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- 저자 : Tina Huang (검색결과 4 건)
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Huang, Yun,Kwan, Kenneth Kin Leung,Leung, Ka Wing,Yao, Ping,Wang, Huaiyou,Dong, Tina Tingxia,Tsim, Karl Wah Keung The Korean Society of Ginseng 2019 Journal of Ginseng Research Vol.43 No.4
Background: The root of Panax ginseng, a member of Araliaceae family, has been used as herbal medicine and functional food in Asia for thousands of years. According to Traditional Chinese medicine, ginseng is the most widely used "Qi-invigorating" herbs, which provides tonic and preventive effects by resisting oxidative stress, influencing energy metabolism, and improving mitochondrial function. Very few reports have systematically measured cell mitochondrial bioenergetics after ginseng treatment. Methods: Here, H9C2 cell line, a rat cardiomyoblast, was treated with ginseng extracts having extracted using solvents of different polarity, i.e., water, 50% ethanol, and 90% ethanol, and subsequently, the oxygen consumption rate in healthy and tert-butyl hydroperoxideetreated live cultures was determined by Seahorse extracellular flux analyzer. Results: The 90% ethanol extracts of ginseng possessed the strongest antioxidative and tonic activities to mitochondrial respiration and therefore provided the best protective effects to H9C2 cardiomyocytes. By increasing the spare respiratory capacity of stressed H9C2 cells up to three-folds of that of healthy cells, the 90% ethanol extracts of ginseng greatly improved the tolerance of myocardial cells to oxidative damage. Conclusion: These results demonstrated that the low polarity extracts of ginseng could be the best extract, as compared with others, in regulating the oxygen consumption rate of cultured cardiomyocytes during mitochondrial respiration.
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Yun Huang,Kenneth Kin Leung Kwan,Ka Wing Leung,Ping Yao,HuaiyouWang,Tina Tingxia Dong,Karl Wah Keung Tsim 고려인삼학회 2019 Journal of Ginseng Research Vol.43 No.4
Background: The root of Panax ginseng, a member of Araliaceae family, has been used as herbal medicineand functional food in Asia for thousands of years. According to Traditional Chinese medicine, ginseng isthe most widely used “Qi-invigorating” herbs, which provides tonic and preventive effects by resistingoxidative stress, influencing energy metabolism, and improving mitochondrial function. Very few reportshave systematically measured cell mitochondrial bioenergetics after ginseng treatment. Methods: Here, H9C2 cell line, a rat cardiomyoblast, was treated with ginseng extracts having extractedusing solvents of different polarity, i.e., water, 50% ethanol, and 90% ethanol, and subsequently, theoxygen consumption rate in healthy and tert-butyl hydroperoxideetreated live cultures was determinedby Seahorse extracellular flux analyzer. Results: The 90% ethanol extracts of ginseng possessed the strongest antioxidative and tonic activities tomitochondrial respiration and therefore provided the best protective effects to H9C2 cardiomyocytes. Byincreasing the spare respiratory capacity of stressed H9C2 cells up to three-folds of that of healthy cells,the 90% ethanol extracts of ginseng greatly improved the tolerance of myocardial cells to oxidativedamage. Conclusion: These results demonstrated that the low polarity extracts of ginseng could be the bestextract, as compared with others, in regulating the oxygen consumption rate of cultured cardiomyocytesduring mitochondrial respiration.
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Kenneth Kin Leung Kwan,Huang Yun,Tina Ting Xia Dong,Karl Wah Keung Tsim 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.4
Background: Mitochondrial dysfunction is one of the significant reasons for Alzheimer"s disease (AD). Ginsenosides, natural molecules extracted from Panax ginseng, have been demonstrated to exert essential neuroprotective functions, which can ascribe to its anti-oxidative effect, enhancing central metabolism and improving mitochondrial function. However, a comprehensive analysis of cellular mitochondrial bioenergetics after ginsenoside treatment under Aβ-oxidative stress is missing. Methods: The antioxidant activities of ginsenoside Rb₁, Rd, Re, Rg₁ were compared by measuring the cell survival and reactive oxygen species (ROS) formation. Next, the protective effects of ginsenosides of mitochondrial bioenergetics were examined by measuring oxygen consumption rate (OCR) in PC12 cells under Aβ-oxidative stress with an extracellular flux analyzer. Meanwhile, mitochondrial membrane potential (MMP) and mitochondrial dynamics were evaluated by confocal laser scanning microscopy. Results: Ginsenoside Rg₁ possessed the strongest anti-oxidative property, and which therefore provided the best protective function to PC12 cells under the Ab oxidative stress by increasing ATP production to 3 folds, spare capacity to 2 folds, maximal respiration to 2 folds and non-mitochondrial respiration to 1.5 folds, as compared to Aβ cell model. Furthermore, ginsenoside Rg1 enhanced MMP and mitochondrial interconnectivity, and simultaneously reduced mitochondrial circularity. Conclusion: In the present study, these results demonstrated that ginsenoside Rg₁ could be the best natural compound, as compared with other ginsenosides, by modulating the OCR of cultured PC12 cells during oxidative phosphorylation, in regulating MMP and in improving mitochondria dynamics under Aβ-induced oxidative stress.
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The Role of Inflammatory Mediators in the Pathogenesis of Otitis Media and Sequelae
Steven K. Juhn,정민교,Mark D. Hoffman,Brian R. Drew,Diego A. Preciado,Nicholas J. Sausen,Timothy T.K. Jung,Bo Hyung Kim,박상유,Jizhen Lin,Frank G. Ondrey,David R. Mains,Tina Huang 대한이비인후과학회 2008 Clinical and Experimental Otorhinolaryngology Vol.1 No.3
This review deals with the characteristics of various inflammatory mediators identified in the middle ear during otitis media and in cholesteatoma. The role of each inflammatory mediator in the pathogenesis of otitis media and cholesteatoma has been discussed. Further, the relation of each inflammatory mediator to the pathophysiology of the middle and inner ear along with its mechanisms of pathological change has been described. The mechanisms of hearing loss including sensorineural hearing loss (SNHL) as a sequela of otitis media are also discussed. The passage of inflammatory mediators through the round window membrane into the scala tympani is indicated. In an experimental animal model, an application of cytokines and lipopolysaccharide (LPS), a bacterial toxin, on the round window membrane induced sensorineural hearing loss as identified through auditory brainstem response threshold shifts. An increase in permeability of the blood-labyrinth barrier (BLB) was observed following application of these inflammatory mediators and LPS. The leakage of the blood components into the lateral wall of the cochlea through an increase in BLB permeability appears to be related to the sensorineural hearing loss by hindering K+ recycling through the lateral wall disrupting the ion homeostasis of the endolymph. Further studies on the roles of various inflammatory mediators and bacterial toxins in inducing the sensorineumral hearing loss in otitis media should be pursued.
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