基于肺虚络瘀理论探究肺间质纤维化的凝血机制
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辽宁省“兴辽英才计划”项目(XLYC1808011)


Study on Coagulation Mechanism of Pulmonary Interstitial Fibrosis Based on the Theory of Lung Deficiency and Collateral Stasis
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    摘要:

    肺间质纤维化发病机制复杂,近些年的研究证实Th1/Th2细胞因子失衡、细胞外基质重塑、成纤维细胞活化增殖、血液凝血机制、局部炎性反应浸润、肺泡上皮损伤等方面学说均在其发病过程中起到重要作用。本文从体内凝血机制角度探究在肺间质纤维化发病中,凝血—纤溶机制的异常改变所起的作用,并提出“肺虚络瘀”的中医现代辨证论治理念,治疗上以“补虚通络”为治则治疗肺间质纤维化,为中医理论指导下治疗肺间质纤维化提供新的理论依据与治疗方法。

    Abstract:

    The pathogenesis of pulmonary interstitial fibrosis is complex.Recent studies have demonstrated that imbalance of Th1/Th2 cytokines, remodeling of extracellular matrix, activation and proliferation of fibroblasts, blood coagulation mechanism, local inflammatory infiltration and alveolar epithelial injury play an important role in its onset.This paper explores the role of abnormal changes in the mechanism of coagulation-fibrinolysis during the onset of pulmonary interstitial fibrosis from the perspective of coagulation mechanism in vivo, and puts forward a modern concept of syndrome differentiation in traditional Chinese medicine(TCM), “lung deficiency and collateral stasis”.“Tonifying deficiency and dredging collateral” is the principle of treatment in pulmonary interstitial fibrosis, providing a new theoretical basis and therapy for the treatment of pulmonary interstitial fibrosis under the guidance of TCM theory.

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朱凌云,吕晓东,高嘉营.基于肺虚络瘀理论探究肺间质纤维化的凝血机制[J].世界中医药,2020,(03).

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  • 收稿日期:2018-11-06
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  • 在线发布日期: 2020-03-16
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