In lactic acid fermentation, the end product inhibition by lactic acid causes several problems. The most important of which are low lactate formation rate and its recovery from fermentation broth. To overcome these problems, extractive lactic acid fermentation was carried out in a bioreactor, which was connected to a column packed with anion exchange resin (Amberlite IRA-400, 250 g). The system was started as a batch process, and then the separation process was started when the lactic acid concentration reached 10 g/L, 20 g/L or 30 g/L. In each case, total lactic acid concentration was reached to 48.6, 53.6, 52.6 g/L with its productivity of 1.2 g/L $.$ h, 1.6 g/L $.$ h, and 1.3 g/L $.$ h, respectively Especially, in the case of the 20 g/L recycling-initiation process, extractive fermentation reduced tie fermentation time (17 hrs) by 34% in comparison with the conventional batch process. The direct consequence of this time reduction was shown by a 1.8 fold increase in overall lactic acid productivity.
The purpose of this study was designed to observe the effects of the feeding Cynanchum wilfordii extract on the improvement of the blood glucose, lipid components in the serum of dietary hyperlipidemic and streptozotocin(STZ) -induced diabetic rats(S.D. strain, ♂) fed the experimental diets for 5 weeks. Concentrations of total cholesterol, atherosclerotic index, LDL, LDL-Cholesterol, free-cholesterol. cholesteryl ester, TG, PL and blood glucose in serum were significantly higher in the cholesterol administration groups((group 2(cholesterol+water), 4(cholesterol+Cynanchum WIlfordii 3.5g% extract)) than those in the control group (group1 , basal diet+water). But the concentrations of total cholesterol. atherosclerotic index, LDL, LDL- cholesterol. free-cholesterol, cholesteryl ester, TG, PL and blood glucose in serum were remakably lower in the group 4 than those in the group 2. In the STZ(55mg/kg B.W.)-induced diabetic groups((group 3(STZ, IP.)+water), 5(STZ(IP.)+Cynanchum WIlfordii 3.5g% extract? the serum total cholesterol, atherosclerotic index, LDL, LDL-cholesterol, free-cholesterol. cholesteryl ester, TG, PL and blood glucose concentrations actions were rather lower in the group 5 than those in the group 3. In the ratio of HDL -cholesterol concentration to total cholesterol and HDL-cholesterol concentration, Cynanchum wilfordii extract administration groups were higher percentage than III the groups 2 and 3. The activities of aspartate aminotransferase(AST), alanine aminotransferase(ALT), alkaline phosphatase (ALP) and lactate dehydrogenase(LDH) in serum were rather lower in the Cynanchum wllfordii extract administration groups (group 4,5) than in the cholesterol diet group(group 2) and STZ-induced diabetic group (group 3). From the above research, the physiological activity substances in Cynanchum wllfordii were effective on the improvement of the blood glucose, lipid compositions in serum of dietary hyperlipidemic and STZ-induced diabetic rats. And particularly, physiological activity substance in Cynanchum wilfordii was more effective therapeutic regimen for the control of metabolic derangements in adult disease.
Oxygen free radicals can generated during metabolic processes in normal cells and by exposure of cells to toxic substances. These radicals have been recogenized to playa critical role in several pathological conditions including carcinogenesis and aging, and they have been implicated in pathogenesis of various diseases such as seizure, Alzheimer's disease, Parkinson's disease, myocardial infarction, respiratory distress syndrome, and rheumatoid arthritis. This study was undertaken to determine if Juglandis semen herb-acupuncture solution (JSHAS) has a protective effect against cell injury caused by oxidants, t-butylhydroperoxide (t-BHP) and $H_{2}O_2$. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release and lipid perexidation was estimated by measurimg malondialdehyde, a product of lipid peroxidation. JSHAS significantly prevented LDH release induced by t-BHP or $H_{2}O_2$ in a dose-dependent manner at concentrations of 0.5-10%. Such protective effect was observed in control tissues untreated with oxidants. JSHAS, at 5% concentration, significantly reduced LDH release even when the concentrations of t-BHP and $H_{2}O_2$ increased to 5 and 200 mM, respectively. JSHAS, at 5% concentration, significantly reduced the lipid peroxidation by t-BHP and $H_{2}O_2$. These results indicate that JSHAS prevents cell injury and lipid peroxidation induced by oxidants in rabbit kidney cells. However, the underlying mechanisms remain to determined.
