Kim, Hyungkuen;Jeon, Eek Hyung;Park, Byung-Chul;Kim, Sung-Jo
Asian-Australasian Journal of Animal Sciences
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제32권11호
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pp.1789-1800
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2019
Objective: Although alveolar macrophages play a key role in the respiratory immunity of livestock, studies on the mechanism of differentiation and survival of alveolar macrophages are lacking. Therefore, we undertook to investigate changes in the lipid metabolism and survival rate, using 3D4/31 macrophages and Dudleya brittonii which has been used as a traditional asthma treatment. Methods: 3D4/31 macrophages were used as the in vitro porcine alveolar macrophages model. The cells were activated by exposure to phorbol 12-myristate 13-acetate (PMA). Dudleya brittonii extraction was performed with distilled water. For evaluating the cell survival rate, we performed the water-soluble tetrazolium salt cell viability assay and growth curve analysis. To confirm cell death, cell cycle and intracellular reactive oxygen species (ROS) levels were measured using flow cytometric analysis by applying fluorescence dye dichlorofluorescein diacetate and propidium iodide. Furthermore, we also evaluated cellular lipid accumulation with oil red O staining, and fatty acid synthesis related genes expression levels using quantitative polymerase chain reaction (qPCR) with SYBR green dye. Glycolysis, fatty acid oxidation, and tricarboxylic acid (TCA) cycle related gene expression levels were measured using qPCR after exposure to Dudleya brittonii extract (DB) for 12 h. Results: The ROS production and cell death were induced by PMA treatment, and exposure to DB reduced the PMA induced downregulation of cell survival. The PMA and DB treatments upregulated the lipid accumulation, with corresponding increase in the acetyl-CoA carboxylase alpha, fatty acid synthase mRNA expressions. DB-PMA co-treatment reduced the glycolysis genes expression, but increased the expressions of fatty acid oxidation and TCA cycle genes. Conclusion: This study provides new insights and directions for further research relating to the immunity of porcine respiratory system, by employing a model based on alveolar macrophages and natural materials.
Panax ginseng (family- Araliaceae) is a native plant of Korea and has been used for past several years among oriental people. To evaluate the radioprotective potential of P. ginseng on the formation of giant cells in the testis of Swiss albino mice, the animals were divided into four groups: -(I)-Only vehicle was administered. (II)P. ginseng treated group: -The animals received 10 mg/kg body weight P. ginseng root extract (in DDW) i.p. continuously for 30 days. (III) Irradiated group: -The animals were exposed to 8 Gy gamma radiation at the dose rate of 1.69 Gy/min at the distance of 80 ems. (IV) Combined treatment group: -Animals were given P. ginseng extract for four days and on fourth day they were irradiated to 8 Gy gamma radiation after 30 minute of extract administration. The animals of these three groups were autopsied on day 1,3, 7, 14 and 30 days. In ginseng treated group, active spermatogenesis was observed without any toxic effect. Histopathological studies of irradiated group (II) revealed reduction in germ cell count, loss of sperms and formation of multinucleated giant cells on day 7th. These giant cells were formed by round nuclei of early or late spermatids. In combination group (III), although germinal epithelium was still disorganized with loss of cells in few tubules, but no giant cell formation was observed. In order to know the mechanism of radioprotection of ginseng, LPO and GSH were estimated. It was observed that pretreated irradiated animals showed inhibition of LPO and increase in GSH. Thus the present study suggests ginseng protects male gonads. This may be attributed to the inhibition of LPO and increase synthesis of GSH byginseng.
