In this paper, through the mutual interpretation and verification of the ancient Korean history books with different origin that have been suspected as false documents, it proves that they could be logically real records and reveal that the substance of the legendary 'medicine for anti-aging and longevity', which also had been mentioned in Chinese old books, is Korean ginseng. Furthermore, with reference to the modern Y chromosomal map of the migratory routes of mankind corresponding to these routes recorded in 「Budoji」, the core history book, the formation of the four ethnic constitution groups (Sasang Constitution) based on the life style of each human group has been estimated. And the cause of Korean ginseng with fever problem for Southeast Asians is their pharmacogenomic constitution problem by protopanaxatriol (PPT) type ginsenosides in ginseng. It was resolved with over production of protopanaxdiol (PPD) type ginsenosides against PPT type in Korean red ginseng as historical or scientific point of view. In addition, by explaining that the processing method to Korean red ginseng could increase red ginseng acidic polysaccharides (RGAP), the RGAP, PPD type ginsenosides, and arginine which is originally abundant in Korean ginseng could increase the expression of the 'heat shock proteins' as a kind of chaperone in the body, this paper presents the theory allowing the scientific interpretation of the efficacy of Korean red ginseng as an 'adaptogen' or 'medicine for anti-aging and longevity'. Lastly, through the consideration of the growing environment of American ginseng and Korean ginseng, the differences are presented.
Po, Wah Wah;Thein, Wynn;Khin, Phyu Phyu;Khing, Tin Myo;Han, Khin Wah Wah;Park, Chan Hee;Sohn, Uy Dong
Biomolecules & Therapeutics
/
v.28
no.2
/
pp.202-210
/
2020
Fluoxetine is used widely as an antidepressant for the treatment of cancer-related depression, but has been reported to also have anti-cancer activity. In this study, we investigated the cytotoxicity of fluoxetine to human gastric adenocarcinoma cells; as shown by the MTT assay, fluoxetine induced cell death. Subsequently, cells were treated with 10 or 20 µM fluoxetine for 24 h and analyzed. Apoptosis was confirmed by the increased number of early apoptotic cells, shown by Annexin V- propidium iodide staining. Nuclear condensation was visualized by DAPI staining. A significant increase in the expression of cleaved PARP was observed by western blotting. The pan-caspase inhibitor Z-VAD-FMK was used to detect the extent of caspase-dependent cell death. The induction of autophagy was determined by the formation of acidic vesicular organelles (AVOs), which was visualized by acridine orange staining, and the increased expression of autophagy markers, such as LC3B, Beclin 1, and p62/SQSTM 1, observed by western blotting. The expression of upstream proteins, such as p-Akt and p-mTOR, were decreased. Autophagic degradation was evaluated by using bafilomycin, an inhibitor of late-stage autophagy. Bafilomycin did not significantly enhance LC3B expression induced by fluoxetine, which suggested autophagic degradation was impaired. In addition, the co-administration of the autophagy inhibitor 3-methyladenine and fluoxetine significantly increased fluoxetine-induced apoptosis, with decreased p-Akt and markedly increased death receptor 4 and 5 expression. Our results suggested that fluoxetine simultaneously induced both protective autophagy and apoptosis and that the inhibition of autophagy enhanced fluoxetine-induced apoptosis through increased death receptor expression.
The purpose of this study was to investigate the aflatoxin $B_1$ binding of lactic acid bacteria (LAB) isolated from Korean traditional soybean paste and to evaluate the effect of incubation conditions and physico-chemical factors on the binding ability of LAB to this mutagen. The amount of aflatoxin $B_1$ bound by Enterococcus faecium DJ22, Lactobacillus fermentum DJ35, Lactobacillus rhamnosus DJ42, and Lactobacillus pentosus DJ47 was strain specific with the percent bound ranging from 19.3% to 52.1%. However, Enterococcus faecalis DJ14, Lactobacillus panis DJ29, and Pediococcus halophilus DJ50 strains did not exhibit any of the binding ability to aflatoxin $B_1$. For most strains, the binding ability was significantly affected by the environmental conditions such as the aflatoxin $B_1$ level, incubation time and temperature, and the initial cell count of LAB. The stability of the aflatoxin $B_1$-bacteria complexes was significantly more unstable after washing. In addition, the binding stability between viable and nonviable cells was not statistically significant. Treatment with heating, acidic pH, ${\alpha}$-amylase, protease, lysozyme, or sodium metaperiodate caused a significant (P<0.05) decrease in aflatoxin $B_1$ binding for the tested strains, suggesting that carbohydrates or proteins in the cell walls may be involved in aflatoxin $B_1$ binding ability. Since the aflatoxin $B_1$ binding of LAB was significantly reduced (P<0.05) by the pretreatment of the urea, the binding force observed in this study may have resulted from hydrophobic interaction.
