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铁调蛋白在大鼠酒精性肝损伤中的保护作用及其机制

Protective effect and mechanism of hepcidin in rats with alcoholic liver damage

摘要:

目的 研究铁调蛋白在酒精性肝损伤中的作用机制.方法 30只雄性wistar大鼠随机分为对照组、酒精组及铁调蛋白组,饲养6周后处死.检测血清ALT、AST、铁、总铁结合力(TIBC)、铁蛋白、丙二醛及铁调蛋白含量;肝组织行HE染色、普鲁士蓝铁染色及免疫组织化学染色,观察肝组织病理学改变.结果 (1)对照组、酒精组和铁调蛋白组的血清ALT值分别为(25.2±4.6)U/L、(37.9±14.3)U/L和(40.9±14.1)U/L,F=4.907,P<0.05,差异有统计学意义;血清AST分别为(32.3±13.4)U/L、(55.0±18.6)U/L和(48.3±26.0)U/L,F=3.742,P<0.05,差异有统计学意义.铁蛋白含量分别为(224.72±85.49)ng/ml、(345.59±124.75)ng/ml和(339.47±138.47)ng/ml,F=3.539,P<0.05,差异有统计学意义.血清TIBC值分别为(147.30±31.98)μmol/L、(148.04±58.74)μmol/L和(143.28±37.38)μmol/L,F=1.209,P>0.05,差异无统计学意义.血清铁含量分别为(55.64±13.32)μmol/L、(60.37±25.89)μmol/L和(49.77±17.64)μmol/L,F=0.651,P>0.05,差异无统计学意义.血清丙二醛含量分别为(5.84±2.17)nmol/ml、(6.51±2.23)nmol/ml和(4.27±2.68)nmol/ml,F=2.782,P>0.05,差异无统计学意义.血清铁调蛋白含量分别为(155.96±44.91)ng/ml、(124.11±31.98)ng/ml和(114.96±25.81)ng/ml,F=3.839,P<0.05,差异有统计学意义.(2)组织学显示酒精组肝细胞明显脂肪变,铁调蛋白组肝细胞脂肪病变较酒精组有所改善.对照组、酒精组和铁调蛋白组每5个高倍视野(×400)的肝脏铁染颗粒数分别为(0.8±1.0)个、(1.2±1.6)个和(1.1±1.1)个,F=0.254,P>0.05,差异无统计学意义.肝脏免疫组织化学每5个高倍视野(×400)阳性细胞数分别为(15.0±8.1)个、(6.6±4.2)个和(7.6±3.2)个,F=4.139,P<0.05,差异有统计学意义.结论 酒精性肝病大鼠的铁调蛋白表达下降,伴铁代谢紊乱.补充铁调蛋白可以通过抑制脂质过氧化反应改善肝脏损伤.

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abstracts:

Objective To study the mechanism of how iron-regulatory protein (hepcidin) affect iron overload in alcoholic liver disease (ALD). Methods Thirty male wistar rats were randomly divided into 3 groups:Lieber-Decarli liquid without alcohol group (control group), Lieber-Decarli liquid with alcohol (alcohol group) and hepcidin intraperitoneally injected group (hepcidin group), each rat was fed for 6 weeks. The Serum concentration of Alanine Aminotransferase (ALT), Aspartate Amino Transferase (AST), Iron, Total Iron Binding capacity (TIBC), Ferritin, Malonyl Dialdehyde (MDA) and Hepcidin were determined. Hepatic tissue was examined by hematoxylin and eosin staining, prussian blue iron staining and immunohistochemisty staining. Results (1) Serum concentration of ALT in control group, alcohol group and hepcidin group were (25.2 ± 4.6) U/L, (37.9 ± 14.3) U/L and (40.9 ± 14.1) U/L (F = 4.907, P < 0.05), respectively. Serum AST among three groups were (32.3 ± 13.4) U/L, (55.0 ± 18.6) U/L and (48.3 ± 26.0) U/L (F = 3.742, P < 0.05),respectively. The secretions of ferritin were (224.72 ± 85.49) ng/ml, (345.59 ± 124.75) ng/ml and (339.47 ±138.47) ng/ml (F = 3.539, P < 0.05). The serum concentrations of TIBC were (147.30 ± 31.98) μ mol/L,(148.04 ± 58.74) μmol/L and (143.28 ± 37.38) μmol/L (F = 1.209, P > 0.05), respectively. The serum concentrations of iron were (55.64 ± 13.32) μmol/L, (60.37 ± 25.89) μmol/L and (49.77 ± 17.64) μmol/L (F = 0.651, P > 0.05), respectively. The serum concentration of MDA were (5.84 ± 2.17) nmol/ml, (6.51 ±2.23) nmol/ml and (4.27 ± 2.68) nmol/ml (F = 2.782, P > 0.05), respectively. The serum concentration of Hepeidin were ( 155.96 ± 44.91 )ng/ml, (124.11 ± 31.98) ng/ml and ( 114.96 ± 25.81 ) ng/ml (F = 3.839, P <0.05), respectively. (2) Significant fat change observed in the liver of alcohol group. The positive granulationes of iron staining were (0.8 ± 1.0), (1.2 ± 1.6) and (1.1 ± 1.1) (F = 0.254, P > 0.05), respectively. No differences found of liver iron express among the three groups. Intraperitoneal injection of hepcidin increased hepcidin expression in liver which was inhibited by alcohol (F= 4.139, P < 0.05). Conclusion ALD rats with lower hepcidin expression in liver can result in iron metabolism disorder. Ectogenic hepcidin can protect liver against alcohol damage by inhibiting lipid peroxidation.

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作者: 冀杨 [1] 张亚南 [2] 康熙雄 [2] 徐有青 [1] 王晨 [1]
期刊: 《中华肝脏病杂志》2011年19卷4期 301-304页 MEDLINEISTICPKUCSCDCA
分类号: R5
栏目名称: 其他肝病|%Other liver disease
DOI: 10.3760/cma.j.issn.1007-3418.2011.04.016
发布时间: 2011-06-14
基金项目:
北京市自然科学基金资助项目
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