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基于线粒体功能障碍论中药防治特发性肺纤维化的研究进展 被引量:2

Research progress of traditional Chinese medicine in prevention and treatment of idiopathic pulmonary fibrosis based on mitochondrial dysfunction
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摘要 中医药防治特发性肺纤维化优势显著。线粒体是负责加工、生成人体能量的重要细胞器,线粒体功能障碍引起的代谢障碍、氧化应激损伤、动力学失衡、钙紊乱及线粒体DNA突变与特发性肺纤维化密切相关。基于国内外学者持续关注,维持线粒体功能对治疗特发性肺纤维化至关重要,为中医药干预防治特发性肺纤维化拓展新思路。文章以此新视角作一综述,以期探索改善线粒体功能的中医药靶点,为中药防治特发性肺纤维化提供理论基础。 Traditional Chinese medicine has significant advantages in preventing and treating idiopathic pulmonary fibrosis.Mitochondria is an important organelle responsible for processing and generating human energy.Metabolic disorder,oxidative stress damage,dynamic imbalance,calcium disorder and mitochondrial DNA mutation caused by mitochondrial dysfunction are closely related to idiopathic pulmonary fibrosis.Based on the continuous attention of scholars both domestically and internationally,maintaining mitochondrial function is crucial for the treatment of idiopathic pulmonary fibrosis,expanding new ideas for the prevention and treatment of idiopathic pulmonary fibrosis with traditional Chinese medicine intervention.This article provides a review from this new perspective,with the aim of exploring traditional Chinese medicine targets for improving mitochondrial function,and providing a theoretical basis for the prevention and treatment of idiopathic pulmonary fibrosis with traditional Chinese medicine.
作者 张馨心 吕晓东 庞立健 臧凝子 ZHANG Xin-xin;LYU Xiao-dong;PANG Li-jian;ZANG Ning-zi(Liaoning University of Traditional Chinese Medicine,Shenyang 110847,China;The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110032,China)
出处 《中华中医药杂志》 CAS CSCD 北大核心 2023年第6期2715-2720,共6页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 辽宁省“兴辽英才计划”高水平创新团队(No.XLYC1808011) 辽宁省科技厅重大研发项目(No.2019JH2/10300023) 沈阳市科技局公共卫生研发专项计划项目(No.20-205-4-056)。
关键词 线粒体 功能障碍 特发性肺纤维化 中医药 防治 Mitochondria Dysfunction Idiopathic pulmonary fibrosis Traditional Chinese medicine Prevention and treatment
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  • 1夏豪,李庚山,许家琍,蒋锡嘉.三七总皂甙对动脉损伤后血管平滑肌细胞增殖曲线的影响[J].中国中西医结合杂志,2000,20(S1):10-11. 被引量:2
  • 2于洁,高传玉,许文克,张连仲.超声检查和血管造影对兔动脉粥样硬化狭窄模型的评价[J].中国临床康复,2006,10(40):51-53. 被引量:9
  • 3RUSSELL P B,MIKE N,KARRIE W,et al.Role of extracellular superoxide dismutase in bleomycin-induced pulmonary fibrosis[J].Am J Physiol Lung Cell Mol Physiol,2002,282(4):L719-L726.
  • 4VELSOR L W,KARIYA C,KACHADOURIAN R.Mitochondrial oxidative stress in the lungs of cystic fibrosis transmembrane conductance regulator protein mutant mice[J].Am J Respir Cell Mol Biol,2006,35(5):579-586.
  • 5CHUA F,GAULDIE J,LAURENT G J.Pulmonary fibrosis:searching for model answers[J].Am J Respir Cell Mol Biol,2005,33(1):6891-6900.
  • 6GONG P,HU B,STEWART D,et al.Cobalt induces heme oxygenase21 expression by a hypoxia-inducible factor-independent mechanism in Chinese hamster ovary cells:regulation by Nrf2 and MafG transcription factors[J].J Biol Chem,2001,276(29):27018-27025.
  • 7IZBICKI G,SEGEL M J,CHRISTENSEN T G,et al.Time course of bleomycin-induced lungfibrosis[J].Int J Exp Path,2002,83(3):111-119.
  • 8SHINFIZU S,TSUJIMOTO Y.Proapoptotic BH3-only Bcl-2 family members induce cytochrome crelease.but not mitochondrial membrane potential loss.and do not directly modulate voltage dependent anion channel activity[J].Pro Natl Acad Sci U S A,2000,97(2):577-582.
  • 9LIN H H,HSU H L,YEH N H.Apoptotic cleavage of NuMA at the C-terminal end is related to nuclear disruption and death amplification[J].J Biomed Sci,2007,14(5):681-694.
  • 10CROW M T,MANI K,NAM Y J,et al.The mitochondrial death pathway and cardiac myocyte apoptosis[J].Circ Res,2004,95(10):957-970.

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