目的:分析肝炎后肝硬化患者的生活质量与中医证候的相关性,探讨影响肝炎后肝硬化患者生命质量的主要因素。方法:采用新修订的简明健康生存质量(ShortForm-36Health Survey,SF-36)量表测试108例肝炎后肝硬化患者的生命质量分值,并采集肝炎后肝硬化患者相关临床信息,包括性别、年龄、体质量指数(body mass index,BMI)、病程、疾病的共性证候及主要实验室指标等。运用t检验、方差分析和逐步回归筛选影响肝炎后肝硬化患者生活质量的主要因素。结果:修订后的SF-36量表Cronbachsα系数为0.773,提示各项目间内部有良好的一致性。肝炎后肝硬化组修订后SF-36总评分及躯体功能、躯体角色、机体疼痛、心理健康、社会功能的平均评分显著低于正常对照组(P<0.01);相关分析结果提示,肝炎后肝硬化共性证候评分与躯体功能、心理健康、情感角色、活力、总体健康状况具有相关性(均r>0.6,P<0.01);多元逐步回归分析结果显示,在P=0.05水平,中医肝炎后肝硬化共同证候、天冬氨酸氨基转移酶、总胆红素、白蛋白、凝血酶原时间的回归系数分别是0.262、-0.2978、-0.4839、-0.4839、-0.5123、-0.5719,是影响肝炎后肝硬化患者生活质量的主要因素。结论:肝炎后肝硬化患者的生活质量全面下降,纳入疾病中医共性证候的修订后SF-36量表更为客观,对于肝炎后肝硬化患者生活质量的评价具有一定的临床实用价值。
Objective： To investigate the effects of ancient Chinese medical formula Xiayuxue Decoction （下瘀血汤, XYXD） on activation of hepatic stellate cells （HSCs） and defenestration of sinusoidal endothelial cells （SECs） in CCI4-induced fibrotic liver of mice. Methods： High performance liquid chromatography was used to identify the main components of XYXD and control the quality of extraction. C57BL/6 mice were induced liver fibrosis by CCI4 exposure and administered with XYXD for 6 weeks simultaneously. Liver tissue was investigated by hematoxylin-eosin and Sirius-red staining. Sinusoidal fenestrations were observed by scanning electronic microscopy and fluorescent immunohistochemistry of PECAM-1 （CD31）. Whole liver lysates were detected of α-smooth muscle actin （α-SMA） and type-I collagen by Western blot. Primary rat HSCs-T6 cells were analyzed by detecting α-SMA, F-actin, DNA fragmentation through confocal microscopy, Western blot, terminal-deoxynucleoitidyl transferase mediated nick end labeling （TUNEL） assay and cellomics arrayscan, respectively. Results： Amygdalin and emodin in XYXD were identified. XYXD （993 mg/kg） inhibited Sirius red positive area up to 70.1% （P〈0.01）, as well as protein levels of α-SMA and type- I collagen by 42.0% and 18.5% （P〈0.05） respectively. In vitro, XYXD （12.5 μg/mL, 50 μg/mL） suppressed the activation of HSCs and reversed the myofibroblastic HSCs into quiescent, demonstrated as inhibition of fluorescent F-actin by 32.3% and 46.6% （P〈0.05）. Besides, XYXD induced the apoptosis of HSC-T6 cells by 20.0% （P〈0.05） and 49.5% （P〈0.01）, evidenced by enhanced TUNEL positivity. Moreover, ultrastructural observation suggested XYXD inhibited defenestration of SECs, which was confirmed by 31.1% reduction of protein level of CD31 （P〈0.05）. Conclusions： XYXD inhibited both HSCs activation and SECs defenestration which accompany chronic liver injuries. These data may help to understand the underlying mechanisms of XY
