot phenol-water method. Culture supernatants were collected and assayed for IL-6. We used real-time polymerase chain reaction to detect IL-6 mRNA expression. $I{\kappa}B-{\alpha}$ degradation, nuclear translocation of NF-${\kappa}B$ subunits, and STAT1 phosphorylation were characterized via immunoblotting. DNA-binding of NF-${\kappa}B$ was also analyzed. Results: Curcumin strongly suppressed the production of IL-6 at both gene transcription and translation levels in P. intermedia LPS-activated RAW 264.7 cells. Curcumin did not inhibit the degradation of $I{\kappa}B-{\alpha}$ induced by P. intermedia LPS. Curcumin blocked NF-${\kappa}B$ signaling through the inhibition of nuclear translocation of NF-${\kappa}B$ p50 subunit. Curcumin also attenuated DNA binding activity of p50 and p65 subunits and suppressed STAT1 phosphorylation. Conclusions: Although further study is required to explore the detailed mechanism of action, curcumin may contribute to blockade of the host-destructive processes mediated by IL-6 and appears to have potential therapeutic values in the treatment of inflammatory periodontal disease.

• Korean Journal of Exercise Nutrition
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• v.23 no.2
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• pp.7-12
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• 2019

[Purpose] Eccentric exercise induces a decrease in vascular endothelial function. Curcumin, a major component of turmeric, has potent antioxidant and anti-inflammatory properties that are associated with vascular protective effects. The present study examined the effect of acute supplementation of curcumin on eccentric exercise-induced endothelial dysfunction in healthy young men. [Methods] Fourteen healthy sedentary young men (range, 21-29 years) were assigned to either the curcumin (n = 6) or placebo (n = 8) group. All subjects consumed either curcumin or placebo before exercise, and eccentric exercise of the elbow flexors was performed with their nondominant arm. Before and 60 min after exercise, brachial artery flow-mediated dilation (FMD), as an indicator of endothelial function, was measured in the non-exercised arm. [Results] Brachial artery FMD significantly decreased following eccentric exercise (p < 0.05) in the placebo group, but acute supplementation with curcumin before exercise nullified this change. The change in FMD before and after eccentric exercise between the placebo and curcumin groups was significantly different (p < 0.05). [Conclusion] The present study found that acute curcumin supplementation could attenuate the decrease in endothelial function, as measured by FMD, following eccentric exercise in healthy young men.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.29 no.5
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• pp.272-281
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• 2003

Nontraditional or alternative medicine is becoming an increasingly attractive approach for the treatment of various inflammatory disorders and cancers. Curcumin is the major constitute of turmoric powder extracted from the rhizomes of the plant Curcuma longa. Resveratrol is a phytoalexin present in grapes and a variety of medicinal plants. In this report, We investigated the effect of curcumin and resveratrol on regulatory protein of cell cycle, induction of apoptosis and MMP activity. Treatment with 75 M curcumin for 24 hrs produced morphological changing in HN-4 cells. Curcumin and resveratrol inhibited the cellular growth in HN-4 cells. Inhibition of cell growth was associated with down-regulation of cell cycle regulatory proteins. Curcumin-induced caspase-3 activation and Bax degradation were dose-dependent with a maximal effect at a concentration of 100 M. The elevated caspase-3 activity in curcumin treated HN-4 cells are correlated with down-regulation of survivin and cIAP1, but not cIAP2. Curcumin induced a dose-dependent increase of cytochrome c in the cytosol. Curcumin induced-apoptosis was mediated through the release of cytochrome c. In addition, curcumin-induced apoptosis was caused by the generation of reactive oxygen species, which was prevented by antioxidant N-acetyl-cysteine (NAC). Cotreatment with NAC markedly prevented cytochrome c release, Bax cleavage and cell death. Also resveratrol-induced apoptosis was preceded by down-regulation of the anti-apoptotic Bcl-2, cIAP1, and caspase-3 activity. However, resveratrol-induced apoptosis was not prevented by antioxidant NAC. In addition, HN-4 cells release basal levels of MMP2 when cultured in serum-free medium. Treatment of the cells with various concentrations of PMA for 24 hr induced the expression and secretion of latent MMP9 as determined by gelatin zymography. HN-4 cells were treated with various concentrations of curcumin and resveratrol in the presence of 75 nM PMA, and MMP2 and 9 activities were inhibited by curcumin and resveratrol. These findings have implications for developing curcumin-based anticancer and anti-inflammation therapies.

