• Title, Summary, Keyword: Curcumin

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Effects of Curcumin on Sperm Motility, Viability, Mitochondrial Activity and Plasma Membrane Integrity in Boar Semen

  • Lee, A-Sung;Lee, Sang-Hee;Lee, Seunghyung;Yang, Boo-Keun
    • Biomedical Science Letters
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    • v.23 no.4
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    • pp.406-410
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    • 2017
  • Curcumin is known as a natural antioxidant, decreasing oxidative stress in animal cells. Generally, oxidative stress induces reactive oxygen species in sperm and leads to decreased sperm characteristics in pigs. Therefore, this study investigated the influence of curcumin on sperm motility, viability, mitochondrial activity and plasma membrane integrity in pigs. Curcumin (0, 5 and $10{\mu}M$) was treated in boar semen, which were incubated for 9 hours in $37^{\circ}C$. Then, motility, viability, mitochondrial activity, plasma membrane integrity of sperm was analyzed every 3 hours. In the results, sperm motility was significantly increased by $5{\mu}M$ curcumin after 3 and 9 hours after incubation, and viability was significantly higher in $5{\mu}M$ curcumin treatment at 3 hours (P<0.05). Similarly, sperm mitochondrial activity and plasma membrane integrity were significantly increased by $5{\mu}M$ curcumin at 3, 6 and 9 hours after incubation (P<0.05). There results suggest that curcumin improve sperm characteristics such as motility, viability, mitochondrial activity, and plasma membrane integrity, and may exert a positive effect on sperm fertility in pigs.

Curcumin Inhibits the Activation of Immunoglobulin E-Mediated Mast Cells and Passive Systemic Anaphylaxis in Mice by Reducing Serum Eicosanoid and Histamine Levels

  • Li, Xian;Lu, Yue;Jin, Ye;Son, Jong-Keun;Lee, Seung Ho;Chang, Hyeun Wook
    • Biomolecules & Therapeutics
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    • v.22 no.1
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    • pp.27-34
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    • 2014
  • Curcumin is naturally occurring polyphenolic compound found in turmeric and has many pharmacological activities. The present study was undertaken to evaluate anti-allergic inflammatory activity of curcumin, and to investigate its inhibitory mechanisms in immunoglobulin E (IgE)/Ag-induced mouse bone marrow-derived mast cells (BMMCs) and in a mouse model of IgE/Ag-mediated passive systemic anaphylaxis (PSA). Curcumin inhibited cyclooxygenase-2 (COX-2) dependent prostaglandin $D_2$ ($PGD_2$) and 5-lipoxygenase (5-LO) dependent leukotriene $C_4$ ($LTC_4$) generation dose-dependently in BMMCs. To probe the mechanism involved, we assessed the effects of curcumin on the phosphorylation of Syk and its downstream signal molecules. Curcumin inhibited intracellular $Ca^{2+}$ influx via phospholipase $C{\gamma}1$ ($PLC{\gamma}1$) activation and the phosphorylation of mitogen-activated protein kinases (MAPKs) and the nuclear factor-${\kappa}B$ (NF-${\kappa}B$) pathway. Furthermore, the oral administration of curcumin significantly attenuated IgE/Ag-induced PSA, as determined by serum $LTC_4$, $PGD_2$, and histamine levels. Taken together, this study shows that curcumin offers a basis for drug development for the treatment of allergic inflammatory diseases.

Curcumin Stimulates Proliferation of Spinal Cord Neural Progenitor Cells via a Mitogen-Activated Protein Kinase Signaling Pathway

  • Son, Sihoon;Kim, Kyoung-Tae;Cho, Dae-Chul;Kim, Hye-Jeong;Sung, Joo-Kyung;Bae, Jae-Sung
    • Journal of Korean Neurosurgical Society
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    • v.56 no.1
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    • pp.1-4
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    • 2014
  • Objective : The aims of our study are to evaluate the effect of curcumin on spinal cord neural progenitor cell (SC-NPC) proliferation and to clarify the mechanisms of mitogen-activated protein (MAP) kinase signaling pathways in SC-NPCs. Methods : We established cultures of SC-NPCs, extracted from the spinal cord of Sprague-Dawley rats weighing 250 g to 350 g. We measured proliferation rates of SC-NPCs after curcumin treatment at different dosage. The immuno-blotting method was used to evaluate the MAP kinase signaling protein that contains extracellular signal-regulated kinases (ERKs), p38, c-Jun $NH_2$-terminal kinases (JNKs) and ${\beta}$-actin as the control group. Results : Curcumin has a biphasic effect on SC-NPC proliferation. Lower dosage (0.1, 0.5, $1{\mu}M$) of curcumin increased SC-NPC proliferation. However, higher dosage decreased SC-NPC proliferation. Also, curcumin stimulates proliferation of SC-NPCs via the MAP kinase signaling pathway, especially involving the p-ERK and p-38 protein. The p-ERK protein and p38 protein levels varied depending on curcumin dosage (0.5 and $1{\mu}M$, p<0.05). Conclusion : Curcumin can stimulate proliferation of SC-NPCs via ERKs and the p38 signaling pathway in low concentrations.

