Park, Jae Eun;Lee, Do Kyung;Kim, Min Ji;Kim, Kyung Tae;Choi, Kyung Soon;Seo, Jae Goo;Ha, Nam Joo
Korean Journal of Microbiology
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v.50
no.4
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pp.296-301
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2014
Rotavirus is a major cause of acute gastroenteritis in young children in developed and developing countries. The use of probiotics for the treatment of gastrointestinal diseases is both safe and easily accessible. In this study, we evaluated the anti-rotaviral activities of probiotic mixtures in a Sprague-Dawley rat. 24 litters with their dams were randomly assigned to four groups; placebo, phosphate buffered saline (PBS), and two probiotic mixture (PRO-1 and PRO-2) groups. All rats were inoculated with rotavirus at dose of 8 log plaque forming units per rat at 5 days old. Animals in the PRO-1 and PRO-2 groups were orally administered probiotic mixtures 1 or 2, respectively, at a dose of 8 log colony forming units daily during 4 days. For control purposes, placebo and PBS groups were orally administered the same amount of placebo (containing maltose and polydextrose) or PBS once daily for 4 days, respectively. Antiviral analysis was performed by real-time quantitative PCR (RT-qPCR) and observing intestinal villi. As a result, weights of small intestines were greater in the PRO-1, PRO-2 groups than in control groups. Villi were short and villous epithelial necrosis was exhibited in control groups, but these morphological changes were not observed in PRO-1, PRO-2 treated rats. RT-qPCR analysis showed that VP7 gene level of rotavirus in fecal samples and small intestinal epithelial cells were lower in the PRO-1 and PRO-2 groups. These findings suggest that probiotic mixtures may be useful probiotics for the treatment of or as alternative therapies for rotaviral gastroenteritis.
A Bacillus sp. that produces fibrinolytic enzyme was isolated from Cheonggukjang, a traditional Korean soybean-fermented food. According to 16S rRNA gene base sequencing, the bacillus was identified as a variety of Bacillus subtilis, and named Bacillus subtilis IDCC 9204. Fibrinolytic enzyme NK-IL9204 was stable up to $60^{\circ}C$ and within pH range of 5-10. Purified NK-IL9204 was detected through fibrin zymography. The molecular weight and isoelectric point of the enzyme were estimated to be 27.7 kDa and 6.7 by SDS-PAGE and 2D electrophoresis, respectively. Its amino acid sequence was similar to that of nattokinase (identities 99.5%) and different from that of nattokinase BPN (identities 86.4%). The plasma fibrinolytic activity of NK-IL9204 was measured by euglobulin clot lysis times (ECLT). The NK-IL9204 was orally administered to SD rats for 3 weeks (1,000 FU/rat/day). The ECLT was significantly shortened by supplementation of NK-IL9204.
In order to study the morphologic changes of the unfixed odontoblasts suspended in phenol solution of several different concentrations, the author carried out the extraction of lower incisor of S-D strain rats to collect the odontoblasts, and the cells obtained were suspended immediately in saline solution. After observing the odontoblasts in fresh state, the saline solution was substituted with 0.125%, 0.25% 0.5%, 1% and 2% diluted phenol solutions. The morphologic changes were examined with phase contrast microscope at intervals of 10, 30, and 60 minutes. The results were as follows: 1. In saline solution the odontoblast showed cytoplasmic swelling, slender cytoplasmic process, thick rim nuclear membrane with increased dark contrast, and prominent nucleoli and chromatin granules with lapse of time intervals. In accordance with time intervals, blisters appeared in the supranuclear zone and increased its size and moved outward of the cytoplasmic membrane resulting detachment from the cell membrane. The phase dark cytoplasmic granules were increased in its dark contrast and in its size. 2. In 0.125% and 0.25% phenol solution, the odontoblasts and its nucleus shrunk immeidately and its contrast of cellular components was increased. With the lapse of time, the phase-dark granules in cytoplasm were aggregated, and several blisters were formed in and out of the cells. The outline of cytoplasmic membrane was also obscured. 3. In 0.5% phenol solution, the necleus shrunk at once, but soon after it revealed karyolysis accompanying dark contrast of neclear components such as nuclear membrane, nucleoli, and chromatin granules. On the contrary, the cytoplasmic granules showed aggregation and increased dark contrast, small and large blisters were formed in and out of the odontblasts and the outline of cytoplasmic membrane became obscured. 4. In 1% phenol solution, it showed shrinkage of odontblasts and its nuclei with thick rim nuclear membrane, aggregation of chromatin granules and occasional karyorrhexis. The dark contrast of cytoplasmic granules was increased and aggregated each other. But the blister formation could not be found. 5. In 2% phenol solution, it showed the shrinkage of odontoblasts and pyknotic nuclei with increased dark contrast of nucleoli and chromatin granules. The number of cytoplasmic granules was decreased by aggregation. But the blister formation could not be found as in 1% phenol solution.
