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1.
Plants (Basel) ; 10(8)2021 Aug 09.
Article in English | MEDLINE | ID: mdl-34451678

ABSTRACT

Kadsura coccinea (KC), a beneficial plant for human health, has been used for centuries in China, Thailand, and Korea in folk medicine and food. There is evidence supporting the biological effects of highly bioactive ingredients in KC such as lignans, triterpenoids, flavonoids, phenolic acids, steroids, and amino acids. In this study, we aimed to explore the effects, functions, and mechanisms of the extracts from KC root (KCR), stem (KCS), leaf (KCL), and fruit (KCF) in UVA and UVB-irradiated keratinocytes and α-melanocyte stimulating hormone (α-MSH)-stimulated melanocytes. First, the total polyphenol and flavonoid contents of KCR, KCS, KCL, and KCF and their radical scavenging activities were investigated. These parameters were found to be in the following order: KCL > KCR > KCS > KCF. UVA and UVB-irradiated keratinocytes were treated with KCR, KCS, KCL, and KCF, and keratinocyte viability, LDH release, intracellular ROS production, and apoptosis were examined. Our results demonstrated that KC extracts improved keratinocyte viability and reduced LDH release, intracellular ROS production, and apoptosis in the presence UVA and UVB irradiation. The overall photoprotective activity of the KC extracts was confirmed in the following order: KCL > KCR > KCS > KCF. Moreover, KC extracts significantly decreased the intracellular melanin content and tyrosinase activity in α-MSH-stimulated melanocytes. Mechanistically, KC extracts reduced the protein and mRNA expression levels of tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2) in α-MSH-stimulated melanocytes. In addition, these extracts markedly downregulated myophthalmosis-related transcription factor expression and cAMP-related binding protein phosphorylation, which is upstream of the regulation of Tyrosinase, TRP-1, and TRP-2. The overall anti-melanogenic activity of the KC extracts was established in the following order. KCL > KCR > KCS > KCF. Overall, the KC extracts exert photoprotective and anti-melanogenic effects, providing a basis for developing potential skin-whitening and photoprotective agents.

2.
Arch Biochem Biophys ; 692: 108519, 2020 10 15.
Article in English | MEDLINE | ID: mdl-32763235

ABSTRACT

Melanoma is a dangerous type of skin cancer that develops from the melanocytes. Activation of p53 in melanoma cells has been validated as a strategy for melanoma therapy. S-Petasin, a dietary sesquiterpene isolated from Petasites japonicus, has been shown to possess multiple biological effects. However, no studies have reported that s-petasin exerted anti-melanoma or inhibited activity in melanoma cells. We investigated the effect of s-petasin in B16F10 cells and A375 cells and the underlying molecular mechanism. S-Petasin exerted a significant anti-proliferation effect on B16F10 cells and A375 cells as measured by the MTT assay and crystal violet staining assay. S-Petasin induced cell apoptosis in B16F10 cells and A375 cells as evidenced by flow cytometry assay and western blot assay. Wound healing assay and transwell cell migration and invasion assay revealed that s-petasin suppressed B16F10 cells and A375 cells migration in vitro. For mechanism study, western blot assay indicated that s-petasin activated the p53 pathway signaling. Furthermore, expression of Bcl-2, Bcl-XL, Bax, MMP-2, MMP-9, p21, CDK4 and cyclin D1 were regulated by s-petasin. Taken together, our data suggest that s-petasin is a novel compound which can induce apoptosis and inhibit cell migration through activation of the p53 pathway signaling in melanoma B16F10 cells and A375 cells.


Subject(s)
Apoptosis/drug effects , Melanoma, Experimental/metabolism , Sesquiterpenes/pharmacology , Signal Transduction/drug effects , Tumor Suppressor Protein p53/metabolism , 3T3-L1 Cells , Animals , Cell Proliferation/drug effects , Hep G2 Cells , Humans , Melanoma, Experimental/pathology , Mice
3.
Food Funct ; 11(6): 5664-5673, 2020 Jun 24.
Article in English | MEDLINE | ID: mdl-32542253

