• Korean Journal of Korean Medical Institute of Dermatology and Aesthetics
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• v.1 no.1
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• pp.91-97
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• 2005

(1) Objectives: To discover natural skin-lightening agents, we have evaluated the inhibitory activity of EtOH extracts from 20 medicinal plants against mushroom tyrosinase. (2) Methods: Tyrosinase activity was determined by the dopachrome method using L-tyrosine as the substrates. (3) Results: Of the plant extracts tested, the extracts of 4 plants, Albizzia julibrissin, Curcuma longa, Anethum graveolens and Sophora flavescens, exhibited potent inhibitory activity (> 50%) in mushroom tyrosinase assay. Four plant extract, extracts of Agrimonia pilosa, Paeonia moutan, Magnolia obovata and Eugenia caryophyllata also showed relatively strong inhibitory (> 40%) against mushroom tyrosinase. (4) Conclusion: These active medicinal plants may be useful for the development of skin-whitening agents. Since the active medicinal plants may contain effective tyrosinase inhibitors even more than kojic acid, further study to identify the active constituents from the plants is expected.

• Mycobiology
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• v.32 no.3
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• pp.128-133
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• 2004

Twenty plant extracts were tested against mycelial growth, sclerotium formatiom and dry weight of mycelium with sclerotia of Sclerotium rolfsii Sacc. The highest(90 mm) mycelial growth was measured in Adhatoda vasica, Tegetes erecta, Allium cepa, and Curcuma longa. The lowest(25 mm) was in Azadirachta indica. No mycelial growth was found in any concentration of cow, buffalo, and goat urine. The highest(90 mm) and the lowest(15 mm) mycelial growth were measured in Biomil and Urea, respectively. No mycelial growth was observed in Zinc. The highest(60 mm) and the lowest(2 mm) mycelial growth were recorded in Macuprex(Dodine; 65% WP) and Boron(100% Boric acid and 17% Boron) respectively. Mycelial growth was totally inhibited in Rovral(Iprodione; 50% WP).

• Toxicological Research
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• v.35 no.1
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• pp.65-74
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• 2019

Tetrahydrocurcumin (THC) is a major metabolite of curcumin, which is obtained from Curcuma longa. THC has various benefits and overcomes the bioavailability issue of curcumin. To establish it as a pharmacologically active molecule, its safety profile has to be determined. Thus, the present study aimed to determine the preclinical safety profile of THC in a 90-day subchronic and reproductive/developmental toxicity study in Wistar rats. THC at oral doses of 100, 200, and 400 mg/kg was administered daily for 90 days. Rats in the recovery group were kept for 14 days after treatment termination. The animals were observed for treatment-related morbidity, mortality, and changes in clinical signs, clinical pathology, and histopathology. In the reproductive/developmental toxicity study, THC at 100, 200, and 400 mg/kg was administered orally to rats and the reproductive/developmental parameters in adult male and female rats and pups were observed. THC at up to 400 mg/kg/day of did not have any significant effect on all parameters in male and female rats in both toxicity studies. Thus, 400 mg/kg/day can be considered as the no-observed-adverse-effect-level of THC in rats.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.3
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• pp.181-189
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• 2019

Curcumin, an active ingredient of Curcuma longa L., can reduce the concentration of low-density lipoproteins in plasma, in different ways. We had first reported that curcumin exhibits hypocholesterolemic properties by improving the apolipoprotein B (apoB) mRNA editing in primary rat hepatocytes. However, the role of curcumin in the regulation of apoB mRNA editing is not clear. Thus, we investigated the effect of curcumin on the expression of multiple editing components of apoB mRNA cytidine deamination to uridine (C-to-U) editosome. Our results demonstrated that treatment with $50{\mu}M$ curcumin markedly increased the amount of edited apoB mRNA in primary mouse hepatocytes from 5.13%-8.05% to 27.63%-35.61%, and significantly elevated the levels of the core components apoB editing catalytic polypeptide-1 (APOBEC-1), apobec-1 complementation factor (ACF), and RNA-binding-motif-protein-47 (RBM47), as well as suppressed the level of the inhibitory component glycine-arginine-tyrosine-rich RNA binding protein. Moreover, the increased apoB RNA editing by $50{\mu}M$ curcumin was significantly reduced by siRNA-mediated APOBEC-1, ACF, and RBM47 knockdown. These findings suggest that curcumin modulates apoB mRNA editing by coordinating the multiple editing components of the edito-some in primary hepatocytes. Our data provided evidence for curcumin to be used therapeutically to prevent atherosclerosis.