Leptin, the product of the ob gene, is a small peptide molecule synthesized by white adipocytes with an important role in the regulation of body fat and food intake. Based on the evidence that synthesis of leptin is regulated by female sex hormone, estrogen, this present study was investigated whether sex hormone precursor DHEA, can regulate obese gene expression in lean and genetically obese (ob/ob) mice. Antiobesity activity of DHEA was evaluated by determining body weight, food consumption, epididymal fat weight and serum levels of cholesterol and triglyceride in ICR, C57BL/6J, and ob/ob mice. The treatment of C57BL/6J lean and obese mice with a diet containing 0.3% and 0.6% DHEA resulted in lowered rates of weight gain in comparison to non-treated mice, although much greater response was found in the obese mice. All other concentrations of DHEA (0.015%, 0.06%, 0.15%, 0.3%) except the highest one(0.6%) showed no significant effects on weight gain in ICR mice. Food consumption was significantly decreased in all mice treated with 0.6% DHEA, whereas it was not decreased in ICR mice at lower concentrations than 0.6% DHEA. DHEA decreased significantly epididymal adipose tissue weight and serum triglyceride levels dose dependently in lean and obese mice. However serum cholesterol levels were decreased at lower concentrations than 0.15% DHEA and increased at concentrations of 0.3% and 0.6% DHEA in lean and obese mice. These increases in serum cholestrol levels at high concentrations of DHEA might result from the fact that DHEA has a cholesterol moiety thereby interfered the assay system. As an approach to elucidate the mechanism for antiobesity activity of DHEA, we examined mRNA levels of obese gene in the adipocyte and obese gene product (leptin) in the serum. The results showed that DHEA did not affect obese gene expression in ICR and C57BL/6J mice. Therefore, we concluded that antiobesity activity of DHEA was not modulated by obese gene expression.
Power to gas (P2G) is one of the energy storage technologies that can increase the storage period and storage capacity compared to the existing battery type. One of P2G technology produces hydrogen by decomposing water from renewable energy (electricity) and the other produces CH4 by reacting hydrogen with CO2. This study is an experimental study to produce CH4 by reacting CO2 of biogas with hydrogen using a 40 wt% Ni-Mg-Al catalyst and a commercial catalyst. Catalyst characteristics were analyzed through H2-TPR, XRD, and XPS instruments of 40% Ni catalyst and commercial catalyst. The effect on the CO2 conversion rate and CH4 selectivity was analyzed, and the activities of a 40% Ni catalyst and a commercial catalyst were compared. As a result of experiment, In the case of a 40 wt% catalyst, the maximum CO2 conversion rate showed 77% at the reaction temperature of 400℃. Meanwhile, the commercial catalyst showed a maximum CO2 conversion rate of 60% at 450℃. When 50% of CO was added to the CO2 methanation reaction, the CO2 conversion rate was increased by about 5%. This is considered to be due to the atmosphere in which the CO reaction can occur without the process of converting to CH4 after forming carbon and CO as intermediates in terms of the CO2 mechanism on the catalyst surface.
7-Hydroxy-4-methylcoumarin (7H-4MC) inhibits hyaluronan production in multiple cell lines and tissue types both in vitro and in vivo. It is a commercially available drug approved for human use, called hymecromone, in European and Asian countries to prevent biliary spasms. Nevertheless, as the pharmacological efficacy of 7H-4MC has not yet been reported in macrophages, this study investigated its anti-inflammatory effects and mechanism of action using lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. LPS-induced RAW 264.7 cells were treated with various concentrations of 7H-4MC (62.5, 125, 250, and 500 μM). The application of 7H-4MC significantly reduced nitric oxide and prostaglandin E2 production without cytotoxic effects. Additionally, 7H-4MC strongly decreased the expression of inducible nitric oxide synthase and cyclooxygenase. Furthermore, 7H-4MC reduced the production of proinflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. Finally, 7H-4MC exerted its potent anti-inflammatory actions via the upregulation of IκB-α production, which led to the inhibition of nuclear factor-κB (NF-κB) activity. These results, obtained in macrophage cell lines, suggest that 7H-4MC prevents inflammatory diseases via the NF-κB signaling pathway and that its use could be beneficial for human health. Ultimately, this is the first report describing the anti-inflammatory activity of 7H-4MC in a macrophage cell line.
