期刊文献+

葛根素对胰岛素抵抗-高血压大鼠自由基损伤的拮抗作用 被引量:7

Antagonistic effect of puerarin on injury of free radical in insulin-resistant-hypertensive rats
暂未订购
导出
摘要 目的:观察葛根素对胰岛素抵抗-高血压大鼠自由基损伤的作用。方法:①实验于2003-12/2004-03在广州市中医中药研究所药理教研室完成。选用出生6~8d的健康SD大鼠71只,雌雄不拘。②随机抽出20只为正常对照组,饮用蒸馏水和喂饲普通饲料;其余大鼠给予饮用50g/L蔗糖水和20g/L盐水及喂饲高脂高盐高糖饲料造成胰岛素抵抗-高血压病理模型。造模8周后,挑选血压和糖耐量异常的胰岛素抵抗-高血压造模成功大鼠51只,随机分为5组:模型组(n=11)、卡托普利组(n=10)、葛根素高剂量组(n=10)、葛根素中剂量组(n=10)、葛根素低剂量组(n=10)。各组均照上述方法继续造模4周。同时,正常对照组和模型组:肌肉注射500g/L丙二醇,0.8mL/kg,1次/d,共4周;卡托普利组:肌肉注射卡托普利注射液7mg/kg,1次/d,共4周;葛根素高、中、低剂量组:按华兴帮《大鼠穴位图谱的研制》及《实验动物与动物实验》中的取穴方法,选取大鼠双侧足三里(后三里)、脾俞、肾俞,按80,40,20mg/kg给予葛根素进行穴位注射,每天1组穴位,交替使用,1次/d,共4周。③分别给药4周后,用大鼠血压仪测定大鼠尾动脉收缩压;用ONETOUCHⅡ血糖仪测定大鼠血糖;采用生化分析仪测定血清一氧化氮水平及一氧化氮合酶、丙二醛、超氧化歧化酶活性和空腹血糖水平;用酶联免疫分析仪测定血浆胰岛素含量,计算胰岛素敏感指数[1/(空腹血糖×空腹胰岛素)]。④计量资料差异比较采用组间t检验(方差不齐,用t’检验)。结果:SD大鼠71只均进入结果分析。①卡托普利组、葛根素高、中剂量组给药4周后血压明显低于模型组(P<0.01)。卡托普利组和葛根素高、中剂量组血浆胰岛素水平明显低于模型组,胰岛素敏感指数明显高于模型组(P<0.05~0.01);而葛根素低剂量组上述指标与模型组比较,差异不明显(P>0.05)。②模型组血清一氧化氮和丙二醛水平,一氧化氮合酶和诱导型一氧化氮合酶活力明显高于正常对照组(P<0.01);超氧化物歧化酶活力明显低于正常对照组(P<0.01)。卡托普利和葛根素高剂量组血清超氧化物歧化酶活力明显高于模型组(P<0.05,0.01);卡托普利组和葛根素高、中剂量组血清丙二醛水平均明显低于模型组(P<0.05~0.01);葛根素低剂量组上述指标与模型组比较,差异不明显(P>0.05)。卡托普利组,葛根素高、中剂量组血清一氧化氮水平和一氧化氮合酶及诱导型一氧化氮合酶活力均明显低于模型组(P<0.05~0.01);葛根素低剂量组血清诱导型一氧化氮合酶水平也明显低于模型组(P<0.01),但一氧化氮水平及诱导型一氧化氮合酶活力与模型组相近(P>0.05)。结论:葛根素能增强胰岛素抵抗-高血压大鼠的抗氧化能力,减轻自由基损伤,降血压,改善胰岛素抵抗,增强胰岛素敏感性。 AIM: To observe the effects of puerarin on injury of free radical in insulin-resistant-hypertensive (IRH) rats. METHODS: ① The experiment was completed in Guangzhou Institute of Traditional Chinese Medicine from December 2003 to March 2004. Totally 71 healthy SD rats, aged 6-8 days, of either gender, were selected in this study. ② Twenty were randomly selected as normal control group and fed with distilled water and general feed. Another rats were treated with 50 g/L saccharu, 20 g/L saline and high fat-sugar-salt feed to establish IRH models. After 8 weeks, 51 IRH rats with normal blood pressure and glucose tolerance were divided randomly into 5 groups: model group (n =11), captopril group (n=10), high-dose, middle-dose and low-dose puerarin groups with 10 in each group. Model was performed for 4 weeks according to methods mentioned above. Meanwhile, rats in normal control group and model group were injected with 500 g/L propylene glycol (0.8 mL/kg) once a day for 4 weeks; rats in captopril group were injected with 7 mg/kg captopril solution once a day for 4 weeks; rats in dose groups were acupunctured at bilateral Zusanli (rear Sanli), .Piyu and Shenyu with 80, 40 and 20 mg/kg puerarin on the basis of Rats Points Atlas Research and Experimental Animal & Animal Experiment once a day for 4 weeks.③ After 4-week medication, systolic pressure of caudal artery was assayed with hemomanometer, blood glucose with ONE TOUCH II blood-sugar detector;, levels of serum nitric oxide (NO), nitric oxide synthase (NOS), malondialdehyde (MDA) and fasting insulin and activity of superoxide dismutase (SOD) with biochemical analyzer, content of plasma insulin with enzyme linked immunoassay analyzer. Sensitive index of insulin was calculated as [1/(fasting blood glucosexfasting insulin)].④ Measurement data were compared with t test (irregular variance was analysed with t' test). RESULTS: Totally 71 SD rats entered the final analysis. ①After 4 weeks, value of blood pressure in captopril group, high and middle-dose puerarin groups was lower than that in model group (P 〈 0.01); level of plasma insulin in captopril group, high and middle-dose puerarin group was lower than that in model group; and sensitive index of insulin was higher than that in model group (P 〈 0.05-0.01). However, indexes mentioned above in low-dose puerarin group were not significantly different from those in model group (P 〉 0.05).②Levels of serum NO and MDA and activities of NOS and induced NOS were higher in model group than those in normal control group (P 〈 0.01), and SOD activity was lower than that in normal control group (P 〈 0.01). Activities of serum SOD in captopril group and high-dose puerarin group were higher than those in model group (P 〈 0.05, 0.01); serum MDA content in captopril group, high and middle-dose puerarin groups was lower than that in model group (P 〈 0.05-0.01); However, indexes mentioned above in low-dose puerarin group were not significantly different from those in model group (P 〉 0.05). Serum NO content and activities of NOS and induced NOS in captopril group, high and middle-dose puerarin groups was lower than that in model group (P 〈 0.05- 0.01). Level of induced NOS in low-dose puerarin group was also lower than that in model group (P 〈 0.01), but activities of NOS and induced NOS were close to those in model group (p 〉 0.05). CONCLUSION: Puerarin can enhance anti-oxidation of IRH rats, relieve injury of free radical, decrease blood pressure, improve resistance of insulin, and increase sensitivity of insulin.
出处 《中国临床康复》 CSCD 北大核心 2006年第11期71-73,共3页 Chinese Journal of Clinical Rehabilitation
基金 广东省中医药局滚动资助项目(302003) 广州市中医药 中西医结合项目资助(200237)~~
  • 相关文献

