• Journal of Microbiology and Biotechnology
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• 제22권12호
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• pp.1629-1635
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• 2012

Previously, we demonstrated that the erythropoietin receptor (EpoR) is present on fibroblasts, where it regulates focal contact. Here, we assessed whether this action of EpoR is involved in the reduced cell adhesion observed in colonocytes exposed to Clostridium difficile toxin A. EpoR was present and functionally active in cells of the human colonic epithelial cell line HT29 and epithelial cells of human colon tissues. Toxin A significantly decreased activating phosphorylations of EpoR and its downstream signaling molecules JAK-2 (Janus kinase 2) and STAT5 (signal transducer and activator of transcription 5). In vitro kinase assays confirmed that toxin A inhibited JAK 2 kinase activity. Pharmacological inhibition of JAK2 (with AG490) abrogated activating phosphorylations of EpoR and also decreased focal contacts in association with inactivation of paxillin, an essential focal adhesion molecule. In addition, AG490 treatment significantly decreased expression of occludin (a tight junction molecule) and tight junction levels. Taken together, these data suggest that inhibition of JAK2 by toxin A in colonocytes causes inactivation of EpoR, thereby enhancing the inhibition of focal contact formation and loss of tight junctions known to be associated with the enzymatic activity of toxin A.

• 한국식품영양과학회지
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• 제29권5호
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• pp.922-934
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• 2000

To investigate the composition of carotenoids present in marine organisms and the biological activity of the carotenoids, carotenoids of the muscles and tunic of tunicates and shellfishes were isolated and identified. Anitmutagenic activities of the carotenoids for S. typhimurium TA 98 and cytotoxic activity for cancer cell lines were determined. Total carotenoid contents in the muscle of tunicata ranged from 18.65 mg% to 2.39 mg%. The highest amount of the total carotenoid was found in the muscle of Halocynthia aurantium, followed by Styela clava (HERDMAN), H. roretzi, H. hilgendorfi f. igaboya, H. hilgendorfi f. retteri, S. plicata (LESUEUR) in order. Interestingly, total carotenoid content in the muscle of S. clava (HERDAMAN) was higher than that of H. roretzi. Total carotenoid content of all tunicata, other than H. aurantium and H. roretzi, were higher in muscle than tunic. The major carotenoids in H. roretzi, H. aurantium, S. plicata (LESUEUR), and S. clava (HERDAMAN) were cynthiaxanthin (25.1∼42.2%), halocynthiaxanthin (9.7∼26.3%), diatoxanthin (8.0∼18.7%) and β-carotene (7.7%∼21.7%). Similarly, cantaxanthin (19.6%), cynthiaxanthin (15.4%), halocynthiaxanthin (14.8%), and (3R, 3'R), (3S, 3'S)-astaxanthin (22.6%) in H. hilgendorfi f. retteri and fucoxanthin (26.6%), cynthiaxanthin (21.8%), halocynthiaxanthin (15.2%), and β-carotene (9.3%) in H. hilgendorfi f. igaboya were major carotenoids in both tunicate. However, the composition of carotenoids in muscle and tunic of tunicata was similar each other. Among the shellfishes examined, total carotenoid content of the muscle of Peronidia venulosa (Schrenck) and Corbicula fluminea, and of the gonad of Atrina pinnata and Chlamys farreri, was ranged from 2.51 to 6.83 mg% which were relatively higher than that of other shellfishes. The composition of the carotenoids of shellfishes, which might depend upon their living environments, was varied. But cynthiaxanthin (15.9∼39.0%) and zeaxanthin (9.6∼21.9%) in gonad of C. farreri, and muscles of Buccinum Volutharpa perryi (JAY) and Crassostrea gigas, cynthiaxanthin (21.5∼48.6%) and mytiloxanthin (14.6%) in muscle of C.fluminea and gonad of A. pinnata, and canthaxanthin (60.6%) and isozeaxanthin (20.5%) in muscles of P. venulosa (Schrenck), and β-carotene (23.7%∼37.8%) and zeaxanthin (18.2∼20.4) in muscles of Semisulcospira libertina and Meretrix lusoria were major carotenoids. Interestingly, diester type-carotenoids were present along with free type-carotenoids in muscles of C. gigas. antimutagenic effect of the carotenoids isolated from tunicata and shellfishes against 2-amino-3-methylimidazol [4,5-f]quinoline (IQ) for S. typhimurium TA 98 was proportional to the amount (20, 50 and 100㎍/plate) treated. Mutagenicity of IQ was significantly reduced by astaxanthin, isozeaxanthin, mytiloxanthin and halocynthiaxanthin, whereas the mutagenicity of aflatoxin B₁(AFB₁) was significantly reduced by β-carotene, isozeaxanthin, and mytiloxnthin. Growth inhibition effect of carotenoids isolated from tunicata and shellfishes for cancer cell was proportional to the amount (5, 10, and 20㎍/plate) treated. The growth of HeLa cell by β-carotene, cynthiaxanthin, astaxanthin and halocynthiaxanthin, NCI-H87 cell by β-carotene, astaxanthin, cynthiaxanthin, and halocynthiaxanthin, HT-29 cell by β-carotene, cynthiaxanthin, mytiloxanthin and halocynthiaxanthin, and MG-63 cells by β-carotene, cynthiaxanthin, astaxanthin, canthaxanthin and halocynthiaxanthin were statistically reduced.

