机构地区:[1]浙江省中西医结合医院消化科,杭州310003
出 处:《浙江中西医结合杂志》2016年第5期430-433,510,共5页Zhejiang Journal of Integrated Traditional Chinese and Western Medicine
基 金:浙江省医药卫生科技项目(No.2011RCB029)
摘 要:目的观察大黄素对肝硬化大鼠高动力循环状态下肠屏障完整性的维持作用。方法 SD雄性大鼠25只,随机分为对照组5只、肝硬化模型组10只、大黄素干预组10只,模型组与干预组予500m L/L四氯化碳(3m L/100g)皮下注射复制肝硬化大鼠模型,对照组大鼠给予生理盐水(3m L/100g)皮下注射,均为8周。干预组制模第15天起予大黄素(5mg/m L,5m L/kg)灌胃,对照组和模型组每日给予相当体积的生理盐水灌胃,均1天1次。8周后处死大鼠,行墨汁推进试验测定肠道传输功能,测定门脉压力,血清生化指标测定,取末端回肠组织及肝脏组织观察组织病理学改变,肠黏膜TUNEL凋亡检测。结果 (1)大鼠小肠黏膜损伤:模型组>干预组>对照组(P<0.05)。(2)门脉压力:模型组(13.73±1.81)mm Hg,较对照组(5.64±0.88)mm Hg显著升高(P<0.05),大鼠明显处于高循环状态;干预组门脉压力(10.25±1.47)mm Hg,较模型组明显降低(P<0.05)。(3)血清生化指标(ALT、AST、TB、ALP)水平:模型组[(594.22±317.82)U/L,(1008.33±778.70)U/L,(6.00±5.29)μmol/L,(802.78±396.94)U/L]较对照组[(60.20±21.30)U/L,(149.80±43.03)U/L,(1.00±0.44)μmol/L,(196.20±31.29)U/L]显著升高(P<0.05);干预组[(292.20±140.12)U/L,(350.40±173.35)U/L,(2.49±1.10)μmol/L,(552.20±303.37)U/L]较模型组明显降低(P<0.05);ALB模型组(16.29±1.26)g/L较对照组(23.42±1.56)g/L明显下降(P<0.05),干预组(18.89±1.02)g/L较模型组明显上升(P<0.05)。(4)肠道黑染百分比:模型组(68.05±2.09)%,较对照组(81.68±3.15)%明显减少(P<0.05);干预组(74.50±4.28)%,较模型组明显增加(P<0.05)。(5)肠黏膜凋亡小体:模型组明显多于对照组,而干预组大黄素干预后的小肠上皮细胞凋亡较模型组明显下降。结论大黄素对肝硬化大鼠高动力循环状态下肠屏障完整性有较好的维持作用。Objective To investigate the effects of emodin on intestinal mucosal barrier in cirrhotic rats with portal hypertension. Methods Twenty-five male SD rats were randomly divided into three groups:control group(n=5), model group(n=10), and emodin group(n=10).The model was induced by thesubcutaneous injection of 500 m L/L CCL4(3m L/100 g, twice a week for 8 weeks), then was intragastrically given saline in model group or emodin(5mg/m L, 5m L/kg, once a day)in emodin group from Day 15. Control group received normal saline(3m L/100g). At 8weeks, rats were sacrificed to determine the changes of Ink propelling test, portal pressure, and serum variable and biopsies from the terminal ileum and liver were made for histology and apoptosis body detection with TUNEL. Results The degree of intestinal mucosal injury was the severest in model group, followed by emodin group and control group(P〈0.05). The portal pressure in model group was higher than that in control group(13.73±1.81 mm Hg vs 5.64±0.88 mm Hg, P〈0.05), indicating a hyperkinetic circulatory state; that in emodin group(10.25±1.47 mm Hg)was lower than that in model group(P〈0.05). ALT, AST, TB, and ALP in model group(594.22 ±317.82U/L,1008.33±778.70U/L, 6.00±5.29μmol/L, 802.78±396.94U/L) were higher than those in control group(60.20±21.30U/L,149.80±43.03U/L, 1.00±0.44μmol/L, 196.20±31.29U/L) and in emodin group(292.20±140.12U/L, 350.40±173.35U/L,2.49±1.10μmol/L 552.20±303.37U/L), ALB in model group(16.29 ±1.26g/L) was lower than that in control group(23.42±1.56g/L) and emodin group(18.89±1.02g/L)(all P〈0.05). The percentage of dyed intestinal black in model group(68.05%±2.09%) was lower than that in control group(81.68%±3.15%) and emodin group(74.50%±4.28%)(all P〈0.05). The number of apoptosis body in model group was more than that in control group and emodin group.Conclusion Emodin could protect intestinal mucosal barrier in the hyperkinetic circulat
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