Curcumin utilizes the anti-inflammatory response pathway to protect the intestine against bacterial invasion

  • Cho, Jin Ah;Park, Eunmi
    • 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.

EFFECT OF CURCUMIN AND RESVERATROL ON THE CELL CYCLE REGULATION, APOPTOSIS AND INHIBITION OF METASTASIS RELATED PROTEINS IN HN-4 CELLS (Curcumin과 resveratrol에 의한 두경부암 유래의 HN-4 세포의 세포주기, 세포사 및 전이관련 단백질의 발현 조절)

  • Kim, Sa-Yub;Lee, Sang-Han;Kwon, Taeg-Kyu
    • 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.

Effects of Curcumin Analogues and Metabolite on Oxidative Stress-induced Cytotoxicity in HepG2 Cells (Curcumin 유도체 및 대사체가 산화스트레스에 의한 HepG2 세포 독성에 미치는 영향)

  • Kim, Ki-Byoung;Lee, Su-Kyung;Kwon, Young-Dal;Yeom, Seung-Ryong;Song, Yung-Sun
    • 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.

The Effect of Curcumin and Human Adipose-derived Stromal Cells on Wound Healing of Lewis Rats (커큐민과 지방 기질세포가 흰 쥐의 창상치유에 미치는 영향)

  • Paik, Hye-Won;Hwang, Dong-Yeon;Yoo, Gyeol;Byeon, Jun-Hee
    • 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.

Curcumin and Vit. E Alleviate Alone or Synergetically Hydrogen Peroxide Induced-Oxidative Stress on Boar Sperm Characteristics during In Vitro Storage

  • Jang, Hyun-Young;Jin, Hyun-A;Lee, Hee-Young;Kim, Dae-Jung;Cheong, Hee-Tae;Kim, Jong-Taek;Park, In-Chul;Park, Choon-Keun;Yang, Boo-Keun
    • Reproductive and Developmental Biology
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    • v.33 no.4
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    • pp.273-281
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    • 2009
  • Antioxidants partially ameliorated the detrimental effects of reactive oxygen species (ROS) on sperm characteristics during in vitro storage. The objective of the present study was to investigate the single or synergetic antioxidative effect of curcumin and Vit. E on the characteristics of fresh boar sperm during in vitro storage. The sperm viability in curcumin, Vit. E supplementation and curcumin+Vit. $E+H_2O_2$ groups remained over 85.0% in 3 hr incubation period, but in 6 hr incubation period, curcumin+Vit. $E+H_2O_2$ groups was sharply dropped than those of curcumin and Vit. E group. The membrane intergrity in all evaluated groups except for $H_2O_2$ group did not significantly difference in 3 hr incubation period. The viability in curcumin or Vit. E supplementation were significantly increased than in curcumin+$H_2O_2$ and Vit. $E+H_2O_2$ group in 6 hr incubation period. The percentage of mitochondrial activity and acrosome intergrity obtained similar trends within same incubation periods irrespective of treatment. The lipid peroxidation of spermatozoal plasma membrane ranged from $11.6{\sim}17.5\;nM/l{\times}10^6$ and $14.0{\sim}19.0\;nM/l{\times}10^6$ in 3 hr and 6 hr incubation periods. In conclusion, curcumin or Vit. E surpplementation alone or cooperatively improved sperm viability index (motility, membrane intergrity, viability and survival rates) and fertility index (mitochondria activity, acrosome intergrity and lipid peroxidation) of fresh boar sperm, indicating that curcumin and Vit. E have a antioxidative properties through its scavenging activity against hydrogen peroxide.

Prostaglandin E2 Reverses Curcumin-Induced Inhibition of Survival Signal Pathways in Human Colorectal Carcinoma (HCT-15) Cell Lines

  • Shehzad, Adeeb;Islam, Salman Ul;Lee, Jaetae;Lee, Young Sup
    • Molecules and Cells
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    • v.37 no.12
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    • pp.899-906
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    • 2014
  • Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.

Induction of MicroRNA-9 Mediates Cytotoxicity of Curcumin Against SKOV3 Ovarian Cancer Cells

  • Zhao, Song-Feng;Zhang, Xiao;Zhang, Xiao-Jian;Shi, Xiu-Qin;Yu, Zu-Jiang;Kan, Quan-Cheng
    • 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.