摘要
目的围绕线粒体蛋白质控(mitochondrial protein quality control, MPQC)探讨脾气虚小肠黏膜细胞线粒体损伤的可能机制。方法 16只雄性SD大鼠随机分为正常组和脾气虚证(模型)组,每组8只;透射电镜观察小肠黏膜细胞线粒体超微结构;分离小肠黏膜细胞线粒体,比色法检测其ATP含量和呼吸链复合物(complex, C)I-IV活性,Western blot法检测呼吸链CV、热休克蛋白70,Lon蛋白酶,酪蛋白裂解蛋白酶XP(caseinolytic protease XP,ClpXP)表达。结果与正常组比较,模型组线粒体嵴减少,ATP水平下降(P<0.05),呼吸链CIII和IV活性及CV表达降低(P<0.01,P<0.01,P<0.05),ClpX和ClpP表达均升高(均P<0.01)。结论脾气虚小肠黏膜细胞线粒体结构和功能损伤与其MPQC异常有关。
Objective To explore the possible mechanism of mitochondrial impairment of small intestinal mucosal cells(SIMCs) in spleen Qi deficiency based on the mitochondrial protein quality control(MPQC). Methods 16 male SD rats were randomly divided into normal and spleen Qi deficiency(model) groups with 8 in each group;transmission electron microscopy was used to observe mitochondrial ultrastructures in SIMCs;after mitochondria in SIMCs were isolated, colorimetry was chosen to test respiratory chain complex(C) I-IV activities, western blot was utilized to detect expressions of respiratory chain CV, hot shock protein 70, Lon protease and caseinolytic protease XP(ClpXP).Results Compared with those in the normal group, the number of mitochondrial cristae was reduced, the ATP level was decreased(P<0.05), respiratory chain CIII and IV activities and CV expression were all reduced(P<0.01,P<0.01,P<0.05), ClpX and ClpP expressions were both increased(Ps<0.01), in the model group.Conclusion Ultrastructural and functional impairment of mitochondria of SIMCs in spleen qi deficiency might be related to abnormality of the MPQC.
作者
孟相泽
刘文俊
许欣竹
马丹
王路
王凌志
于化新
刘慧慧
单德红
MENG Xiang-zhe;LIU Wen-jun;XU Xin-zhu;MA Dan;WANG Lu;WANG Ling-zhi;YU Hua-xin;LIU Hui-hui;SHAN De-hong(Liaoning University of Traditional Chinese Medicine,Shenyang 110847,China)
出处
《时珍国医国药》
CAS
CSCD
北大核心
2020年第5期1258-1260,共3页
Lishizhen Medicine and Materia Medica Research
基金
国家自然科学基金(81673851)。
关键词
脾气虚
小肠黏膜
线粒体蛋白质控
热休克蛋白70
Lon蛋白酶
酪蛋白裂解蛋白酶XP
Spleen Qi deficiency
Small intestinal mucosa
Mitochondrial protein quality control
Hot shock protein 70
Lon protease
Caseinolytic protease XP