Kim Sung-Mun;Kang Sung-Hee;Ma Jin-Yeul;Kim Jin-Hyun
KSBB Journal
/
v.21
no.1
s.96
/
pp.11-15
/
2006
The biological activities of extracts from the fruit, stem, and leaf of Hovenia dulcis were examined. In the batch mode of operation, the fruit, stem, and leaf of Hovenia dulcis were extracted with hot water for 10 hr. The fruit extract of Hovenia dulcis gave the highest activity for decreasing alcohol concentration which was 138% of control. The equilibrium between bioactive compound in the fruit (size : 4 mm) and hot water solution was reached within 6 hr and the recovery was 95% by three-times extraction. The fruit extract of Hovenia dulcis showed significant alcohol decrease in blood and hepatoprotective activity against $CCl_4$-toxicity in rat. The fruit extract significantly inhibited the elevation of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels.
The purpose of this study was to compare the inhibitory effect of bevacizumab on human Tenon's fibroblasts (HTFs) cultured from primary and recurrent pterygium. Cultured HTFs were exposed to 2.0, 5.0, 7.5, and 15.0 mg/mL concentration of bevacizumab for 24 hours. The 3-[4,5-dimethylthiazol- 2-yl]-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase leakage assays were then performed to assess fibroblast metabolism and viability. The matrix metalloproteinase (MMP), procollagen type I C terminal propeptide (PIP), and laminin immunoassays were performed to examine extracellular matrix production. Changes in cellular morphology were examined by phase-contrast and transmission electron microscopy. Both metabolic activity and viability of primary and recurrent pterygium HTFs were inhibited by bevacizumab in a dose-dependent manner, especially at concentrations greater than 7.5 mg/mL. Both types of HTFs had significant decreases in MMP-1, PIP, and laminin levels. Distinctly, the inhibitory effect of bevacizumab on MMP-1 level related with collagenase in primary pterygium HTFs was significantly higher than that of recurrent pterygium. Significant changes in cellular density and morphology both occurred at bevacizumab concentrations greater than 7.5 mg/mL. Only primary pterygium HTFs had a reduction in cellular density at a bevacizumab concentration of 5.0 mg/mL. Bevacizumab inhibits primary and recurrent pterygium HTFs in a dose-dependent manner, especially at concentrations greater than 7.5 mg/mL. As the primary HTFs produces larger amounts of MMP-1 compared to recurrent HTFs, significant reduction in MMP-1 level in primary pterygium HTFs after exposure to bevacizumab is likely to be related to the faster cellular density changes in primary pterygium HTFs.
Park, Ji-Hwan;Kim, Yun-Ha;Moon, Seong-Keun;Kim, Tae-Young;Kim, Jong-Moon
Journal of Korean Neurosurgical Society
/
v.38
no.6
/
pp.456-464
/
2005
Objective : The authors investigated whether rotenone induces cellular death also in non-dopaminergic neurons and high concentration of potassium ion can show protective effect for non-dopaminergic neuron in case of rotenone-induced cytotoxicity. Methods : Neuro 2A cells was treated with rotenone, and their survival as well as cell death mechanism was estimated using 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium[MTT] assay, Lactate dehydrogenase[LDH] release assay, fluorescence microscopy, and agarose gel electrophoresis. The changes in rotenone-treated cells was also studied after co-treatment of 50mM KCl. And the protective effect of KCl was evaluated by mitochondrial membrane potential assay and compared with the effects of various antioxidants. Results : Neuro 2A cells treated with rotenone underwent apoptotic death showing chromosome condensation and fragmentation as well as DNA laddering. Co-incubation of neuro 2A cells with 50mM KCl prevented it from the cytotoxicity induced by rotenone. Intracellular accumulation of reactive oxygen species[ROS] resulting by rotenone were significantly reduced by 50mM KCl. Potassium exhibited significantly similar potency compared to the antioxidants. Conclusion : The present findings showed that potassium attenuated rotenone-induced cytotoxicity, intracellular accumulation of ROS, and fragmentation of DNA in Neuro 2A cells. These findings suggest the therapeutic potential of potassium ion in neuronal apoptosis, but the practical application of high concentration of potassium ion remains to be settled.
