We investigated the anti-obesity effect of Gelidium elegans extract (GE) on 3T3-L1 preadipocytes and a high-fat-diet (HFD)-induced mouse model. The results of the present study demonstrated that GE prevents weight gain induced by a high-fat diet (HFD) by modulating the adenosine monophosphate-activated protein kinase (AMPK)-PR domain-containing 16 (PRDM16)-uncoupling protein-1 (UCP-1) pathway in a mice model. Moreover, in vitro results show that GE suppressed adipocyte differentiation by modulating adipogenic regulators, stimulated lipolysis by activating ATGL, and inhibited adipogenesis by downregulating various enzymes associated with triglyceride synthesis. GE was also found to upregulate AMPK phosphorylation as well as the expression of UCP1 and PRDM16 proteins, leading to measurable changes in the beige-like phenotype differentiation of 3T3-L1 cells. Taken together, these findings suggest the role of GE as a functional food ingredient extracted from Gelidium elegans to increase energy expenditure and anti-obesity efficacy.
Background: Ginseng possesses antitumor effects, and ginsenosides are considered to be one of its main active chemical components. Ginsenosides can further be hydrolyzed to generate secondary saponins, and 20(R)-panaxotriol is an important sapogenin of ginsenosides. We aimed to synthesize a new ginsengenin derivative from 20(R)-panaxotriol and investigate its antitumor activity in vivo and in vitro. Methods: Here, 20(R)-panaxotriol was selected as a precursor and was modified into its derivatives. The new products were characterized by 1H-NMR, 13C-NMR and HR-MS and evaluated by molecular docking, MTT, luciferase reporter assay, western blotting, immunofluorescent staining, colony formation assay, EdU labeling and immunofluorescence, apoptosis assay, cells migration assay, transwell assay and in vivo antitumor activity assay. Results: The derivative with the best antitumor activity was identified as 6,12-dihydroxy-4,4,8,10,14-pentamethyl-17-(2,6,6-trimethyltetrahydro-2H-pyran-2-yl)hexadecahydro-1H-cyclopenta[a]phenanthren-3-yl(tert-butoxycarbonyl)glycinate (A11). The focus of this research was on the antitumor activity of the derivatives. The efficacy of the derivative A11 (IC50 < 0.3 µM) was more than 100 times higher than that of 20(R)- panaxotriol (IC50 > 30 µM). In addition, A11 inhibited the protein expression and nuclear accumulation of the hypoxia-inducible factor HIF-1α in HeLa cells under hypoxic conditions in a dose-dependent manner. Moreover, A11 dose-dependently inhibited the proliferation, migration, and invasion of HeLa cells, while promoting their apoptosis. Notably, the inhibition by A11 was more significant than that by 20(R)-panaxotriol (p < 0.01) in vivo. Conclusion: To our knowledge, this is the first study to report the production of derivative A11 from 20(R)-panaxotriol and its superior antitumor activity compared to its precursor. Moreover, derivative A11 can be used to further study and develop novel antitumor drugs.
Retinal prosthesis is regarded as the most feasible method for the blind caused by retinal diseases such as retinitis pigmentosa (RP) or age related macular degeneration (AMD). Recently Korean consortium launched for developing retinal prosthesis. One of the prerequisites for the success of retinal prosthesis is the optimization of the electrical stimuli applied through the prosthesis. Since electrical characteristics of degenerate retina are expected to differ from those of normal retina, we performed voltage stimulation experiment both in normal and degenerate retina to provide a guideline for the optimization of electrical stimulation for the upcoming prosthesis. After isolation of retina, retinal patch was attached with the ganglion cell side facing the surface of microelectrode arrays (MEA). $8{\times}8$ grid layout MEA (electrode diameter: $30{\mu}m$, electrode spacing: $200{\mu}m$, and impedance: $50k{\Omega}$ at 1 kHz) was used to record in-vitro retinal ganglion cell activity. Mono-polar electrical stimulation was applied through one of the 60 MEA channel, and the remaining channels were used for recording. The electrical stimulus was a constant voltage, charge-balanced biphasic, anodic-first square wave pulse without interphase delay, and 50 trains of pulse was applied with a period of 2 sec. Different electrical stimuli were applied. First, pulse amplitude was varied (voltage: $0.5{\sim}3.0V$). Second, pulse duration was varied $(100{\sim}1,200{\mu}s)$. Evoked responses were analyzed by PSTH from averaged data with 50 trials. Charge density was calculated with Ohm's and Coulomb's law. In normal retina, by varying the pulse amplitude from 0.5 to 3V with fixed duration of $500{\mu}s$, the threshold level for reliable ganglion cell response was found at 1.5V. The calculated threshold of charge density was $2.123mC/cm^2$. By varying the pulse duration from 100 to $1,200{\mu}s$ with fixed amplitude of 2V, the threshold level was found at $300{\mu}s$. The calculated threhold of charge density was $1.698mC/cm^2$. Even after the block of ON-pathway with L-(1)-2-amino-4-phosphonobutyric acid (APB), electrical stimulus evoked ganglion cell activities. In this APB-induced degenerate retina, by varying the pulse duration from 100 to $1200{\mu}s$ with fixed voltage of 2 V, the threshold level was found at $300{\mu}s$, which is the same with normal retina. More experiment with APB-induced degenerate retina is needed to make a clear comparison of threshold of charge density between normal and degenerate retina.