ABSTRACT

Nonalcoholic fatty liver disease (NAFLD) has become one of the most common medical problems. Inhibition of lipogenesis and promotion of lipolysis are two ways to prevent NAFLD. In this study, oleic acid-induced HepG2 cells are used as a NAFLD cell model to test whether s-petasin exerts inhibition of lipogenesis and promotion of the lipolysis effect. The results showed that s-petasin significantly inhibited the lipid level in oleic acid-induced HepG2 cells. Moreover, results showed that the triacylglycerol level was reduced by s-petasin in oleic acid-induced HepG2 cells. Western blot assay revealed that s-petasin stimulated phosphorylation of AMPKα and ACCα. The results also demonstrated that s-petasin can inhibit lipogenesis and enhance triacylglycerol turnover by down-regulation of FAS and SCD-1 and up-regulation of ATGL and HSL through the AMPK signaling-dependent regulation of transcriptional factors, FKHR and SREBP-1. This in vitro study indicates that s-petasin has potential as a candidate compound for NAFLD therapy.


Subject(s)
AMP-Activated Protein Kinases/metabolism , Oleic Acid/adverse effects , Oleic Acid/metabolism , Sesquiterpenes/pharmacology , Signal Transduction/drug effects , Cell Survival , Down-Regulation , Forkhead Box Protein O1/genetics , Forkhead Box Protein O1/metabolism , Hep G2 Cells/drug effects , Humans , Lipid Accumulation Product , Lipogenesis/drug effects , Lipolysis , Non-alcoholic Fatty Liver Disease/metabolism , Phosphorylation , Stearoyl-CoA Desaturase/genetics , Stearoyl-CoA Desaturase/metabolism , Sterol Regulatory Element Binding Protein 1/genetics , Sterol Regulatory Element Binding Protein 1/metabolism , Triglycerides/metabolism , Up-Regulation/drug effects
4.
Arch Biochem Biophys ; 686: 108365, 2020 06 15.
Article in English | MEDLINE | ID: mdl-32315651

ABSTRACT

Pelargonidin is a natural compound that exists widely in fruits, and exerts antioxidant, anti-atherosclerotic, anti-inflammatory, anti-hyperglycemic, and anti-diabetic activities. However, there have not been any studies concerning its anti-obesity potential to date. Therefore, we evaluated the anti-obesity potential of pelargonidin via inhibition of adipogenesis in 3T3-L1 cells. The cellular oil droplet content was decreased to 68.14%, 56.75%, and 48.39% and triglyceride accumulation decreased to 74.53%, 61.54%, and 47.86% after incubation with 5 µM, 10 µM, and 20 µM pelargonidin, respectively, when compared with DMSO group. Furthermore, pelargonidin treatment led to decrease in glucose consumption. Western blot assay illustrated that the expression of PPAR-γ was suppressed to 63.25%, 47.52%, and 21.23% after incubation with 5 µM, 10 µM, and 20 µM pelargonidin when compared with DMSO group. Then, we measured the expression of some target proteins of PPAR-γ, and found that pelargonidin decreased the expressions of HMGCR, LPL, Glut4, and A-FABP. Besides, the result of Luciferase Reporter Assay indicated that pelargonidin inhibited PPAR-γ transcription activity. These results indicated that pelargonidin exerts anti-adipogenic activity in 3T3-L1 cells through inhibition of PPAR-γ signaling pathway, and pelargonidin could be used as a potential anti-obesity agent.


Subject(s)
Adipogenesis/drug effects , Anthocyanins/pharmacology , Anti-Obesity Agents/pharmacology , PPAR gamma/metabolism , 3T3-L1 Cells , Animals , Anthocyanins/metabolism , Anti-Obesity Agents/metabolism , Down-Regulation/drug effects , Fatty Acid-Binding Proteins/genetics , Fatty Acid-Binding Proteins/metabolism , Gene Expression Regulation/drug effects , Glucose/metabolism , Glucose Transporter Type 4/genetics , Glucose Transporter Type 4/metabolism , Lipoprotein Lipase/genetics , Lipoprotein Lipase/metabolism , Mice , Triglycerides/genetics , Triglycerides/metabolism
5.
Food Funct ; 10(7): 4396-4406, 2019 Jul 17.
Article in English | MEDLINE | ID: mdl-31282906