To characterize glutelins, the most abundant storage protein in rice, 13 complete coding sequences of glutelin genes from the database were analyzed. According to the phylogenic analysis, these genes could be classified into 5 groups, Group I to V. The degrees of homology were calculated to be in the range of 90 to 60%, but the patterns of hydrophobicity were similar in all the groups. Also, each group was found to have similar amino acid composition with variations in lysine content from 2.5 to 3.6% due to the point mutation of arginine to lysine. The isoelectric points of mature proteins and their basic chains of all the groups showed the value of about 9.0 and 10.0, respectively, while the isoelectric points of acidic chains in these groups showed the distinct value of 6.6, 6.7, 7.2, 8.4 and 7.9. The plot of the fraction of G+C at synonimous site in codons (GC3s) against effective codon numbers suggest no major difference in translational efficiency in the expression of glutelin multigenes.
Decalcification is routinely performed to obtain a pathological diagnosis using bone marrow biopsy. During the decalcification process using a conventional acidic solution, such as HCl, the antigenicity of tissue is damaged. Especially DNA and RNA in the bone marrow are impaired. Hence, there is the need for a standardized decalcification protocol that preserves the antigenicity of tissue. To this end, we compared the effects of two commonly used decalcifiers: Commercial decalcifier (Calcl-Clear Rapid, HCl) and the EDTA (12.5%, pH 7.0). Bone marrow biopsies sampled from 71 patients were decalcified in accordance with the protocols of respective groups-HCI versus EDTA. The differences of decalcification protocols were analyzed with respect to Hematoxylin & Eosin staining, Gomori'sreticulum staining, and immunohistochemical staining and molecular analysis. Immunohistochemical staining used Ki-67, CD20 and CD138 as primary antibodies and molecular analysis was conducted through the DNA concentration analysis, in situ hybridization (ISH) and immunoglobulin heavy chain (IGH) gene rearrangement. On the routine histopathology analysis, there was no difference between HCl and EDTA. Moreover, in case of immunohistochemical staining, the cytoplasmic membrane or cytoplasmic CD markers was well preserved. However, nuclear proteins, such as Ki-67, were stained with low quality. Conversely, according to the molecular analysis, the EDTA protocol preserved the DNA and RNA compared with the HCI. The differences of DNA quantity and quality were statistically significant between protocols of HCl and EDTA. We used 38 cases in HCl and 12 cases in EDTA. Consequently, the EDTA protocol maintains the antigenicity of the protein on tissue and is acceptable for examination with molecular base analysis. Decalcification of bone marrow biopsy by EDTA is highly recommended for the examination of immunohistochemical staining and molecular analysis.
Dental caries is initiated by the acid accumulated in dental plaque. Streptococcus mutans, one of a major causal agents of dental caries, is component of the dental plaque and produces various organic acids such as lactic acid as the end-product of glycolysis. As a consequence, we investigated the acid stress response of S. mutans KCTC 3065 in this study. The addition of lactic acid to the growth media had a concentration-dependent effect on the growth of S. mutans. S. mutans exhibited higher maximum culture OD compared with the more acidic growth pH values. At treatment of centration of 20 mmol/L lactic acid in the mid-log phage, cell growth was reduced to 40% relative to the control. The following results were obtained with the treatment of cells with a concentration of 20 mmol/L lactic acid in the mid-log phage for 2hrs: Analysis of fatty acids extracted from cells showed that growth at a concentration of 20 mmol/L lactic acid resulted in changes in $C_{14:0}$, $C_{16:0}$, $C_{18:0}$ and $C_{18:1}$ fatty acids. Protein profiles investigated by SDS-PAGE showed that approximately 70, 60, 45, 40 and 23 kDa proteins were highly expressed in S. mutans KCTC 3065.
Objective : This research investigates the effect of the Jangwon-Dan,(JWD) on Alzheimer's disease. Method : The effects of the JWN extract on (1) $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ mRNA of PC-12 cells treated with LPS; (2) amyloid precursor proteins(APP), acetylcholinesterase(AChE), and glial fibrillary acidic protein(GFAP) mRNA, the AChE activity and the APP production of PC-12 cell treated with CT-105; (3) the behavior; (4) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, $IL-1{\beta}$ mRNA, and $TNF-{\alpha}$ mRNA, (5) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. Result : 1. The JWN extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in THP-1 cells treated with LPS. 2. The JWN extract suppressed the expression of APP, AChE, and GFAP mRNA in PC-12 cells treated with CT-105. 3. The JWN extract suppressed the AChE activity, and the production of APP significantly in PC-12 cells treated with CT-105. 4. For the JWN extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 5. The JWN extract suppressed the over-expression of $IL-1{\beta}$ protein, $TNF-{\alpha}$ protein, MDA, $IL-1{\beta}$ mRNA, $TNF-{\alpha}$ mRNA, and CD68/GFAP, in the mice with Alzheimer's disease induced by ${\beta}A$. 6. The JWN extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusion : These results suggest that the JWN extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the JWN extract for Alzheimer's disease is suggested for future research.