Flavonoids have been shown to affect calcium signaling in neurons. However, there are no reports on the effect of apigenin on glutamate-induced calcium signaling in neurons. We investigated whether apigenin affects glutamate-induced increase of free intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in cultured rat hippocampal neurons, using fura-2-based digital calcium imaging and microfluorimetry. The hippocampal neurons were used between 10 and 13 days in culture from embryonic day 18 rats. Pretreatment of the cells with apigenin ($1{\mu}M$ to $100{\mu}M$) for 5 min inhibited glutamate ($100{\mu}M$, 1 min) induced $[Ca^{2+}]_i$ increase, concentration-dependently. Pretreatment with apigenin ($30{\mu}M$) for 5 min significantly decreased the $[Ca^{2+}]_i$ responses induced by two ionotropic glutamate receptor agonists, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA, $10{\mu}M$, 1 min) and N-methyl-D-aspartate (NMDA, $100{\mu}M$, 1 min), and significantly inhibited the AMPA-induced peak currents. Treatment with apigenin also significantly inhibited the $[Ca^{2+}]_i$ response induced by 50 mM KCl solution, decreased the $[Ca^{2+}]_i$ responses induced by the metabotropic glutamate receptor agonist, (S)-3,5-dihydroxy-phenylglycine (DHPG, 100 $[Ca^{2+}]_i$, 90 s), and inhibited the caffeine (10 mM, 2 min)-induced $[Ca^{2+}]_i$ responses. Furthermore, treatment with apigenin ($30{\mu}M$) significantly inhibited the amplitude and frequency of 0.1 mM $[Mg^{2+}]_o$-induced $[Ca^{2+}]_i$ spikes. These data together suggest that apigenin inhibits glutamate-induced calcium signaling in cultured rat hippocampal neurons.
Purpose : Transcranial electromagnetic stimulation(TMS) is a noninvasive method which stimulates the central nervous system through pulsed magnetic fields without direct effect on the neurons. Although the neurobiologic mechanisms of magnetic stimulation are unknown, the effects on the brain are variable according to the diverse stimulation protocols. This study aims to observe the effect of the magnetic stimulation with two different stimulation methods on the cultured hippocampal slices. Methods : We obtained brains from 8-days-old Spague-Dawley rats and dissected the hippocampal tissue under the microscope. Then we chopped the tissue into 450 µm thickness slices and cultured the hippocampal tissue by Stoppini's method. We divided the inserts, which contained five healthy cultured hippocampal slices respectively, into magnetic stimulation groups and a control group. To compare the different effects according to the frequency of magnetic stimulation, stimulation was done every three days from five days in vitro at 0.67 Hz in the low stimulation group and at 50 Hz in the high stimulation group. After N-methyl-D-aspartate exposure to the hippocampal slices at 14 days in vitro, magnetic stimulation was done every three days in one and was not done in another group. To evaluate the neuronal activity after magnetic stimulation, the $NeuN/{\beta}$-actin ratio was calculated after western blotting in each group. Results : The expression of NeuN in the magnetic stimulation group was stronger than that of the control group, especially in the high frequency stimulation group. After N-methyl-D-aspartate exposure to hippocampal slices, the expression of NeuN in the magnetic stimulation group was similar to that of the control group, whereas the expression in the magnetic non-stimulation group was lower than that of the control group. Conclusion : We suggest that magnetic stimulation increases the neuronal activity in cultured hippocamal slices, in proportion to the stimulating frequency, and has a neuroprotective effect on neuronal damage.