参考文献7

二级参考文献99

  • 1景永奎,韩锐.大豆甙元(S86019)与乳香有效成分Bc-4或阿糖胞苷对HL-60细胞分化的联合诱导[J].药学学报,1993,28(1):11-16. 被引量:31
  • 2石昌顺.中药葛根的研究进展[J].中草药,1994,25(9):496-497. 被引量:84
  • 3李博萍 潘竞锵 等.苦丁茶及其制剂的药理、毒理和药效学研究进展[J].中华中西医结合杂志,2001,1(8):9-12.
  • 4罗雪琚 李秀钩.胰岛素抵抗与高血压.胰岛素抵抗综合征[M].北京:人民卫生出版社,2001.101-107.
  • 51,Hotarnisigil GS,Shargill NS, Spiegelman BM. Adipose expression of tumor necrosis factor-alpha:direct role in obesity-linked insulin resistance .Science,1993,259:87
  • 62,Pring JB, Niesler CU, Winterford CM, et al. Tumor necrosis fac tor-alpha induces apoptosis of human adipose cells.Diabetes,1997,46(12):1939~19 44
  • 73,Maegawa H, Kashiwagi A. Molecular mechanism and clinical impac t of insulin resistance in type 2 diabetes mellitus.Nippon Rinsho,1999,57(3):539 ~544
  • 84,Lang Ch, Dobrescu C, Bagby GJ. Tumor necrosis factor-alpha imp airs insulin action on peripheral glucose disposal and hepatic glucose output.En docrinology,1992,130:43
  • 95,Stephens JM and Pekala PH. Transcriptional expression of the g lut4 and O/EBP genes in 3T3-L1 adipocytes by tumor necrosis factor-alpha. J Biol Chem, 1991,266:21839
  • 106,Storz P, Doppler H, Wernig A, et al. TNF inhibits insulin indu ced STAT5 activation in differentiated mouse muscle cells pmi28. FEBS Lett, 1998 ,27:440(1-2):41~45

共引文献253

同被引文献116

引证文献7

二级引证文献45

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部