This research investigates the effect of the Hibiscus syriacus(HSS) on Alzheimer's disease. Specifically, the effects of the HSS extract on (1) $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ mRNA of PC-12 cells treated with LPS; (2) amyloid precursor proteins(APP), acetylcholinesterase(AChE), and glial fibrillary acidic protein(GFAP) mRNA of PC-12 cells treated with CT-105; (3) the AChE activity and the APP production of PC-12 cell treated with CT-105; (4) the behavior; (4) expression of $IL-1{\beta}$, $TNF-{\alpha}$, $IL-1{\beta}$ mRNA, $TNF-{\alpha}$ mRNA, and reactive oxygen species(ROS); (5) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. The results were summarized below ; 1. The HSS extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in THP-l cells treated with LPS. 2. The HSS extract suppressed the expression of APP, AChE, and GFAP mRNA in PC-12 cells treated with CT-105. 3. The HSS extract suppressed the AChE activity, and the production of APP significantly in PC-12 cells treated with CT-105. 4. For the HSS extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 5. The HSS extract suppressed the over-expression of $IL-1{\beta}$, $TNF-{\alpha}$, $IL-1{\beta}$ and $TNF-{\alpha}$ mRNA, CD68/GFAP, ROS in the mice with Alzheimer's disease induced by ${\beta}A$. 6. The HSS extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. These results suggest that the HSS extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the HSS extract for Alzheimer's disease is suggested for future research.
Phenyllactic acid (PLA) which is known as antimicrobial compound can be synthesized through the reduction of phenylpyruvic acid (PPA) by lactate dehydrogenase (LDH) of lactic acid bacteria (LAB). LAB producing PLA was isolated from Korea Kimchi and identified to Lactobacillus plantarum SJ21 by 16 rRNA gene sequence analysis. Cell-free supernatant (CFS) from L. plantarum SJ21 was assessed for both the capability to produce the antimicrobial compound PLA and the antifungal activity against four fungal pathogens (Rhizoctonia solani, Aspergillus oryzae, Botrytis cinerea, and Collectotricum aculatum). PLA concentration was investigated to be 3.23mM in CFS when L. plantarum SJ21 was grown in MRS broth containing 5mM PPA for 16 h. PLA production also could be promoted by the supplement of PPA and phenylalanine in MRS broth, but inhibited by the supplement of 4-hydroxyphenylpyruvic acid and tyrosine as precursors. Antifungal activity demonstrated that all fungal pathogens were sensitive to 5% CFS (v/v) of L. plantarum SJ21 with average growth inhibitions ranging from 27.32% to 69.05% (p<0.005), in which R. solani was the most sensitive to 69.05% and followed by B. cinerea, C. aculatum, and A. oryzae. The minimum inhibitory concentration (MIC) for commercial PLA was also investigated to show the same trend in the range from $0.35mg\;mL^{-1}$ (2.11 mM) to $0.7mg\;mL^{-1}$ (4.21 mM) at pH 4.0. The inhibition ability of CFS against the pathogens was not affected by heating or protease treatment. However, pH modification in CFS to 6.5 caused an extreme reduction in their antifungal activity. These results may indicate that antifungal activities in CFS were caused by acidic compounds like PLA or organic acids rather than proteins or peptides molecules.
Seo, Gyoo-Tae;Lee, Eun-Kyung;Choi, Cheol-Hong;Chung, Dae-Kyoo
Journal of Oriental Neuropsychiatry
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v.18
no.2
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pp.101-132
/
2007
Objective : This research investigates the effect of the NogYongDaeBoTang,(NYDBT) on Alzheimer's disease. Method : The effects of the NYDBT extract on (1) $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ mRNA of PC-12 cells treated with LPS; (2) acetylcholinesterase(AChE), amyloid precursor proteins(APP), and glial fibrillary acidic protein(GFAP) mRNA the AChE activity and the APP production of PC-12 cell treated with CT-105; (3) the behavior; (4) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, $IL-1{\beta}$ mRNA, and $TNF-{\alpha}$ mRNA; (5) the infarction area of the hippocampus, and brain tissue injury in Alzheimer‘s diseased mice induced with ${\beta}A$ were investigated. Results : 1. The NYDBT extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in BV2 microglia cell line treated with LPS. 2. The NYDBT extract suppressed the expression of $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ protein production in BV2 microglia cell line treated with LPS. 3. For the NYDBT extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by $A{\beta}$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 4. The NYDBT extract suppressed the over-expression of $IL-1{\beta}$ protein, $TNF-{\alpha}$ protein, MDA, and CD68/CD11b, in the mice with Alzheimer's disease induced by $A{\beta}$. 5. The NYDBT extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by $A{\beta}$. 6. The NYDBT extract reduced the Tau protein, GFAP protein, and presenilin1/2 protein (immunohistochemistry) of hippocampus in the mice with Alzheimer's disease induced by $A{\beta}$. Conclusions : These results suggest that the NYDBT extract may be effective for the prevention and treatment of Alzheimer's disease.
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