Kim, Dong-Hyeon;Amanullah, Sadar M.;Yoon, Hee;Lee, Hyuk-Jun;Kong, Il-Keun;Kim, Sam-Churl;Cho, Kyu-Woan;Kim, Sang-Bum
Journal of agriculture & life science
/
v.46
no.3
/
pp.79-85
/
2012
This study was conducted to examine the effect of dietary n-3/n-6 fatty acid (FA) ratio on in vitro dry matter digestibility (IVDMD), fermentation indices and FA profile. Rice bran was mixed with oil sources (cotton seed oil and linseed oil) to make the diets at 0.02, 0.29 and 0.61 of dietary n-3/n-6 FA ratio. These diets (0.5g) were placed into the incubation bottles with 40 ml of anaerobic culture medium, which contained rumen fluid and Van Soest medium at 1:2 ratio. Five replicates of each diet and two blanks were incubated at $39^{\circ}C$ for 48 hours. After incubation, the incubated contents were centrifuged. The residues were freeze-dried for DMD and FA analyses. The supernatant was used for pH, $NH_3-N$ and volatile fatty acid analyses. The concentrations of lactate (p<0.001) and iso-valerate (p<0.001) decreased linearly with increasing dietary n-3/n-6 FA ratio, but acetate concentration (p=0.056) and the ratio of acetate to propionate (p=0.005) was increased linearly. The concentrations of n-3, n-6 FA and the ratio of n-3/n-6 FA in residues increased (p<0.001) linearly with increasing dietary n-3/n-6 FA ratio, but C18:1n-9 FA concentration was decreased (p<0.001) linearly. With these results, it could affect fermentation characteristics and FA profile of rumen content by dietary n-3/n-6 FA ratio.
Kim, Yeo Jin;Cho, Eun Ju;Lee, Ah Young;Seo, Weon Taek
Microbiology and Biotechnology Letters
/
v.49
no.2
/
pp.138-147
/
2021
The overproduction of reactive nitrogen species (RNS) and reactive oxygen species (ROS) causes oxidative damage to neuronal cells, leading to the progression of neurodegenerative diseases. In this study, we determined the nitric oxide radical (NO), hydroxyl radical (·OH), and superoxide anion radical (O2-) scavenging activities of apigenin. Our results showed that apigenin exhibited remarkable, concentration-dependent ·OH, O2-, and NO radical scavenging activities. Particularly, apigenin indicated the strongest ·OH radical scavenging activity with 93.38% in the concentration of 100 µM. Furthermore, we also investigated the protective effects of apigenin against hydrogen peroxide (H2O2)-induced oxidative stress in SH-SY5Y cells. The H2O2 treatment resulted in a significant decrease in cell viability, as well as an increase in lactate dehydrogenase (LDH) release and ROS production compared with the H2O2-nontreated SH-SY5Y cells. However, the cell viability significantly increased in the apigenin-treated group, as well as inhibited ROS generation and LDH release compared with the H2O2-induced control group. To elucidate the protective mechanisms of apigenin against oxidative stress in SH-SY5Y, we analyzed the apoptosis-related protein expression. The apigenin treatment resulted in the downregulated expression of apoptosis-related protein markers, such as cytochrome C, cleaved caspase-3, poly (ADP)-ribose polymerase (PARP), and B-cell lymphoma 2-associated X (Bax), as well as the upregulated expression of anti-apoptosis markers such as B-cell lymphoma 2 (Bcl-2). In this study, we report that apigenin exhibits a neuroprotective effect against oxidative stress in SH-SY5Y cells. These results suggest that apigenin may be considered as a potential agent for neurodegenerative disease prevention.
