丁酸钠对肝性脑病大鼠血氨浓度的影响初探
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摘要
目的观察不同浓度丁酸钠对肝性脑病(HE)大鼠血氨浓度的影响以及对HE的防治效果。方法采用腹腔注射硫代乙酰胺(TAA)诱导急性肝性脑病模型。饲喂两周后造模两天,观察大鼠一般情况,并进行神经反射评级,血浆TBil、DBil、AST、ALT、血氨和肠道p H值等指标的测定。结果丁酸钠各组HE大鼠TBil、DBil、ALT、AST均有所下降,其中丁酸钠A组的肠道p H值较模型组差异有统计学意义(P<0.05),丁酸钠A、B两组的血氨浓度较模型组明显降低(P均<0.001)。丁酸钠处理可改善大鼠的神经反射,降低大鼠肝性脑病的分期。结论丁酸钠通过酸化肠道,降低HE大鼠的血氨浓度,进而改善HE大鼠所表现出来的精神症状。
Objective To observe the effect of ammonia concentrations and the preventing and treating effects on hepatic encephalopathy(HE) in rats by different concentrations of sodium butyrate. Methods The hepatic encephalopathy rat models were induced by intraperitoneal injection thioacetamide(TAA) after fed two weeks made mould for two days. General condition and the nerve refl ection, the level of TBil, DBil, ALT, AST, NH3 in serum, the intestinal p H values and liver histopathology were detected. Results TBil, DBil, ALT, AST of each sodium butyrate groups were decreased. The intestinal p H value of sodium butyrate group A compared with model group was statistically significant(P < 0.05), blood ammonia concentrations of sodium butyrate group A and group B were significantly lower than that in model group(P < 0.001). In addition, sodium butyrate treatment can improve neuro-refl ex, decrease the staging of HE. Conclusions The results indicated that the ammonia concentrations can be reduced because of the souring of the intestinal tract by sodium butyrate, which could also improve the psychiatric symptoms of the hepatic encephalopathy.
Objective To observe the effect of ammonia concentrations and the preventing and treating effects on hepatic encephalopathy(HE) in rats by different concentrations of sodium butyrate. Methods The hepatic encephalopathy rat models were induced by intraperitoneal injection thioacetamide(TAA) after fed two weeks made mould for two days. General condition and the nerve refl ection, the level of TBil, DBil, ALT, AST, NH3 in serum, the intestinal p H values and liver histopathology were detected. Results TBil, DBil, ALT, AST of each sodium butyrate groups were decreased. The intestinal p H value of sodium butyrate group A compared with model group was statistically significant(P < 0.05), blood ammonia concentrations of sodium butyrate group A and group B were significantly lower than that in model group(P < 0.001). In addition, sodium butyrate treatment can improve neuro-refl ex, decrease the staging of HE. Conclusions The results indicated that the ammonia concentrations can be reduced because of the souring of the intestinal tract by sodium butyrate, which could also improve the psychiatric symptoms of the hepatic encephalopathy.
引文
[1]葛均波,徐永健.内科学[M].第8版.北京:人民卫生出版社,2013:434-438.
[2]金惠铭,王建枝.病理生理学[M].第7版.北京:人民卫生出版社,2008:237-245.
[3]杨莉丽,邹兵,王俊萍,等.乳果糖和益生菌制剂预防肝性脑病的临床疗效观察[J].中国医药导报,2011,8:75-76.
[4]Velazquez OC,Lederer HM,Rombeau JL.Butyrate and the colonocyte.Production,absorption,metabolism,and therapeutic implications[J].Adv Exp Med Biol,1997,427:123-134.
[5]韩晓风,王鹏远,马元元,等.丁酸钠对腹膜炎小鼠肠道屏障功能的保护[J].中华实验外科杂志,2012,2:1765-1767.
[6]刘赫,梁妍,刘雁勇,等.地黄苏合香合剂对轻微肝性脑病模型大鼠治疗的实验研究[J].中国康复理论与实践,2012,16:904-906.
