• 제목/요약/키워드: Huizhou Medicine

검색결과 3건 처리시간 0.021초

명(明)·청시대(淸時代)의 신안(新安)(휘주(徽州))의학(醫學)-유(儒)·상(商)·의(醫) 삼위일체(三位一體)의 문화구조(文化構造) (Huizhou Medicine (Xīn'ān medicine) in the Ming-Ching Dynasty -The Confucian-Merchants-Doctors triad(triarchy) in the culture & structure)

  • 이민호;안상우
    • 한국의사학회지
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    • 제22권2호
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    • pp.15-22
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    • 2009
  • In this thesis, the emphasis is laid especially on the culture & structure of Huizhou Province, China as the prime mover of the specifically-regional Huizhou $X{\bar{i}}n^{\prime}{\bar{a}}n$ medicine. Huizhou was the home town & stronghold of Neo-coufucian masters Cheng-Zhu (Cheng brothers and Zhu-hsi)". The tradition of the region as "The arts province" resulted in the flourishing trend of nurturing prominent Confucian-doctors. The remarkable all round activities of Huizhou Merchants (新安商人 $X{\bar{i}}n^{\prime}{\bar{a}}nsh{\bar{a}}ngr{\acute{e}}n$), as the reigning power merchant at the period were the second mover of the Zeitgeist. Their nation-wide network all over China made it possible to gain valuable inlormation and access to news including the field of medicine in time. Some merchants actually have "abandoned their own jobs to become doctors of medicine". This Confucian-Merchant culture was one of intrinsic characteristics of Huizhou region, inducing "Pragmatic Scholarship". With the enlargement of the population of Confucian-tumed doctors and improvement of the societal status of doctors, the resultant occupational triad of local Confucian govemment officials, local $X{\bar{i}}n^{\prime}{\bar{a}}nsh{\bar{a}}ngr{\acute{e}}n$ merchants, and local doctors was established after the Middle-Ming Dynasty. Ultimately, the two prime movers of the concomitant development of medicine in the Province Huizhou in this study are concluded to be the synergy effects of the Neo-Confucian tradition and economic power of the prevalent Huizhou Merchants ($X{\bar{i}}n^{\prime}{\bar{a}}nsh{\bar{a}}ngr{\acute{e}}n$).

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Ginsenoside Ro, an oleanolic saponin of Panax ginseng, exerts anti-inflammatory effect by direct inhibiting toll like receptor 4 signaling pathway

  • Xu, Hong-Lin;Chen, Guang-Hong;Wu, Yu-Ting;Xie, Ling-Peng;Tan, Zhang-Bin;Liu, Bin;Fan, Hui-Jie;Chen, Hong-Mei;Huang, Gui-Qiong;Liu, Min;Zhou, Ying-Chun
    • Journal of Ginseng Research
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    • 제46권1호
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    • pp.156-166
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    • 2022
  • Background: Panax ginseng Meyer (P. ginseng), a herb distributed in Korea, China and Japan, exerts benefits on diverse inflammatory conditions. However, the underlying mechanism and active ingredients remains largely unclear. Herein, we aimed to explore the active ingredients of P. ginseng against inflammation and elucidate underlying mechanisms. Methods: Inflammation model was constructed by lipopolysaccharide (LPS) in C57BL/6 mice and RAW264.7 macrophages. Molecular docking, molecular dynamics, surface plasmon resonance imaging (SPRi) and immunofluorescence were utilized to predict active component. Results: P. ginseng significantly inhibited LPS-induced lung injury and the expression of proinflammatory factors, including TNF-α, IL-6 and IL-1β. Additionally, P. ginseng blocked fluorescencelabeled LPS (LPS488) binding to the membranes of RAW264.7 macrophages, the phosphorylation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs). Furthermore, molecular docking demonstrated that ginsenoside Ro (GRo) docked into the LPS binding site of toll like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD2) complex. Molecular dynamic simulations showed that the MD2-GRo binding conformation was stable. SPRi demonstrated an excellent interaction between TLR4/ MD2 complex and GRo (KD value of 1.16 × 10-9 M). GRo significantly inhibited LPS488 binding to cell membranes. Further studies showed that GRo markedly suppressed LPS-triggered lung injury, the transcription and secretion levels of TNF-α, IL-6 and IL-1β. Moreover, the phosphorylation of NF-κB and MAPKs as well as the p65 subunit nuclear translocation were inhibited by GRo dose-dependently. Conclusion: Our results suggest that GRo exerts anti-inflammation actions by direct inhibition of TLR4 signaling pathway.