We have examined the effects of S-nitroso-N-acetylpenicillamine (SNAP), prostaglandin $E_2$ (PG $E_2$) and dibutric cyclic AMP (dbcAMP) on the methylation of interferon- ${\gamma}$ (IFN- ${\gamma}$ ) gene in human Jurkat T cells. The CpG dinucleotide which is critical for promoter function of IFN- ${\gamma}$ gene was methylated by treatment with SNAP, PG $E_2$ and dbcAMP, respectively. The DNA methylation induced by PG $E_2$ was suppressed by the addition of 2',5'-dideoxyadenosine (DDA), an inhibitor of adenylyl cyclase, but the suppression was not observed in SNAP treated cells. The NO production was not enhanced in PG $E_2$ or dbcAMP treated cells. The methylation induced by PG $E_2$ and dbcAMP was not suppressed by the addition of $N^{G}$-methyl-L-arginine (L-NMMA), NO synthase inhibitor. In conclusion, the inhibition of INF- ${\gamma}$ gene expression by PG $E_2$ was associated with the methylation of INF- ${\gamma}$ gene by elevation of intracellular cAMP in human Jurkat T cells. However, the methylation induced by PG $E_2$ might not be mediated through the NO production.rough the NO production.
Kang, Ki Ung;Oh, Jun Young;Lee, Yun Ha;Lee, Hye Sun;Jin, Seo Yeon;Bae, Sun Sik
Journal of Life Science
/
v.28
no.12
/
pp.1516-1522
/
2018
Atherosclerosis is an obstructive vessel disease mainly caused by chronic arterial inflammation to which the proliferation and migration of vascular smooth muscle cells (VSMCs) is the main pathological response. In the present study, the primary responsible inflammatory cytokine and its signaling pathway was investigated. The proliferation and migration of VSMCs was significantly enhanced by the prostaglandin $F_{2{\alpha}}$ ($PGF_{2{\alpha}}$), while neither was affected by tumor necrosis factor ${\alpha}$. Prostacyclin $I_2$ was seen to enhance the proliferation of VSMCs while simultaneously suppressing their migration. Both prostaglandin $D_2$ and prostaglandin $E_2$ significantly enhanced the migration of VSMCs, however, proliferation was not affected by either of them. The proliferation and migration of VSMCs stimulated by $PGF_{2{\alpha}}$ progressed in a dose-dependent manner; the $EC_{50}$ value of both proliferation and migration was $0.1{\mu}M$. VSMCs highly expressed the phospholipase isoform $C-{\beta}3$ ($PLC-{\beta}3$) while others such as $PLC-{\beta}1$, $PLC-{\beta}2$, and $PLC-{\beta}4$ were not expressed. Inhibition of the PLCs by U73122 completely blocked the $PGF_{2{\alpha}}$-induced migration of VSMCs, and, in addition, silencing $PLC-{\beta}3$ significantly diminished the $PGF_{2{\alpha}}$-induced proliferation and migration of VSMCs. Given these results, we suggest that $PGF_{2{\alpha}}$ plays a crucial role in the proliferation and migration of VSMCs, and activation of $PLC-{\beta}3$ could be involved in their $PGF_{2{\alpha}}$-dependent migration.