ABSTRACT

Petasites japonicus is an edible and medicinal plant with a good flavor, and it is a rich source of bioactive compounds. S-Petasin has been isolated from Petasites hybridus (L.), Petasites officinalis (L.) and Petasites formosanus, but not from Petasites japonicus. In this study, we found that hexane extracts of Petasites japonicus inhibited adipogenesis in 3T3-L1 cells. After this we isolated s-petasin from Petasites japonicus. Subsequently, the 3T3-L1 pre-adipocytes were used to test whether s-petasin exerts an anti-adipogenic effect. The results showed that s-petasin presented strong anti-adipogenic activity. Further studies illustrated that s-petasin reduced glucose uptake. Moreover, results showed that triglyceride accumulation was inhibited by s-petasin in differentiated 3T3-L1 cells. Western blot assay indicated that s-petasin down-regulated the expression of PPAR-γ and its target genes in a dose dependent manner. In conclusion, we isolated s-petasin from Petasites japonicus and found that it exerted anti-adipogenic activity against 3T3-L1 cell differentiation through inhibition of the expression of PPAR-γ pathway signaling.


Subject(s)
Adipogenesis/drug effects , PPAR gamma/metabolism , Petasites/chemistry , Plant Extracts/isolation & purification , Plant Extracts/pharmacology , Sesquiterpenes/isolation & purification , Sesquiterpenes/pharmacology , Signal Transduction/drug effects , 3T3-L1 Cells/drug effects , Animals , Cell Differentiation/drug effects , Down-Regulation/drug effects , Mice , Plant Extracts/chemistry , Plants, Medicinal , Sesquiterpenes/chemistry , Triglycerides/metabolism
6.
J Sci Food Agric ; 97(4): 1084-1092, 2017 Mar.
Article in English | MEDLINE | ID: mdl-27264863

ABSTRACT

BACKGROUND: There is a need to minimize economic damage by sorting infected seeds from healthy seeds before seeding. However, current methods of detecting infected seeds, such as seedling grow-out, enzyme-linked immunosorbent assays, the polymerase chain reaction (PCR) and the real-time PCR have a critical drawbacks in that they are time-consuming, labor-intensive and destructive procedures. The present study aimed to evaluate the potential of visible/near-infrared (Vis/NIR) hyperspectral imaging system for detecting bacteria-infected watermelon seeds. RESULTS: A hyperspectral Vis/NIR reflectance imaging system (spectral region of 400-1000 nm) was constructed to obtain hyperspectral reflectance images for 336 bacteria-infected watermelon seeds, which were then subjected to partial least square discriminant analysis (PLS-DA) and a least-squares support vector machine (LS-SVM) to classify bacteria-infected watermelon seeds from healthy watermelon seeds. The developed system detected bacteria-infected watermelon seeds with an accuracy > 90% (PLS-DA: 91.7%, LS-SVM: 90.5%), suggesting that the Vis/NIR hyperspectral imaging system is effective for quarantining bacteria-infected watermelon seeds. CONCLUSION: The results of the present study show that it is possible to use the Vis/NIR hyperspectral imaging system for detecting bacteria-infected watermelon seeds. © 2016 Society of Chemical Industry.


Subject(s)
Bacteria/growth & development , Citrullus/microbiology , Food Microbiology/methods , Seeds/microbiology , Spectroscopy, Near-Infrared/methods , Humans
7.
Int J Mol Med ; 35(2): 525-32, 2015 Feb.
Article in English | MEDLINE | ID: mdl-25503787

ABSTRACT

Since oxidative stress is critically involved in excitotoxic damage, we sought to determine whether the activation of the transcription factors, cAMP-responsive element binding protein (CREB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2, also known as NFE2L2), by α-iso-cubebene is involved in its protective effects against glutamate-induced neuronal cell death. Pre-treatment with α-iso-cubebene significantly attenuated glutamate-induced cytotoxicity in mouse hippocampus-derived neuronal cells. α-iso-cubebene also reduced the glutamate-induced generation of reactive oxygen species and calcium influx, thus preventing apoptotic cell death. α-iso-cubebene inhibited glutamate-induced mitochondrial membrane depolarization and, consequently, inhibited the release of the apoptosis-inducing factor from the mitochondria. Immunoblot anlaysis revealed that the phosphorylation of extracellular signal-regulated kinase (ERK) by glutamate was reduced in the presence of α-iso-cubebene. α-iso-cubebene activated protein kinase A (PKA), CREB and Nrf2, which mediate the expression of the antioxidant enzymes, heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase [quinone] 1 (NQO1), involved in neuroprotection. In addition, α-iso-cubebene induced the expression of antioxidant responsive element and CRE transcriptional activity, thus conferring neuroprotection against glutamate-induced oxidative injury. α-iso-cubebene also induced the expression of Nrf2-dependent genes encoding HO-1 and NQO1. Furthermore, the knockdown of CREB and Nrf2 by small interfering RNA attenuated the neuroprotective effects of α-iso-cubebene. Taken together, our results indicate that α-iso-cubebene protects HT22 cells from glutamate-induced oxidative damage through the activation of Nrf2/HO-1/NQO-1, as well as through the PKA and CREB signaling pathways.