The reactive intermediates formed during the metabolism of therapeutic agents, toxicants and carcinogens by cytochromes P450 are frequently capable of covalently binding to tissue macromolecules and causing tissue damage. It has been shown that YH439, a congener of malotilate, is effective in suppressing hepatic P450 2E1 expression. The present study was designed to further establish the mechanistic basis of YH439 protection against toxicant by assessing its effects against chemical-mediated potentiated hepatotoxicity. Retinoyl palmitate (Vit-A) pretreatment of rats for 7 days substantially enhanced carbon tetrachloride hepatotoxicity, as supported by an ${\sim}5-fold$ increase in serum alanine aminotransferase (ALT) activity, as compared to $CCl_4$ treatment alone. The elevation of ALT activity due to Vit-A was completely blocked by the treatment of $GdCl_3$ a selective inhibitor of Kupffer cell activity. Concomitant pretreatment of rats with both YH439 and Vit-A resulted in a 94% decrease in Vit-A-potentiated $CCl_4$ hepatotoxicity. YH439 was also effective against propyl sulfide-potentiated $CCl_4-induced$ hepatotoxicity. Whereas propyl sulfide (50 mg/kg, 7d) enhanced $CCl_4-induced$ hepatotoxicity by >5-fold, relative to $CCl_4$ treatment alone, concomitant treatment of animals with both propyl sulfide and YH439 at the doses of 100 and 200 mg/kg prevented propyl sulfide-potentiated $CCl_4$ hepatotoxicity by 35% and 90%, respectively. Allyl sulfide, a suppressant of hepatic P450 2E1 expression, completely blocked the propyl sulfide-enhanced hepatotoxicity, indicating that propyl sulfide potentiation of $CCl_4$ hepatotoxicity was highly associated with the expression of P450 2E1 and that YH439 blocked the propyl sulfide-enhanced hepatotoxicity through modulation of P450 2E1 levels. Propyl sulfide- and $CCl_4-induced$ stimulation of lipid peroxidation was also suppressed by YH439 in a dose-related manner, as supported by decreases in malonedialdehyde production. The role of P450 2E1 induction in the potentiation of $CCl_4$ toxicity and the effects of YH439 were further evaluated using pyridine as a P450 2E1 inducer. Pyridine pretreatment substantially enhanced the $CCl_4$ hepatotoicity by 23-fold, relative to $CCl_4$ alone. YH439, however, failed to reduce the pyridine-potentiated toxicity, suggesting that the other form(s) of cytochroms P450 inducible by pyridine, but not suppressible by YH439 treatment, may play a role in potentiating $CCl_4-induced$ hepatotoxicity. YH439 was capable of blocking cadmium chloride-induced liver toxicity in mice. These results demonstrated that YH439 efficiently blocks Vit-A-enhanced hepatotoxiciy through Kupffer cell inactivation and that the suppression of P450 2E1 expression by YH439 is highly associated with blocking of propyl sulfide-mediated hepatotoxicity.
The previous extensive in vitro studies on the antioxidative activities of a number of Korean grains, vegetables, seaweeds and mushrooms, and the various combinations of these food source exhibited a wide range of antioxidative activities, and four food mixtures composed of 5 kinds of foods (5A, 5B, 5C and 5D) were designed from 16 selective foods showing. high antioxidant effect, in vitro, to find the good combinations for the meal planning. Mixture 5B or 5C contained very high levels of total flavonoid and polyphenol, and ethanol extract from 5A, 5B or 5C showed very strong inhibitory effects against in vitro $Fe^{2+}-induced$ lipid peroxidation and ethanol extract from 5B or 5C showed remarkable DPPH radical scavenging effect and lipid peroxide-protein conjugation inhibition effect. And in vivo study was also carried out with two mixtures (5B, 5C). Powders (P5B, P5C) or ethanol extracts (E5B, E5C) of these mixtures were supplemented to Sprague-Dawley rats fed on high fat $(15\%)-high$ cholesterol $(1\%)$ semipurified diet for 5 weeks. The total antioxidant power in serum was significantly higher in P5B, P5C, E5B and E5C groups than in high fat control group, and $ascorbate-Fe^{2+}-induced$ TBARS was significantly lowered by E5B supplementation in rat liver. In liver tissue, Cu, Zn-SOD activity was significantly higher in P5B and E5B groups than in high fat control group, while catalase or GSH-peroxidase (GPx) activity was not changed by any supplementations. In kidney, Cu, ZnSOD activity was significantly higher in P5B group than in high fat control group, while GPx activity was not changed by any supplementations. Taken together, mixture 5B and 5C showed very strong antioxidative effects both in vitro and in vivo. Therefore, the ingredient Korean foods of 5B and 5C could be recommended to take a lot together for prevention from age-related chronic diseases.