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.6
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• pp.1014-1019
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• 2011

Curcumin is a natural phytochemical present in turmeric, the ground powder of the rhizomes of Curcuma longa. Curcumin has been described as having antioxidant, anti-inflammatory, and anti-carcinogenic properties. However, it is still largely unknown whether curcumin inhibits the UVB-induced inflammatory reaction in HaCaT keratinocyte cell lines. In this study, to confirm the photoprotection properties of curcumin, HaCaT keratinocyte cells were irradiated by UVB, and then treated with curcumin. UVB irradiation induced the increased expressions of IL-$1{\beta}$, TNF-${\alpha}$, IL-6, IL-8, and COX-2 in HaCaT cells. These increased expressions of cytokines (IL-$1{\beta}$, TNF-${\alpha}$, IL-6, IL-8, and COX-2) were down-regulated by curcumin treatment in UVB-irradiated HaCaT cells. In addition skin of hairless mice were damaged by UVB irradiation, which were evidenced by atrophy of epidermis and decrease of collagen in dermis. However, these damages were protected partially by co-treatment of curcumin. Taken together, this data indicate that curcumin may be a promising photoprotection agent, when used in massage pack or sunscreen product, to reduce cell death in UV-damaged skin.

• Archives of Plastic Surgery
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• v.37 no.2
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• pp.110-114
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• 2010

Purpose: On this study, we investigated the effects of curcumin and adipose-derived stromal cells (ADSCs) in wound healing process, especially in the aspect of synergic effects when they were administrated simultaneously. Methods: Curcumin (40 mg/kg) and/or $1.0{\times}10^6$ ADSCs were applied to an $1.5{\times}1.5\;cm$-sized full thickness wound on the backs of male Lewis rats (n=5 in each group). In control group (n=5), saline was administrated instead of curcumin and ASCs. The wound size was followed by computer planimetry in 5, 7, and 14 days, and wounds were harvested for histological analysis in 7 and 14 days. Results: The dimensions of wounds of curcumin, ADSCs, and curcumin-ADSCs group significantly decreased in 5, 7, 14 days compared with those of control group (p<0.05), but there were no significant differences among three groups. The wound sizes were lowest in curcumin-ADSCs group compared with the other groups, but the differences were insignificant (p>0.05). There were infiltration of more epithelization and more precisely organization of extracellular matrix in curcumin, ADSCs, and curcumin-ADSCs group compared with those of control group. Conclustion: The results suggest that curcumin and ADSCs have beneficial effects in the acceleration of wound healing. Although the simultaneous application of curcmin and ADSCs also has beneficial effects on wound healing, there are no significant synergic effects.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3363-3368
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• 2014

Background: Curcumin, a phenolic compound extracted from the rhizomes of Curcuma longa, has shown cytotoxic effects against a variety of cancers. The aim of this study was to identify potential microRNA (miRNA) mediators of the anticancer effects of curcumin in ovarian cancer cells. Materials and Methods: SKOV3 ovarian cancer cells were treated with curcumin ($10-60{\mu}M$) and miR-9 expression, cell proliferation, and apoptosis were assessed. The effects of miR-9 depletion on curcumin-mediated growth suppression were also examined. Phosphorylation of Akt and forkhead box protein O1 (FOXO1) was measured in cells with miR-9 overexpression or curcumin treatment. Results: Curcumin caused a significant and dose-dependent increase of miR-9 expression in SKOV3 cells, while significantly impeding cell proliferation and stimulating apoptosis. Depletion of miR-9 significantly (p<0.05) attenuated the growth-suppressive effects of curcumin on SKOV3 cells, coupled with reduced percentages of apoptotic cells. In contrast, overexpression of miR-9 significantly enhanced the cleavage of caspase-3 and poly(ADP-ribose) polymerase and promoted apoptotic death in SKOV3 cells. Western blot analysis showed that both miR-9 overexpression and curcumin similarly caused a significant (p<0.05) decline in the phosphorylation of Akt and FOXO1, compared to untreated cells. Conclusions: The present study provided evidence that curcumin exerts its cytotoxic effects against SKOV3 ovarian cancer cells largely through upregulation of miR-9 and subsequent modulation of Akt/FOXO1 axis. Further studies are needed to identify direct targets of miR-9 that mediate the anticancer effects of curcumin in ovarian cancer cells.