• Biomolecules & Therapeutics
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• v.27 no.5
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• pp.484-491
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• 2019

Glioblastoma is the most aggressive common brain tumor in adults. Curcumin, from Curcuma longa, is an effective antitumor agent. Although the same proteins control both autophagy and cell death, the molecular connections between them are complicated and autophagy may promote or inhibit cell death. We investigated whether curcumin affects autophagy, which regulates curcumin-mediated tumor cell death in A172 human glioblastoma cells. When A172 cells were incubated with $10{\mu}M$ curcumin, autophagy increased in a time-dependent manner. Curcumin-induced cell death was reduced by co-incubation with the autophagy inhibitors 3-methyladenine (3-MA), hydroxychloroquine (HCQ), and LY294002. Curcumin-induced cell death was also inhibited by co-incubation with rapamycin, an autophagy inducer. When cells were incubated under serum-deprived medium, LC3-II amount was increased but the basal level of cell viability was reduced, leading to the inhibition of curcumin-induced cell death. Cell death was decreased by inhibiting curcumin-induced autophagy using small interference RNA (siRNA) of Atg5 or Beclin1. Therefore, curcumin-mediated tumor cell death is promoted by curcumin-induced autophagy, but not by an increase in the basal level of autophagy in rapamycin-treated or serum-deprived conditions. This suggests that the antitumor effects of curcumin are influenced differently by curcumin-induced autophagy and the prerequisite basal level of autophagy in cancer cells.

• Toxicological Research
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• v.35 no.4
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• pp.403-410
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• 2019

Curcumin, a hydrophobic polyphenol isolated from the Curcuma longa L. plant, has many pharmacological properties, including antioxidant, anti-inflammatory, and chemo-preventive activities. Curcumin has been shown to have potential in preventing nonalcoholic fatty liver disease (NAFLD). However, the low bioavailability of curcumin has proven to be a major limiting factor in its clinical adoption. Theracurmin, a highly bioavailable curcumin that utilizes micronized technology showed improved biological absorbability in vivo. The aim of this study was to investigate the role of theracurmin in modulating hepatic lipid metabolism in vivo. A fatty liver mouse model was produced by feeding mice a high fat diet (HFD; 60% fat) for 12 weeks. We found that treatment for 12 weeks with theracurmin significantly lowered plasma triacylglycerol (TG) levels and reduced HFD-induced liver fat accumulation. Theracurmin treatment lowered hepatic TG and total cholesterol (T-CHO) levels in HFD-fed mice compared to controls. In addition, theracurmin administration significantly reduced lipid peroxidation and cellular damage caused by reactive oxygen species in HFD-fed mice. Overall, these results suggest that theracurmin has the ability to control lipid metabolism and can potentially serve as an effective therapeutic remedy for the prevention of fatty liver.

• 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.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.9
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• pp.3987-3992
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• 2014

Curcumin, a polyphenol compound derived from the rhizome of the plant Curcuma longa L. has been verified as an anticancer compound against several types of cancer. However, understanding of the molecular mechanisms by which it induces apoptosis is limited. In this study, the anticancer efficacy of curcumin was investigated in human gastric adenocarcinoma SGC-7901 cells. The results demonstrated that curcumin induced morphological changes and decreased cell viability. Apoptosis triggered by curcumin was visualized using Annexin V-FITC/7-AAD staining. Curcumin-induced apoptosis of SGC-7901 cells was associated with the dissipation of mitochondrial membrane potential (MMP) and the release of cytochrome c into the cytosol. Furthermore, the down-regulation of Bcl-2 and up-regulation of Bax that led to the cleavage of caspase-3 and increased cleaved PARP was observed in SGC-7901 cells treated with curcumin. Therefore, curcumin-induced apoptosis of SGC-7901 cells might be mediated through the mitochondria pathway, which gives the rationale for in vivo studies on the utilization of curcumin as a potential cancer therapeutic compound.