Rhim, Byung-Yong;Kim, Chi-Dae;Kim, Dong-Heon;Biancani, Piero;Behar, Jose
The Korean Journal of Pharmacology
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v.32
no.1
/
pp.67-74
/
1996
Cholecystokinin octapeptide (CCK-8), acetylcholine (ACh) and KCl caused a dose dependent contraction in muscle cells enzymatically digested from cat gallbladder. Maximal contraction was obtained at concentration of $10^{-9}M$ for CCK-8, $10^{-5}M$ for ACh and 20mM for KCl. CCK-8 induced contraction was unaffected in calcium free physiological salt solution (PSS) and was completely blocked by strontium substitution for calcium (p<0.001). In contrast, KCl evoked contraction was blocked in calcium free PSS (p<0.01) but was unaffected by strontium replacement of calcium. The contraction elicited by ACh was only slightly reduced in calcium free PSS (p<0.05) and was unaltered by strontium. Muscle cells permeabilized with saponin contracted in response to inositol 1,4.5-trisphosphate $(IP_3)$ and CCK-8. The contraction was blocked by the calmodulin antagonist CGS 9343B (p<0.001), whereas heparin completely blocked the effect of $IP_3$ (p<0.001). The protein kinase C (PKC) antagonist H7 had no effect on either agonist. We conclude that CCK-8 induced gallbladder muscle contraction is mediated by $IP_3$ dependent intracellular calcium release from intracellular stores and a calmodulin dependent pathway; ACh may utilize both extracellular and intracellular calcium. KCl causes muscle contracrion through influx of extracellular calcium and a calmodulin independent machanism.
In this study, chemical compositions - holocellulose, lignin and monomeric sugars - were characterized with two poplar wood cell walls, one of which was grown at normal condition (CPW) and the other was genetically modified by antisence suppression of CCoAOMT gene expression (ACPW). Milled wood lignins were isolated from CPW and ACPW and subjected to methoxyl group, DFRC, Py-GC/MS, GPC, $^{13}C$-NMR analysis, respectively. There were few differences in holocellulose contents in both cell walls, which were determined to 81.6% in CPW and to 82.3% in ACPW. However, lignin contents in ACPW was clearly decreased by the suppression of CCoAOMT gene expression. In CPW 21.7% of lignin contents was determined, while lignin contents in ACPW was lowered to 18.3%. The relative poor solubility of ACPW in alkali solution could be attributed to the reduction of lignin content. The glucose contents of CPW and ACPW were measured to 511.0 mg/g and 584.8 mg/g and xylose contents 217.8 mg/g and 187.5 mg/g, respectively, indicating that suppression of CCoAOMT gene expression could be also influenced to the formation of monomeric sugar compositions. In depth investigation for milled wood lignin (MWL) isolated from both samples revealed that the methoxyl contents at ACPW was decreased by 7% in comparison to that of CPW, which were indirectly evidenced by $^{13}C$-NMR spectra and Py-GC/MS. According to the data from Py-GC/MS S/G ratios of lignin in CPW and ACPW were determined to 0.59 and 0.44, respectively. As conclusive remark, the biosynthesis of syringyl unit could be further influenced by antisense suppression of CCoAOMT during phenylpropanoid pathway in the plant cell wall rather than that of guaiacyl unit.
Inflammation is a complex process resulting from a variety of mechanisms. Combined inhibition of the activities of enzymes involved in the process may therefore be considered more important in anti-inflammatory property of plant extracts than any single contribution. In this study, the inhibitory effects of the ethanol extracts of thirty plant foods on the activities of secretory phospholipase $A_{2}$ ($sPLA_{2}$), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and 12-lipoxygenase (12-LOX) were examined. Several legumes, mungbean sprout and some leaf vegetables inhibited the activity of $sPLA_2$, upstream enzyme of inflammation pathway. Only soybean sprout and mungbean sprout significantly inhibited 12-LOX activity. Although most of extracts inhibited the activities of both COX-1 and COX-2, water dropwort and amaranth showed selectivity for the inhibition of COX-2 over COX-1. Especially, mungbean showed anti-inflammatory property at both upstream and downstream of inflammation pathway with relatively low $IC_{50}$ values for $sPLA_{2}$ and COX-2 enzymes. Mungbean sprout exhibited inhibitory effects on all enzymes related to early and late inflammation and soybean sprout suppressed 12-LOX and COX-2 simultaneously, although the activities of these plants were showed at relatively high concentration. Therefore, mungbean, mungbean sprout, and soybean sprout appear to exhibit anti-inflammatory effects by combined inhibition of inflammatory enzymes.