A novel sensor material of Au nanoparticles (NPs) functionalized 1D ${\alpha}-MoO_3$ nanobelts (NBs) was fabricated by a facile lysine-assisted approach. The obtained $Au/{\alpha}-MoO_3$ product was characterized by means of X-ray diffraction (XRD), scanning electron microscope (SEM), transmission electron microscope (TEM) and energy dispersive X-ray (EDX), and X-ray photoelectron spectra (XPS). Then, in order to investigate the gas sensing performances of our samples, a comparative gas sensing study was carried out on both the ${\alpha}-MoO_3$ NBs before and after Au NPs decoration by using ethanol vapor as the molecular probe. The results turned out that, after the functionalization of Au NPs, the sensor exhibited improved gas-sensing characteristics than the pure ${\alpha}-MoO_3$, such as response and recovery time, optimal operating temperature (OT) and excellent selectivity. Take for example 200 ppm of ethanol, the response/recovery times were 34 s/43 s and 5.7 s/10.5 s, respectively, while the optimal operating temperature (OT) was lower to $200^{\circ}C$ rather than $250^{\circ}C$. Besides, the functionalized sensor showed a higher response to ethanol at $200^{\circ}C$, and response was 1.6 times higher than the pure $MoO_3$. The mechanism of such improved sensing properties was interpreted, which might be attributed to the spillover effect of Au NPs and the electronic metal-support interaction.
Background/Aims Irritable bowel syndrome (IBS) is a common disease characterized by intestinal dysmotility, the mechanism of which remains elusive. We aim to determine whether the high-affinity choline transporter 1 (CHT1), a determinant of cholinergic signaling capacity, modulates intestinal motility associated with stress-induced IBS. Methods A rat IBS model was established using chronic water avoidance stress (WAS). Colonic pathological alterations were evaluated histologically and intestinal motility was assessed by intestinal transit time and fecal water content (FWC). Visceral sensitivity was determined by visceromotor response to colorectal distension. RT-PCR, western blotting, and immunostaining were performed to identify colonic CHT1 expression. Contractility of colonic muscle strips was measured using isometric transducers. enzyme-linked immunosorbent assay was used to measure acetylcholine (ACh). We examined the effects of MKC-231, a choline uptake enhancer, on colonic motility. Results After 10 days of WAS, intestinal transit time was decreased and fecal water content increased. Visceromotor response magnitude in WAS rats in response to colorectal distension was significantly enhanced. Protein and mRNA CHT1 levels in the colon were markedly elevated after WAS. The density of CHT1-positive intramuscular interstitial cells of Cajal and myenteric plexus neurons in WAS rats was higher than in controls. Ammonium pyrrolidine dithiocarbamate partly reversed CHT1 upregulation and alleviated colonic hypermotility in WAS rats. Pharmacological enhancement of CHT1 activity by MKC-231 enhanced colonic motility in control rats via upregulation of CHT1 and elevation of ACh production. Conclusion Upregulation of CHT1 in intramuscular interstitial cells of Cajal and myenteric plexus neurons is implicated in chronic stress-induced colonic hypermotility by modulation of ACh synthesis via nuclear factor-kappa B signaling.
Ruiz-Torres, Claudio Adrian;Araujo-Martinez, Rene Fernando;Martinez-Castanon, Gabriel Alejandro;Morales-Sanchez, J. Elpidio;Lee, Tae-Jin;Shin, Hyun-Sang;Hwang, Yuhoon;Hurtado-Macias, Abel;Ruiz, Facundo
Environmental Engineering Research
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제24권3호
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pp.463-473
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2019
Nanoscale zero-valent iron (nZVI) has proved to be an effective tool in applied environmental nanotechnology, where the decreased particle diameter provides a drastic change in the properties and efficiency of nanomaterials used in water purification. However, the agglomeration and colloidal instability represent a problematic and a remarkable reduction in nZVI reactivity. In view of that, this study reports a simple and cost-effective new strategy for ultra-small (< 7.5%) distributed functionalized nZVI-EG (1-9 nm), with high colloidal stability and reduction capacity. These were obtained without inert conditions, using a simple, economical synthesis methodology employing two stabilization mechanisms based on the use of non-aqueous solvent (methanol) and ethylene glycol (EG) as a stabilizer. The information from UV-Vis absorption spectroscopy and Fourier transform infrared spectroscopy suggests iron ion coordination by interaction with methanol molecules. Subsequently, after nZVI formation, particle-surface modification occurs by the addition of the EG. Size distribution analysis shows an average diameter of 4.23 nm and the predominance (> 90%) of particles with sizes < 6.10 nm. Evaluation of the stability of functionalized nZVI by sedimentation test and a dynamic light-scattering technique, demonstrated very high colloidal stability. The ultra-small particles displayed a rapid and high nitrate removal capacity from water.