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.10
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• pp.1495-1500
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• 2003

Two bio-assays were conducted to evaluate turmeric root powder and mannan-oligosaccharides (MOS) as alternatives to feed antibiotics for broilers. In one trial, one hundred and eighty 19-days old broilers assigned to 18 groups of 10 were fed on one of six experimental diets with three replicates during four weeks. The diets included a basal feed without additives and with either virginiamycin, MOS, or turmeric at 1, 2 and 3 g/kg, respectively. In the second trial, one hundred and forty four 21-days old broilers arranged in 16 groups of nine were fed on the first four diets with four replicates for a similar period. Virginiamycin, MOS and turmeric (1 g/kg) in the first trial generally improved the weight gain of broilers by 3.4, 6.2 and 5.3%, respectively. In the second trial they increased the weight gain significantly (p<0.05) by 8.8, 8.0 and 15.1%, respectively. Additives improved the feed efficiency up to 15.1% and carcass recovery up to 3.1% (p<0.05). Virginiamycin, MOS and turmeric (1 g/kg) markedly reduced the abdominal fat content from 1.91% BW in the control to 1.44, 0.97 and 1.2% BW, respectively, in the first trial. The corresponding values obtained in the second trial were 1.01, 0.55 and 0.6%, respectively as compared to 1.22% in the control group. All additives showed a remarkable inhibition of duodenal coliform bacteria, yeast and mould in the caecum, and all viable microbes in the ileum. A significant (p<0.05) improvement in energy and protein utilization could be recorded with supplemented diets except for high turmeric diets. Dietary 2 and 3 g/kg addition of turmeric reduced energy and protein utilization as well as fat deposition. Present results reveal that turmeric and MOS are satisfactory alternatives to antibiotics in broiler feeds. Both MOS and turmeric possess an antimicrobial effect in vivo. Turmeric may also depress fat deposition in broilers.

• BMB Reports
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• v.34 no.3
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• pp.189-193
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• 2001

Curcumin a yellow pigment from Curcuma Tonga, has been known to possess antioxidative and anticarcinogenic properties, as well as to induce apoptosis in some cancer cells. There have been, however, several contradictory reports that hypothesized curcumin (a hydrophobic molecule) can bind a membrane Gpid bilayer and induce nonspecific cytotoxicity in some cell lines. Why curcumin shows these contradictory effects is unknown. In A-431 cells, growth inhibition by curcumin is due mostly to the specific inhibition of the intrinsic tyrosine kinase activity of the epidermal growth factor receptor, as reported earlier by Korutla et al. Thus, we assumed that the cell death of A-431 by curcumin might be due to the specific induction of apoptosis. In this paper we clearly show that curcumin induces apoptosis in A-431 cells. The cureumin-induced cell death of A-431 exhibited various apoptotic features, including DNA fragmentation and nuclear condensation. Furthermore, the curcumin-induced apoptosis of A-431 cells involved activation of caspase-3-like cysteine protease. Involvement of caspase-3 was further confirmed by using a caspase-3 specific inhibitor, DEVD-CHO. In another study, decreased nitric oxide (NO) production was also shown in A-431 cells treated with curcumin, which seems to be the result of the inhibition of the iNOS expression by curcumin, as in other cell lines. However, 24 h after treatment of curcumin there was increased NO production in A-431 cells. This observation has not yet been clearly explained. We assumed that the increased NO production may be related to denitrosylation of the enzyme catalytic site in caspase-3 when activated. Taken together, this study shows that the cell death of A-431 by curcumin is due to the induction of apoptosis, which involves caspase-3 activation.