Subject(s)
Glutamic Acid/toxicity , Hippocampus/metabolism , Neurons/metabolism , Neuroprotective Agents/pharmacology , Oxidative Stress/drug effects , Sesquiterpenes/pharmacology , Animals , Cell Line , Hippocampus/pathology , Mice , Nerve Tissue Proteins/metabolism , Neurons/pathology , Signal Transduction/drug effects
8.
Biochem Biophys Res Commun ; 427(3): 547-52, 2012 Oct 26.
Article in English | MEDLINE | ID: mdl-23022181

ABSTRACT

α-Iso-cubebenol, a natural compound isolated from the Schisandra chinensis fruit, strongly enhances survival rate in cecal ligation and puncture (CLP) challenge-induced sepsis. Mechanistically, α-iso-cubebenol markedly reduces viable bacteria in the peritoneal fluid and peripheral blood, by increasing production of superoxide anion. α-Iso-cubebenol also significantly attenuates widespread immune cell apoptosis in a mouse CLP sepsis model, and inhibits the production of proinflammatory cytokines including interleukin-1ß (IL-1ß) and IL-6 in CLP mice and lipopolysaccharide-stimulated splenocytes. Taken together, the results indicate that α-iso-cubebenol can reverse the progression of septic shock by triggering multiple protective downstream signaling pathways to enhance microbial killing and maintain organ function and leukocyte survival.


Subject(s)
Biological Products/therapeutic use , Schisandra/chemistry , Sepsis/drug therapy , Sesquiterpenes/therapeutic use , Animals , Bacteria/drug effects , Disease Models, Animal , Fruit/chemistry , Male , Mice , Mice, Inbred ICR , Sesquiterpenes/administration & dosage
9.
J Med Food ; 14(12): 1519-26, 2011 Dec.
Article in English | MEDLINE | ID: mdl-22145771

ABSTRACT

Periodontitis, a chronic inflammatory periodontal disease that develops from gingivitis, is caused by periodontal pathogenic bacteria such as Porphyromonas gingivalis. Recent studies have focused on the antioxidant, anti-human immunodeficiency virus, anticarcinogenic, and anti-inflammatory properties of gomisins. However, the anti-inflammatory activities of gomisin plants through heme oxygenase-1 (HO-1) signals remain poorly defined. We found that gomisins' anti-inflammatory activity occurs via the induction of HO-1 expression. Gomisins G and J inhibit the production of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1ß, and interleukin-6 and also block nuclear factor-κB activation in Raw264.7 cells stimulated with P. gingivalis lipopolysaccharide. Furthermore, pro-inflammatory cytokine production is inhibited through the induction of HO-1 expression. HO-1 expression is induced by all gomisins, but their anti-inflammatory activity via HO-1 signaling is observed with gomisins G and J, and not A. We found that gomisins G and J extracted from Schisandria chinensis can inhibit the P. gingivalis lipopolysaccharide induced-inflammatory responses in Raw264.7 cells.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Cyclooctanes/pharmacology , Dioxoles/pharmacology , Heme Oxygenase-1/metabolism , Lignans/pharmacology , Lipopolysaccharides/pharmacology , Membrane Proteins/metabolism , Animals , Cell Line , Fruit/chemistry , Heme Oxygenase-1/genetics , Inflammation/metabolism , Interleukin-1beta/antagonists & inhibitors , Interleukin-1beta/biosynthesis , Interleukin-6/antagonists & inhibitors , Interleukin-6/biosynthesis , Membrane Proteins/genetics , Mice , NF-kappa B/antagonists & inhibitors , NF-kappa B/metabolism , Plant Extracts/pharmacology , Polycyclic Compounds/pharmacology , Porphyromonas gingivalis/pathogenicity , Schisandra/chemistry , Signal Transduction , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Necrosis Factor-alpha/biosynthesis
10.
Biochem Biophys Res Commun ; 391(4): 1687-92, 2010 Jan 22.
Article in English | MEDLINE | ID: mdl-20040359