Choi, Jong Hee;Jang, Minhee;Kim, Eun-Jeong;Lee, Min Jung;Park, Kyoung Sun;Kim, Seung-Hyun;In, Jun-Gyo;Kwak, Yi-Seong;Park, Dae-Hun;Cho, Seung-Sik;Nah, Seung-Yeol;Cho, Ik-Hyun;Bae, Chun-Sik
Journal of Ginseng Research
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v.44
no.6
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pp.790-798
/
2020
Background: Beneficial effects of Korean Red Ginseng (KRG) on polycystic ovarian syndrome (PCOS) remains unclear. Methods: We examined whether pretreatment (daily from 2 hours before PCOS induction) with KRG extract in water (KRGE; 75 and 150 mg/kg/day, p.o.) could exert a favorable effect in a dehydroepian-drosterone (DHEA)-induced PCOS rat model. Results: Pretreatment with KRGE significantly inhibited the elevation of body and ovary weights, the increase in number and size of ovarian cysts, and the elevation of serum testosterone and estradiol levels induced by DHEA. Pretreatment with KRGE also inhibited macrophage infiltration and enhanced mRNA expression levels of chemokines [interleukin (IL)-8, monocyte chemoattractant protein-1), proinflammatory cytokines (IL-1β, IL-6), and inducible nitric oxide synthase in ovaries induced by DHEA. It also prevented the reduction in mRNA expression of growth factors (epidermal growth factor, transforming growth factor-beta (EGF, TGF-β)) related to inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cell pathway and stimulation of the nuclear factor erythroid-derived 2-related factor 2 pathway. Interestingly, KRGE or representative ginsenosides (Rb1, Rg1, and Rg3(s)) inhibited the activity of inflammatory enzymes cyclooxygenase-2 and iNOS, cytosolic p-IκB, and nuclear p-nuclear factor kappa-light-chain-enhancer of activated B in lipopolysaccharide-induced RAW264.7 cells, whereas they increased nuclear factor erythroid-derived 2-related factor 2 nuclear translocation. Conclusion: These results provide that KRGE could prevent DHEA-induced PCOS via antiinflammatory and antioxidant activities. Thus, KRGE may be used in preventive and therapeutic strategies for PCOS-like symptoms.
Koh, Chang-Soon;Rhee, Chong-Heon;Chang, Ko-Chang;Hong, Chang-Gi D.
The Korean Journal of Nuclear Medicine
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v.3
no.1
/
pp.73-82
/
1969
The newly developed diagnostic method with application of $^{113}Sn-^{113m}In$ cow system ($^{113}Sn:\;T\frac{1}{2}$ 118 days, $^{113m}In:\;T\frac{1}{2}$ 1.7 hrs, 390 Kev, Single ${\gamma}$) has the remarkable advantages such as increased diagnostic ability by single large dose administration of $^{113m}In$ with no subsequent radiation hazard and shortened examining time. We reformed the research of following scope with the use of developed $^{113}Sn-^{113m}In$ cow (25 mCi) generator: The sizes of particles produced under various conditions were investigated, and possibility for application to the scannings of various organs such as brain, liver, lung, bone marrow and blood pool etc. were studied. Results: $^{113m}InCl_3$ solution eluted from diluted HCl solution (pH 1.5) passed through $^{113}Sn-^{113m}In$ generator, and there can be produced various sized particles of colloidal indium. And there observed the state of distribution of $^{113m}In$ in each organ which showed many differences according to the particle sizes of colloidal indium. The results are stated as follows: 1. The adjustment of pH is the most important factor in making the desirable particle size of colloidal indium. The colloid for blood pool showed the highest level as 7.1%/gm blood, at pH 1.7, the colloid of pH 3.5 for liver scanning showed the highest level, 88.4%, in the liver, the colloid pH 6 showed the highest level, 3.1%, in the spleen, and the colloid of pH 11.0 showed the highest level, 85.3%/gm, in the lung. 2. The colloid for liver scanning made with NaCl-NaOH system showed the highest liver uptake at pH 7.2, and at either higher or lower pH than 7.2 showed decrease of liver uptake more or less. 3. The activity of $^{113m}In$ eluted through $^{113}Sn-^{113m}In$ generator indicated over 90% in the initial 4 ml, and particularly 88.1%-86.0% in the initial 2 ml. 4. The incubation time, tempertaure and mechanical irritation related to colloid formation and coating of colloid were not the definite condition of influence.
Benign prostatic hyperplasia (BPH) is the most common urogenital disorder in men, benign tumor and is a typical disease deteriorating the quality of old men's lives, and its prevalence increases with age. Though the molecular pathogenesis of BPH has not yet been clearly revealed, it is known that the variation and aging of the endocrine including sex hormone may cause BPH. Especially the hypertrophy of the prostate cell by the formation of the excessive dihydrotestosterone (DHT) is estimated to cause BPH. If testosterone exists excessively in blood, a lot of DHT is produced in prostate by $5{\alpha}-reductase$. Thus, in this study we tried to analyze haematological change and histopathological change by using the model rat with BPH caused by hypodermic injection of testosterone to prove the effect of Houttuynia cordata extracts on BPH. Rats were divided into four experimental groups: no treatment group (N), the testosterone injection and D.W treatment group (DO), the testosterone injection and Houttuynia cordata treatment group (HO) and testosterone injection and finasteride treatment group (FO). Prostate weight, volume and weight ratio in the HO and FO groups were significantly lower than the DO group. Testosterone and DHT levels in the HO group were significantly lower than the DO group. The HO and FO groups showed trophic symptoms and were lined by flattened epithelial cells, thus, the stromal proliferation is relatively low as compared to the DO group. These results suggest that Houttuynia cordata may control benign prostatic hyperplasia.
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