Journal of the Society of Cosmetic Scientists of Korea
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v.26
no.1
/
pp.149-162
/
2000
Coenzyme Q10 is found in all tissues including skin and it is the well-known coenzyme for mitochondrial enzymes. The electron and proton transfer functions of the quinone ring are of fundamental importance for the oxidative phosphorylation pathway to generate energy in the cells. Coenzyme Q10 has been studied as a potent antioxidant molecule in the skin. It is involved in the skin's response to UVR irradiation. The concentration of this antioxidant in UVR exposed skin is higher than in non-exposed skin. However, recent studies have also shown that coenzyme Q10 is one of the first antioxidants to be depleted when skin is UVR-irradiated. This indicates that coenzyme Q10 is primarily involved in defense mechanisms of the skin. Therefore, we questioned whether coenzyme Q10 shows reulatory effect of melanogenesis. Here we report that coenzyme Q10 inhibits melanin neosynthesis of normal human melanocytes grown in culture, and lightens UVB-induced hyperpigmentation of the guinea pig skin in vivo. We treated human melanocytes with 0.05mM to 0.5mM of coenzyme Q10 for a total of two days. This inhibited melanin neosynthesis of cultured human melanocytes dose-dependently. The inhibitory effect of coenzyme Q10 was as effective as kojic acid or vitamin C on cultured human melanocytes. CoQ10 didn't have direct inhibitory effect on tyrosinase activity in in vitro tyrosine hydroxylase activity To further clarify the effect of coenzyme Q10 on the melanogenesis, we established UVB-induced hyperpigmentation on the shaved backs of brownish guinea pigs. The UVB intensity was 500mJ/$\textrm{cm}^2$ and the total energy dose was 1,500 mJ/$\textrm{cm}^2$. The animals were exposed to UVB radiation one times a week for three consecutive weeks. Coenzyme Q10, kojic acid, Arbutin, vitamin C(1% in vehicle) or vehicle alone as a control were then topically applied daily to the hyperpigmented areas twelve times per week far four successive weeks. The lightening effect was evaluated by visual scoring, chromameter and immunohistochemistry. Coenzyme Q10 had lightening effect on the UVB-induced hyperpigmentation without any other side effects, whereas another compounds showed weak lightening efficacies. Therefore, these results suggest that coenzyme Q10 may be useful for solving physiological hyperpigmenting problems for cosmetic purposes.
In this study we purified a fibrinolytic enzyme from Cordyceps militaris using a combination of ion-exchange chromatography on a DEAE Sephadex A-50 column, gel filtration chromatography on a Sephadex G-75 column, and FPLC on a HiLoad 16/60 Superdex 75 column. This purification protocol resulted in a 191.8-fold purification of the enzyme and a final yield of 12.9 %. The molecular mass of the purified enzyme was estimated to be 52 kDa by SDS-PAGE, fibrin-zymography, and gel filtration chromatography. The first 19 amino acid residues of the N-terminal sequence were ALTTQSNV THGLATISLRQ, which is similar to the subtilisin-like serine protease PR1J from Metarhizium anisopliae var. anisopliase. This enzyme is a neutral protease with an optimal reaction pH and temperature of 7.4 and $37^{\circ}C$, respectively. Results for the fibrinolysis pattern showed that the enzyme rapidly hydrolyzed the fibrin $\alpha$-chain followed by the $\gamma$-$\gamma$ chains. It also hydrolyzed the $\beta$-chain, but more slowly. The A$\alpha$, B$\beta$, and $\gamma$ chains of fibrinogen were also cleaved very rapidly. We found that enzyme activity was inhibited by $Cu^{2+}$ and $Co^{2+}$, but enhanced by the additions of $Ca^{2+}$ and $Mg^{2+}$ ions. Furthermore, fibrinolytic enzyme activity was potently inhibited by PMSF and APMSF. This enzyme exhibited a high specificity for the chymotrypsin substrate S-2586 indicating it's a chymotrypsin-like serine protease. The data we present suggest that the fibrinolytic enzyme derived from the edible and medicinal mushroom Cordyceps militaris has fibrin binding activity, which allows for the local activation of the fibrin degradation pathway.
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