• BMB Reports
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• 제56권4호
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• pp.234-239
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• 2023

Thioredoxin-like protein 1 (TXNL1), one of the thioredoxin superfamily known as redox-regulator, plays an essential in maintaining cell survival via various antioxidant and anti-apoptotic mechanisms. It is well known that relationship between ischemia and oxidative stress, however, the role of TXNL1 protein in ischemic damage has not been fully investigated. In the present study, we aimed to determine the protective role of TXNL1 against on ischemic injury in vitro and in vivo using cell permeable Tat-TXNL1 fusion protein. Transduced Tat-TXNL1 inhibited ROS production and cell death in H₂O₂-exposed hippocampal neuronal (HT-22) cells and modulated MAPKs and Akt activation, and pro-apoptotic protein expression levels in the cells. In an ischemia animal model, Tat-TXNL1 markedly decreased hippocampal neuronal cell death and the activation of astrocytes and microglia. These findings indicate that cell permeable Tat-TXNL1 protects against oxidative stress in vitro and in vivo ischemic animal model. Therefore, we suggest Tat-TXNL1 can be a potential therapeutic protein for ischemic injury.

• Mycobiology
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• 제40권3호
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• pp.181-188
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• 2012

This study was initiated in order to investigate the anticancer and immunomodulating activities of crude polysaccharides extracted in methanol, neutral saline, and hot water (hereinafter referred to as Fr. MeOH, Fr. NaCl, and Fr. HW, respectively) from the fruiting bodies of Panellus serotinus. Content of ${\beta}$-glucan and protein in Fr. MeOH, Fr. NaCl, and Fr. HW extracts of P. serotinus ranged from 22.92~28.52 g/100 g and 3.24~3.68 g/100 g, respectively. In vitro cytotoxicity tests, none of the various fractions of crude polysaccharides were cytotoxic against sarcoma 180, HT-29, NIH3T3, and RAW 264.7 cell lines at the tested concentration. Intraperitoneal injection with crude polysaccharides resulted in a life prolongation effect of 23.53~44.71% in mice previously inoculated with sarcoma 180. Treatment with Fr. HW resulted in an increase in the numbers of spleen cells by 1.3 fold at the concentration of $50{\mu}g/mL$ compared with control. Treatment with Fr. NaCl resulted in improvement of the immuno-potentiating activity of B lymphocytes by increasing the alkaline phosphatase activity by 1.4 fold, compared with control, at the concentration of $200{\mu}g/mL$. Among the three fractions, maximum nitric oxide ($13.48{\mu}M$) was recorded at $500{\mu}g/mL$ in Fr. HW. Production of tumor necrosis factor alpha, interleukin-$1{\beta}$, and interleukin-6 was significantly higher, compared to the positive control, concanavalin A, at the tested concentration. Therefore, treatment with crude polysaccharides extracted from the fruiting body of P. serotinus could result in improvement of antitumor activity.

• Journal of Ginseng Research
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• 제44권3호
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• pp.442-452
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• 2020

Backgroud: Sleep deprivation (SD) impairs learning and memory by inhibiting hippocampal functioning at molecular and cellular levels. Abnormal autophagy and apoptosis are closely associated with neurodegeneration in the central nervous system. This study is aimed to explore the alleviative effect and the underlying molecular mechanism of stem-leaf saponins of Panax notoginseng (SLSP) on the abnormal neuronal autophagy and apoptosis in hippocampus of mice with impaired learning and memory induced by SD. Methods: Mouse spatial learning and memory were assessed by Morris water maze test. Neuronal morphological changes were observed by Nissl staining. Autophagosome formation was examined by transmission electron microscopy, immunofluorescent staining, acridine orange staining, and transient transfection of the tf-LC3 plasmid. Apoptotic event was analyzed by flow cytometry after PI/annexin V staining. The expression or activation of autophagy and apoptosis-related proteins were detected by Western blotting assay. Results: SLSP was shown to improve the spatial learning and memory of mice after SD for 48 h, accomanied with restrained excessive autophage and apoptosis, whereas enhanced activation of phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway in hippocampal neurons. Meanwhile, it improved the aberrant autophagy and apoptosis induced by rapamycin and re-activated phosphoinositide 3-kinase/Akt/mammalian target of rapamycin signaling transduction in HT-22 cells, a hippocampal neuronal cell line. Conclusion: SLSP could alleviate cognitive impairment induced by SD, which was achieved probably through suppressing the abnormal autophagy and apoptosis of hippocampal neurons. The findings may contribute to the clinical application of SLSP in the prevention or therapy of neurological disorders associated with SD.