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 : Guo Jianshuang (검색결과 1 건)
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        ACT001 alleviates inflammation and pyroptosis through the PPAR-γ/NF-κB signaling pathway in LPS-induced alveolar macrophages

        Fu Qiang,Shen Na,Fang Tao,Zhang Hewei,Di Yanbo,Liu Xuan,Du Chao,Guo Jianshuang 한국유전학회 2024 Genes & Genomics Vol.46 No.3

        Background ACT001 is an anti-inflammatory agent that has been widely investigated for its role in tumors, intracranial diseases, and fibrotic diseases, but its effect on acute lung injury is less known. Objective The purpose of this study was to investigate the effect and mechanism of ACT001 on regulating inflammation and pyroptosis in lipopolysaccharide (LPS)-induced alveolar macrophages. Methods NR8383 alveolar macrophages treated with LPS were used to replicate the proinflammatory macrophage phenotype observed during acute lung injury. After ACT001 treatment, we measured the secretion and expression levels of critical inflammatory cytokines, the rate of pyroptosis, and the expression of NLRP3 inflammasome-associated proteins and pyroptosis-associated proteins. In addition, we assessed the role of the PPAR-γ/NF-κB signaling pathways and further validated the results with a PPAR-γ inhibitor. Results Our findings confirmed that ACT001 reduced the expression and release of inflammatory factors, attenuated cell pyroptosis, and downregulated the expression of NLRP3, ASC, caspase-1 p20, and GSDMD-N. These effects may be achieved by activating PPAR-γ expression and then inhibiting the NF-κB signaling pathway. When macrophages were treated with the PPAR-γ inhibitor, the protective effects of ACT001 were reversed. Conclusion ACT001 significantly ameliorated inflammation and pyroptosis via the PPAR-γ/NF-κB signaling pathways in LPS-induced NR8383 alveolar macrophages. Background ACT001 is an anti-inflammatory agent that has been widely investigated for its role in tumors, intracranial diseases, and fibrotic diseases, but its effect on acute lung injury is less known. Objective The purpose of this study was to investigate the effect and mechanism of ACT001 on regulating inflammation and pyroptosis in lipopolysaccharide (LPS)-induced alveolar macrophages. Methods NR8383 alveolar macrophages treated with LPS were used to replicate the proinflammatory macrophage phenotype observed during acute lung injury. After ACT001 treatment, we measured the secretion and expression levels of critical inflammatory cytokines, the rate of pyroptosis, and the expression of NLRP3 inflammasome-associated proteins and pyroptosis-associated proteins. In addition, we assessed the role of the PPAR-γ/NF-κB signaling pathways and further validated the results with a PPAR-γ inhibitor. Results Our findings confirmed that ACT001 reduced the expression and release of inflammatory factors, attenuated cell pyroptosis, and downregulated the expression of NLRP3, ASC, caspase-1 p20, and GSDMD-N. These effects may be achieved by activating PPAR-γ expression and then inhibiting the NF-κB signaling pathway. When macrophages were treated with the PPAR-γ inhibitor, the protective effects of ACT001 were reversed. Conclusion ACT001 significantly ameliorated inflammation and pyroptosis via the PPAR-γ/NF-κB signaling pathways in LPS-induced NR8383 alveolar macrophages.

      맨처음 페이지로1맨끝 페이지로

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