[7]邱华毛,德文,韦艾凌.大黄煎剂对急性肝衰竭大鼠肝性脑病防治机制的实验研究[J].中国中医急症,2007,16:195-197.
[8]张美华,贾林,杜洪,等.硫代乙酰胺致大鼠肝性脑病模型的量-效关系[J].广州医学院学报,2004,32:72-74.
[9]陆伦根.肝性脑病的发病机制[J].中华肝脏病杂志,2004,12:304-304.
[10]许瑞玲,尹镭,陈贤明,等.暴发性肝衰血脑屏障通透性改变对肝性脑病发生发展的影响[J].中国病理生理杂志,1994,10:160-163.
[11]周勤飞,王永才.丁酸钠对动物肠道影响及其应用进展[J].家畜生态学报,2009,30:104-105.
[12]李军,周祯祥.生大黄对肝性脑病大鼠肿瘤坏死因子-α和血氨水平的影响[J].中国中医急症,2011,20:1265-1266.
[13]Faijam M,Dehdab P,Abbassnia F,et al.Thioacetamide-induced acute hepatic encephalopathy in rat:behavioral,biochemical and histological changes[J].Iran Red Crescent Med J,2012,14:164-170.
[14]狄茜,李扬.丁酸钠对前列腺癌PC-3M细胞的增殖抑制和凋亡诱导作用[J].吉林大学学报(医学版),2004,9:710-712.
[15]姚咏明,徐珊,盛志勇.高迁移率族蛋白B1的组织损伤效应及其干预途径[J].中国医学科学医学报,2007,29:459-465.
[2]金惠铭,王建枝.病理生理学[M].第7版.北京:人民卫生出版社,2008:237-245.
[3]杨莉丽,邹兵,王俊萍,等.乳果糖和益生菌制剂预防肝性脑病的临床疗效观察[J].中国医药导报,2011,8:75-76.
[4]Velazquez OC,Lederer HM,Rombeau JL.Butyrate and the colonocyte.Production,absorption,metabolism,and therapeutic implications[J].Adv Exp Med Biol,1997,427:123-134.
[5]韩晓风,王鹏远,马元元,等.丁酸钠对腹膜炎小鼠肠道屏障功能的保护[J].中华实验外科杂志,2012,2:1765-1767.
[6]刘赫,梁妍,刘雁勇,等.地黄苏合香合剂对轻微肝性脑病模型大鼠治疗的实验研究[J].中国康复理论与实践,2012,16:904-906.
[7]邱华毛,德文,韦艾凌.大黄煎剂对急性肝衰竭大鼠肝性脑病防治机制的实验研究[J].中国中医急症,2007,16:195-197.
[8]张美华,贾林,杜洪,等.硫代乙酰胺致大鼠肝性脑病模型的量-效关系[J].广州医学院学报,2004,32:72-74.
[9]陆伦根.肝性脑病的发病机制[J].中华肝脏病杂志,2004,12:304-304.
[10]许瑞玲,尹镭,陈贤明,等.暴发性肝衰血脑屏障通透性改变对肝性脑病发生发展的影响[J].中国病理生理杂志,1994,10:160-163.
[11]周勤飞,王永才.丁酸钠对动物肠道影响及其应用进展[J].家畜生态学报,2009,30:104-105.
[12]李军,周祯祥.生大黄对肝性脑病大鼠肿瘤坏死因子-α和血氨水平的影响[J].中国中医急症,2011,20:1265-1266.
[13]Faijam M,Dehdab P,Abbassnia F,et al.Thioacetamide-induced acute hepatic encephalopathy in rat:behavioral,biochemical and histological changes[J].Iran Red Crescent Med J,2012,14:164-170.
[14]狄茜,李扬.丁酸钠对前列腺癌PC-3M细胞的增殖抑制和凋亡诱导作用[J].吉林大学学报(医学版),2004,9:710-712.
[15]姚咏明,徐珊,盛志勇.高迁移率族蛋白B1的组织损伤效应及其干预途径[J].中国医学科学医学报,2007,29:459-465.