RISS 학술연구정보서비스

검색
자동완성 버튼
다국어입력
다국어 입력
あ ぁ か が さ ざ た だ な は ば ぱ ま や ゃ ら わ ゎ ん い ぃ き ぎ し じ ち ぢ に ひ び ぴ み り う ぅ く ぐ す ず つ づ っ ぬ ふ ぶ ぷ む ゆ ゅ る え ぇ け げ せ ぜ て で ね へ べ ぺ め れ お ぉ こ ご そ ぞ と ど の ほ ぼ ぽ も よ ょ ろ を
ア ァ カ サ ザ タ ダ ナ ハ バ パ マ ヤ ャ ラ ワ ヮ ン イ ィ キ ギ シ ジ チ ヂ ニ ヒ ビ ピ ミ リ ウ ゥ ク グ ス ズ ツ ヅ ッ ヌ フ ブ プ ム ユ ュ ル エ ェ ケ ゲ セ ゼ テ デ ヘ ベ ペ メ レ オ ォ コ ゴ ソ ゾ ト ド ノ ホ ボ ポ モ ヨ ョ ロ ヲ ―

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
ㅥ ㅦ ㅧ ㅨ ㅩ ㅪ ㅫ ㅬ ㅭ ㅮ ㅯ ㅰ ㅱ ㅲ ㅳ ㅴ ㅵ ㅶ ㅷ ㅸ ㅹ ㅺ ㅻ ㅼ ㅽ ㅾ ㅿ ㆀ ㆁ ㆂ ㆃ ㆄ ㆅ ㆆ ㆇ ㆈ ㆉ ㆊ ㆋ ㆌ ㆍ ㆎ
Α Β Γ Δ Ε Ζ Η Θ Ι Κ Λ Μ Ν Ξ Ο Π Ρ Σ Τ Υ Φ Χ Ψ Ω α β γ δ ε ζ η θ ι κ λ μ ν ξ ο π ρ σ τ υ φ χ ψ ω
á à Á À é è É È ç Ç ê
Ä Ö Ü ä ö ü ß
ְ ֳ ֲ ֱ ָ ַ ֵ ֶ ִ ֹ ּ ֻ ׂ ׁ ּ פ ם ן ו ט א ר ק ף ך ל ח י ע כ ג ד ש ץ ת צ מ נ ה ב
‘ ’ “ ” 〔 〕 〈 〉 「 」 『 』 【 】 ＂ （ ） ［ ］ ｛ ｝
± × ÷ ≠ ≤ ≥ ∞ ∴ ♂ ♀ ∠ ⊥ ⌒ ∂ ∇ ≡ ≒ ≪ ≫ √ ∽ ∝ ∵ ∫ ∬ ∈ ∋ ⊆ ⊇ ⊂ ⊃ ∪ ∩ ∧ ∨ ￢ ⇒ ⇔ ∀ ∃ ∮ ∑ ∏ ＋ － ＜ ＝ ＞
、 。 · ‥ … ¨ 〃 ― ∥ ＼ ∼ ´ ～ ˇ ˘ ˝ ˚ ˙ ¸ ˛ ¡ ¿ ː ！ ＇ ， ． ／ ： ； ？ ＾ ＿ ｀ ｜
½ ⅓ ⅔ ¼ ¾ ⅛ ⅜ ⅝ ⅞ ¹ ² ³ ⁴ ⁿ ₁ ₂ ₃ ₄
Æ Ð Ħ IJ Ł Ø Œ Þ Ŧ Ŋ æ đ ð ħ ı ij ĸ ŀ ł ø œ ß þ ŧ ŋ ʼn
А Б В Г Д Е Ё Ж З И Й К Л М Н О П Р С Т У Ф Х Ц Ч Ш Щ Ъ Ы Ь Э Ю Я а б в г д е ё ж з и й к л м н о п р с т у ф х ц ч ш щ ъ ы ь э ю я
′ ″ ℃ Å ￠ ￡ ￥ ¤ ℉ ‰ ＄ ％ Ｆ ￦ ㎕ ㎖ ㎗ ℓ ㎘ ㏄ ㎣ ㎤ ㎥ ㎦ ㎙ ㎚ ㎛ ㎜ ㎝ ㎞ ㎟ ㎠ ㎡ ㎢ ㏊ ㎍ ㎎ ㎏ ㏏ ㎈ ㎉ ㏈ ㎧ ㎨ ㎰ ㎱ ㎲ ㎳ ㎴ ㎵ ㎶ ㎷ ㎸ ㎹ ㎀ ㎁ ㎂ ㎃ ㎄ ㎺ ㎻ ㎽ ㎾ ㎿ ㎐ ㎑ ㎒ ㎓ ㎔ Ω ㏀ ㏁ ㎊ ㎋ ㎌ ㏖ ㏅ ㎭ ㎮ ㎯ ㏛ ㎩ ㎪ ㎫ ㎬ ㏝ ㏐ ㏓ ㏃ ㏉ ㏜ ㏆
§ ※ ☆ ★ ○ ● ◎ ◇ ◆ □ ■ △ ▽ → ← ↑ ↓ ↔ 〓 ◁ ◀ ▷ ▶ ♤ ♠ ♡ ♥ ♧ ♣ ⊙ ◈ ▣ ◐ ◑ ▒ ▤ ▥ ▨ ▧ ▦ ▩ ♨ ☏ ☎ ☜ ☞ † ‡ ↕ ↗ ↙ ↖ ↘ ♭ ♩ ♪ ♬ ㉿ ㈜ № ㏇ ™ ㏂ ㏘ ℡ ＃ ＆ ＊ ＠ ª º
ⅰ ⅱ ⅲ ⅳ ⅴ ⅵ ⅶ ⅷ ⅸ ⅹ Ⅰ Ⅱ Ⅲ Ⅳ Ⅴ Ⅵ Ⅶ Ⅷ Ⅸ Ⅹ
ا ب ت ث ج ح خ د ذ ر ز س ش ص ض ط ظ ع غ ف ق ک ل م ن ه و ی
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      검색키워드
      저자 : Mu Yanfei (검색결과 1 건)
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        Allylpyrocatechol ameliorates sepsis-induced lung injury via SIRT1-mediated suppression of p65 and nucleocytoplasmic translocation of HMGB1