Wang, Xiaochen;Yang, Hongyu;Zhou, Wei;Liu, Jun;Xu, Ning
Journal of Microbiology and Biotechnology
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제29권8호
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pp.1288-1298
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2019
Bacterial ATP synthases drive ATP synthesis by a rotary mechanism, and play a vital role in physiology and cell metabolism. Corynebacterium glutamicum is well known as an industrial workhorse for amino acid production, and its ATP synthase operon contains eight structural genes and two adjacent genes, cg1360 and cg1361. So far, the physiological functions of Cg1360 (GenBank CAF19908) and Cg1361 (GenBank CAF19909) remain unclear. Here, we showed that Cg1360 was a hydrophobic protein with four transmembrane helices (TMHs), while no TMH was found in Cg1361. Deletion of cg1360, but not cg1361, led to significantly reduced cell growth using glucose and acetic acid as carbon sources, reduced F1 portions in the membrane, reduced ATP-driven proton-pumping activity and ATPase activity, suggesting that Cg1360 plays an important role in ATP synthase function. The intracellular ATP concentration in the ${\Delta}cg1360$ mutant was decreased to 72% of the wild type, while the NADH and NADPH levels in the ${\Delta}cg1360$ mutant were increased by 29% and 26%, respectively. However, the ${\Delta}cg1361$ mutant exhibited comparable intracellular ATP, NADH and NADPH levels with the wild-type strain. Moreover, the effect of cg1360 deletion on L-valine production was examined in the L-valine-producing V-10 strain. The final production of L-valine in the $V-10-{\Delta}cg1360$ mutant reached $9.2{\pm}0.3g/l$ in shake flasks, which was 14% higher than that of the V-10 strain. Thus, Cg1360 can be used as an effective engineering target by altering energy metabolism for the enhancement of amino acid production in C. glutamicum.
Kim, Min Kyung;Lee, Wooseong;Yoon, Gang-Ho;Chang, Eun-Ju;Choi, Sun-Cheol;Kim, Seong Who
BMB Reports
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제52권3호
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pp.220-225
/
2019
We have identified a mechanism to diminish the proliferative capacity of cells during cell expansion using human adipose-derived stromal cells (hAD-SCs) as a model of replicative senescence. hAD-SCs of high-passage numbers exhibited a reduced proliferative capacity with accelerated cellular senescence. Levels of key bioactive sphingolipids were significantly increased in these senescent hAD-SCs. Notably, the transcription of sphingosine kinase 1 (SPHK1) was down-regulated in hAD-SCs at high-passage numbers. SPHK1 knockdown as well as inhibition of its enzymatic activity impeded the proliferation of hAD-SCs, with concomitant induction of cellular senescence and accumulation of sphingolipids, as seen in high-passage cells. SPHK1 knockdown-accelerated cellular senescence was attenuated by co-treatment with sphingosine-1-phosphate and an inhibitor of ceramide synthesis, fumonisin $B_1$, but not by treatment with either one alone. Together, these results suggest that transcriptional down-regulation of SPHK1 is a critical inducer of altered sphingolipid profiles and enhances replicative senescence during multiple rounds of cell division.
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