首页|期刊导航|北京中医药大学学报|从肝郁脾虚与线粒体自噬的相关性探讨中枢疲劳的病理机制

从肝郁脾虚与线粒体自噬的相关性探讨中枢疲劳的病理机制OA北大核心CSTPCD

Exploration on the pathological mechanism of central fatigue from the correlation between liver stagnation and spleen deficiency and mitophagy

中文摘要英文摘要

中枢疲劳系因精神压力过大或躯体活动过度导致中枢神经系统发生病变,从而表现出一系列疲劳症状.目前中枢疲劳的病理机制尚不明确,以线粒体自噬为代表的线粒体质量控制途径与中枢疲劳的发生发展密切相关.中医学认为,肝郁脾虚是中枢疲劳的关键病机.本文认为,氧化应激可能是中枢疲劳发生的重要基础,能量代谢障碍是肝失疏泄、脾失健运的具体表现,而活性氧的异常积累是中枢疲劳的病理产物.因此,基于氧化应激与能量代谢,从线粒体自噬的角度探讨中枢疲劳肝失疏泄、脾失健运的病理机制具有丰富的理论内涵,可为中枢疲劳的临床治疗提供理论借鉴.

Central fatigue refers to the central nervous system disease caused by excessive mental pressure or excessive physical activity,which shows a series of fatigue symptoms.The pathological mechanism of central fatigue remains unclear,and the mitochondrial quality control pathway represented by mitophagy is closely related to the occurrence and development of central fatigue.Traditional Chinese medicine considers liver stagnation and spleen deficiency as the key pathogenesis of central fatigue.This paper suggests that oxidative stress may be an important basis for the occurrence of central fatigue,energy metabolism disorders are specific manifestations of liver's failure of conveyance and dispersion and spleen's failure of healthy transportation,and the abnormal accumulation of reactive oxygen can be regarded as pathological products of central fatigue.Therefore,based on oxidative stress and energy metabolism,the pathologic mechanism of liver's failure of conveyance and dispersion and spleen's failure of healthy transportation in central fatigue from the perspective of mitophagy has a rich theoretical connotation,and provides a theoretical reference for the clinical treatment of central fatigue.

张翼飞;于清茜;施晴寰;兰碧娟;张泽涵;李峰

北京中医药大学中医学院 北京 102488

中医学

中枢疲劳线粒体自噬肝郁脾虚氧化应激能量代谢

central fatiguemitophagyliver depression and spleen deficiencyoxidative stressenergy metabolism

《北京中医药大学学报》 2024 (012)

1661-1667 / 7

国家自然科学基金面上项目(No.81874428);国家自然科学基金青年科学基金项目(No.82204978) National Natural Science Foundation of China(Nos.81874428 and 82204978)

10.3969/j.issn.1006-2157.2024.12.005

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