        Mu Yanfei,Mu Xiaosong,Yang Yan,Zhou Yanhong 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4

        Background Sepsis is a deadly clinical condition. Allylpyrocatechol is bioactive flavonoid that has shown promising anti-inflammatory and antioxidant activity. The effects of allylpyrocatechol on sepsis-induced lung injury have not been fully established. Objective This study investigated the effects of allylpyrocatechol in a mouse model of sepsis-induced lung injury. Results RAW264.7 macrophages were used for in vitro studies. A mouse model of sepsis was established by cecal ligation and puncture (CLP). The PaO2/FiO2 ratio was measured in conjunction with lung tissue histology, and edema was determined by the wet:dry tissue ratio. ELISA was performed to analyze levels of IL-6, TNF-α, NOx, and HMGB1. Malondialdehyde (MDA) levels were measured to determine lipid peroxidation status. Protein expression was investigated via Western blotting analyses. Molecular docking studies were done to study the affinity of SIRT1 with Allylpyrocatechol. It was observed that Allylpyrocatechol inhibited the production of HMGB1 and suppressed pro-inflammatory responses in macrophages treated with bacterial lipopolysaccharide (LPS) in vitro, and in CLP sepsis mice in vivo. Moreover, it ameliorated the reduction of SIRT1 levels in both LPS-treated macrophages and CLP mice, alleviated sepsis-induced lung edema, reduced lipid peroxidation, improved lung tissue histology findings, reduced mortality, and improved the PaO2/FiO2 ratio in CLP mice. Allylpyrocatechol caused significant reductions in serum levels of IL-6, nitric oxide, TNF-α, and HMGB1, as well as nuclear translocation of inducible nitric oxide synthase, SIRT1, and HMGB1 in lungs of CLP mice. Molecular docking analysis suggested affinity of SIRT1 with Allylpyrocatechol. Conclusion The findings suggest that Allylpyrocatechol protects mice against lung injury via SIRT1-mediated suppression of HMGB1 nuclear translocation and p-p65 activation. Background Sepsis is a deadly clinical condition. Allylpyrocatechol is bioactive flavonoid that has shown promising anti-inflammatory and antioxidant activity. The effects of allylpyrocatechol on sepsis-induced lung injury have not been fully established. Objective This study investigated the effects of allylpyrocatechol in a mouse model of sepsis-induced lung injury. Results RAW264.7 macrophages were used for in vitro studies. A mouse model of sepsis was established by cecal ligation and puncture (CLP). The PaO2/FiO2 ratio was measured in conjunction with lung tissue histology, and edema was determined by the wet:dry tissue ratio. ELISA was performed to analyze levels of IL-6, TNF-α, NOx, and HMGB1. Malondialdehyde (MDA) levels were measured to determine lipid peroxidation status. Protein expression was investigated via Western blotting analyses. Molecular docking studies were done to study the affinity of SIRT1 with Allylpyrocatechol. It was observed that Allylpyrocatechol inhibited the production of HMGB1 and suppressed pro-inflammatory responses in macrophages treated with bacterial lipopolysaccharide (LPS) in vitro, and in CLP sepsis mice in vivo. Moreover, it ameliorated the reduction of SIRT1 levels in both LPS-treated macrophages and CLP mice, alleviated sepsis-induced lung edema, reduced lipid peroxidation, improved lung tissue histology findings, reduced mortality, and improved the PaO2/FiO2 ratio in CLP mice. Allylpyrocatechol caused significant reductions in serum levels of IL-6, nitric oxide, TNF-α, and HMGB1, as well as nuclear translocation of inducible nitric oxide synthase, SIRT1, and HMGB1 in lungs of CLP mice. Molecular docking analysis suggested affinity of SIRT1 with Allylpyrocatechol. Conclusion The findings suggest that Allylpyrocatechol protects mice against lung injury via SIRT1-mediated suppression of HMGB1 nuclear translocation and p-p65 activation.

      맨처음 페이지로1맨끝 페이지로

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