ABSTRACT

A novel alpha-iso-cubebenol, which has anti-inflammatory effects in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages, was isolated from the fruits of Schisandra chinensis. alpha-iso-cubebenolinhibited LPS-induced nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production. Consistent with these findings, alpha-iso-cubebenol also reduced the LPS-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 at the protein and mRNA levels in a concentration-dependent manner. alpha-iso-cubebenol also inhibited LPS-induced nuclear translocation of the NF-kappaB p65 subunit. Furthermore, alpha-iso-cubebenol suppressed the phosphorylation of ERK, JNK, and p38 kinase induced by LPS. Since the novel alpha-iso-cubebenol blocked the production of several pro-inflammatory mediators induced by LPS in macrophages, the molecule can be useful material for the development of anti-inflammatory agents against bacterial infections or endotoxin.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Cyclooxygenase 2 Inhibitors/pharmacology , Enzyme Inhibitors/pharmacology , Macrophages/drug effects , Nitric Oxide Synthase Type II/antagonists & inhibitors , Schisandra/chemistry , Sesquiterpenes/pharmacology , Animals , Anti-Inflammatory Agents, Non-Steroidal/chemistry , Anti-Inflammatory Agents, Non-Steroidal/isolation & purification , Cell Line , Cyclooxygenase 2/biosynthesis , Cyclooxygenase 2/drug effects , Cyclooxygenase 2 Inhibitors/chemistry , Cyclooxygenase 2 Inhibitors/isolation & purification , Enzyme Inhibitors/chemistry , Enzyme Inhibitors/isolation & purification , Lipopolysaccharides/immunology , Macrophages/enzymology , Mice , Mitogen-Activated Protein Kinase Kinases/metabolism , NF-kappa B/metabolism , Nitric Oxide Synthase Type II/biosynthesis , Sesquiterpenes/chemistry , Sesquiterpenes/isolation & purification , Terpenes
11.
Phytomedicine ; 16(6-7): 530-7, 2009 Jun.
Article in English | MEDLINE | ID: mdl-19195857

ABSTRACT

Lignans are major constituents of plant extracts and have important pharmacological effects on mammalian cells. Here we showed that pinoresinol-4,4'-di-O-beta-D-glucoside (PDG) from Valeriana officinalis induced calcium mobilization and cell migration through the activation of lysophosphatidic acid (LPA) receptor subtypes. Stimulation of mouse embryo fibroblast (MEF) cells with 10 microM PDG resulted in strong stimulation of MEF cell migration and the EC(50) was about 2 microM. Pretreatment with pertussis toxin (PTX), an inhibitor of G(i) protein, completely blocked PDG-induced cell migration demonstrating that PDG evokes MEF cell migration through the activation of the G(i)-coupled receptor. Furthermore, pretreatment of MEF cells with Ki16425 (10 microM), which is a selective antagonist for LPA(1) and LPA(3) receptors, completely blocked PDG-induced cell migration. Likewise, PDG strongly induced calcium mobilization, which was also blocked by Ki16425 in a dose-dependent manner. Prior occupation of the LPA receptor with LPA itself completely blocked PDG-induced calcium mobilization. Finally, PDG-induced MEF cell migration was attenuated by pretreatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor such as LY294002. Cells lacking downstream mediator of PI3K such as Akt1 and Akt2 (DKO cells) showed loss of PDG-induced migration. Re-expression of Akt1 (but not Akt2) completely restored PDG-induced DKO cell migration. Given these results, we conclude that PDG is a strong inducer of cell migration. We suggest that the pharmacological action of PDG may occur through the activation of an LPA receptor whereby activation of PI3K/Akt signaling pathway mediates PDG-induced MEF cell migration.


Subject(s)
Calcium/metabolism , Chemotaxis/drug effects , Embryo, Mammalian/cytology , Glycosides/pharmacology , Lignans/pharmacology , Plant Roots/chemistry , Valerian/chemistry , Animals , Fibroblasts/cytology , Mice , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction
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