萱草花黄酮对免疫性肝损伤小鼠保护作用及机制  

Protective effect of Hemerocallis citrina baroni flavonids on autoimmune liver injury and its mechanism in mice

作　　者：沈楠[1] 黄晓东[1] 王艳春[1] 齐玲[1] 徐博[1] 陈雪[1] 安英[1] 刘婷婷[2] 

机构地区：[1]吉林医药学院基础医学院,吉林吉林132001 [2]吉林医药学院附属医院病理科

出　　处：《中国公共卫生》2017年第2期202-205,共4页Chinese Journal of Public Health

基　　金：吉林省教育厅基金资助课题(2013359)

摘　　要：目的探讨萱草花黄酮对免疫性肝损伤小鼠保护作用及凋亡相关基因bax、bcl-2表达变化。方法使用卡介苗和脂多糖制备小鼠免疫性肝损伤模型,将60只昆明小鼠随机分为对照组、模型组、低、中、高剂量萱草花黄酮(15、30、60 mg/kg)组。苏木素-伊红染色观察肝组织病理损伤程度;比色法测定肝组织中超氧化物歧化酶(SOD)、丙二醛和谷胱甘肽过氧化物酶(GSH-Px)含量;生化分析仪检测血清中谷丙转氨酶(ALT)含量;免疫组化法检测肝脏bax、bcl-2表达。结果与对照组比较,模型组小鼠血清中ALT水平[(105.48±46.34)U/L]、丙二醛含量[(8.57±0.54)nmol/mgprot]明显升高,SOD与GSH-Px活力[分别为(168.14±13.21)、(95.32±1.48)U/mgprot]明显下降(P<0.01);与模型组比较,30、60 mg/kg萱草花黄酮组小鼠血清中ALT水平[分别为(56.38±26.31)、(59.77±13.34)U/L]、丙二醛含量[分别为(5.37±0.34)、(5.52±0.38)nmol/mgprot]降低(P<0.05),SOD与GSH-Px活力[分别为(197.40±25.22)、(249.41±24.08)与(107.32±1.83)、(114.24±1.41)U/mgprot]升高(P<0.05);与对照组比较,模型组小鼠肝脏bax基因表达上调,bcl-2基因表达下调(P<0.0 5);与模型组比较,萱草花黄酮小鼠肝脏bax表达下调,bcl-2表达上调(P<0.05)。结论萱草花黄酮对小鼠免疫性肝损伤具有一定保护作用,其机制可能与提高小鼠抗氧化能力、下调促凋亡基因bax表达、上调抗凋亡基因bcl-2表达有关。Objective To study protective effect of Hemerocallis citrina baroni flavonids （HCBF） on autoimmune liver injury and the influence of HCBF on expressions of BCL-2-associated X protein （bax） and B cell lymyhoma/leuke- mia-2 protein （bcl-2） in mice. Methods The diabetic nephropathy （DN） mice model was established by injections of Bacillus Calmette-Guerin （BCG） and lipopolysaccharide （LPS）. Sixty male Kunming mice were randomly divided into five groups ： a control group, a DN model gourp, and low, moderate, and high treatment groups with HCBF of 15,30,60 mg/kg, respectively. Liver pathological changes were observed with hematoxylin-eosin staining. The contents of superoxide dismutase （SOD）, malondialdehyde （MDA） and glutathione-peroxidase （GSH-Px） were measured with colorimetry. Serum alanine aminotransferase （ALT） was detected with biochemistry analyzer. The expressions of bax and bcl-2 were determined with immunohistochemistry. Results Compared to those of the controls, serum ALT （ 105.48 ± 46. 34 U/L） and MDA （8.57 ±0. 54 nmol/mgprot） increased but SOD （ 168.14 ± 13.21 U/mgprot） and GST-Px （95.32 ±1.48 U/mgprot） decreased in the mice of model group significantly （P 〈0. 01 for all）. Compared to those of the mice of the model group,serum ALT （56. 38 ± 26. 31 and 59. 77 ±/3.34 U/L） and MDA （5. 37 ± 0. 34 and 5.52 ± 0. 38 nmol/mgprot） decreased but SOD （ 197.40 ± 25.22 and 249.41 ± 24.08 nmol/mgprot） and GST-Px （ 107.32±1.83 and 114. 24 ± 1.41 U/mgprot） increased significantly for the mice of 30 and 60 mg/kg HCBF treatment groups （ P 〈 0. 05 for all）. Compared to the mice in the control ,the expression of bax was up-regulated but the expression of bcl-2 was down-regulated for the mice in the model group （both P 〈 0. 05 ）. Compared to the mice in the model group, the expression of bax was down-regulated but the expression of bcl-2 was up-regulated for the mice in the HCBF treatment groups （ P 〈 0. 05 for all）.

关 键 词：萱草花黄酮 免疫性肝损伤 氧化应激 凋亡 

分 类 号：R657.3[医药卫生—外科学]