• The Korean Journal of Pain
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• v.25 no.1
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• pp.1-6
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• 2012

Background: Curcumin has been reported to have anti-inflammatory, antioxidant, antiviral, antifungal, antitumor, and antinociceptive activity when administered systemically. We investigated the analgesic efficacy of intrathecal curcumin in a rat model of inflammatory pain. Methods: Male Sprague Dawley rats were prepared for intrathecal catheterization. Pain was evoked by injection of formalin solution (5%, $50{\mu}l$) into the hind paw. Curcumin doses of 62.5, 125, 250, and $500{\mu}g$were delivered through an intrathecal catheter to examine the flinching responses. The $ED_{50}$ values (half-maximal effective dose) with 95% confidence intervals of curcumin for both phases of the formalin test were calculated from the dose-response lines fitted by least-squares linear regression on a log scale. Results: In rats with intrathecal administration of curcumin, the flinching responses were significantly decreased in both phases. The slope of the regression line was significantly different from zero only in phase 2, and the $ED_{50}$ value (95% confidence interval) of curcumin was $511.4{\mu}g$ (23.5-1126.5). There was no apparent abnormal behavior following the administration of curcumin. Conclusions: Intrathecal administration of curcumin decreased inflammatory pain in rats, and further investigation to elucidate the precise mechanism of spinal action of curcumin is warranted.

• Journal of Korean Medicine Rehabilitation
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• v.20 no.2
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• pp.51-61
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• 2010

Objectives : The purpose of this study was to investigate antioxidant effects of curcumin from Curcumae Longae Radix. Methods : Using HepG2 Iiver-like cells, the antioxidant effects of curcumin, one of main components from Curcumae Longae Radix, and its analogues have been evaluated by measuring their effects on cytotoxicity induced by $H_2O_2$. Results : The pre-incubation for 6 hours with curcumin, bis-demethoxycurcumin, or dimethoxycurcumin protected HepG2 cells from $H_2O_2$-induced toxicity in a dose-dependent manner. However, tetrahydrocurcumin, one of curcumin metabolites, did not protect HepG2 cells from $H_2O_2$-induced toxicity. Interestingly, curcumin, bis-demethoxycurcumin, and dimethoxycurcumin were increased in the protein levels of heme oxygenase-1(HO-1) at concentrations that were also effective in cellular protection. In contrast, tetrahydrocurcumin did not induce HO-1 expression. Tin protoporphyrin-IX, an inhibitor of HO-1 activity, significantly abolished cytoprotection afforded by curcumin, bis-demethoxycurcumin and dimethoxycurcumin. Conclusions : These results demonstrate that curcumin, bis-demethoxycurcumin, and dimethoxycurcumin with two conjugated doble bonds on their structures may reduce $H_2O_2$-induced oxidative stress through HO-1 expression. HO-1 induction may be one of antioxidant pathways by which curcumin protects from oxidative stress-induced cytotoxicity.

• Journal of Microbiology and Biotechnology
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• v.26 no.8
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• pp.1392-1397
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• 2016

Curcumin is a polyphenol derived from the plant Curcuma longa, which is used for the treatment of diseases associated with oxidative stress and inflammation. The present study was undertaken to determine the protective effect of curcumin against naproxen-induced gastric antral ulcerations in rats. Different doses (10, 50, and 100 mg/kg) of curcumin or vehicle (curcumin, 0 mg/kg) were pretreated for 3 days by oral gavage, and then gastric mucosal lesions were caused by 80 mg/kg naproxen applied for 3 days. Curcumin significantly inhibited the naproxen-induced gastric antral ulcer area and lipid peroxidation in a dose-dependent manner. In addition, curcumin markedly increased activities of radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase in a dose-dependent manner. Specifically, 100 mg/kg curcumin completely protected the gastric mucosa against the loss in the enzyme, resulting in a drastic increase of activities of radical scavenging enzymes up to more than the level of untreated normal rats. Histological examination obviously showed that curcumin prevents naproxen-induced gastric antral ulceration as a result of direct protection of the gastric mucosa. These results suggest that curcumin blocks naproxen-induced gastric antral ulcerations through prevention of lipid peroxidation and activation of radical scavenging enzymes, and it may offer a potential remedy of gastric antral ulcerations.