Journal of The Korean Society of Clinical Toxicology
/
v.20
no.2
/
pp.39-44
/
2022
N-Acetylcysteine (NAC) is the standard antidote treatment for preventing hepatotoxicity caused by acetaminophen (AAP) poisoning. This review summarizes the recent evidence for the treatment of AAP poisoning. Several alternative intravenous regimens of NAC have been suggested to improve patient safety by reducing adverse drug reactions and medication errors. A two-bag NAC infusion regimen (200 mg/kg over 4 h, followed by 100 mg/kg over 16 h) is reported to have similar efficacy with significantly reduced adverse reactions compared to the traditional 3-bag regimen. Massive AAP poisoning due to high concentrations (more than 300-lines in the nomogram) needs to be managed with an increased maintenance dose of NAC. In addition to NAC, the combination therapy of hemodialysis and fomepizole is advocated for severe AAP poisoning cases. In the case of a patient presenting with an altered mental status, metabolic acidosis, elevated lactate, and an AAP concentration greater than 900 mg/L, hemodialysis is recommended even if NAC is used. Fomepizole decreases the generation of toxic metabolites by inhibiting CYP2E1 and may be considered an off-label use by experienced clinicians. Since the nomogram cannot be applied to sustained-release AAP formulations, all potentially toxic sustained-release AAP overdoses should receive a full course of NAC regimen. In case of ingesting less than the toxic dose, the AAP concentration is tested twice at an interval of 4 h or more; NAC should be administered if either value is above the 150-line of the nomogram.
This study was undertaken to investigate the mechanism of lipopolysaccharide (LPS) and nitric oxide (NO) as a regulator of vascular smooth muscle cell (VSMC) proliferation. VSMC was primarily cultured from rat aorta and confirmed by the immunocytochemistry with anti-smooth muscle myosin antibody. The number of viable VSMCs were counted, and lactate dehydrogenase (LDH) activity was measured to assess the degree of cell death. Concentrations of nitrite in the culture medium were measured as an indicator of NO production. LPS was introduced into the medium to induce the inducible nitric oxide synthase (iNOS) in VSMC, and Western blot for iNOS protein and RT-PCR for iNOS mRNA were performed to confirm the presence of iNOS. Inhibitors of iNOS and soluble guanylate cyclase (sGC), sodium nitroprusside (SNP) and L-arginine were employed to observe the action of LPS on the iNOS-NO-cGMP signalling pathway. LPS and SNP decreased number of VSMCs and increased the nitrite concentration in the culture medium, but there was no significant change in LDH activity. A cell permeable cGMP derivative, 8-Bromo-cGMP, decreased the number of VSMCs with no significant change in LDH activity. L-arginine, an NO substrate, alone tended to reduce cell count without affecting nitrite concentration or LDH level. Aminoguanidine, an iNOS specific inhibitor, inhibited LPS-induced reduction of cell numbers and reduced the nitrite concentration in the culture medium. LY 83583, a guanylate cyclase inhibitor, suppressed the inhibitory actions of LPS and SNP on VSMC proliferation. LPS increased amounts of iNOS protein and iNOS mRNA in a concentration-dependent manner. These results suggest that LPS inhibits the VSMC proliferation via production of NO by inducing iNOS gene expression. The cGMP which is produced by subsequent activation of guanylate cyclase would be a major mediator in the inhibitory action of iNOS-NO signalling on VSMC proliferation.
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