二氢杨梅素对小鼠葡聚糖硫酸钠结肠炎的疗效

危蓉; 李佩容; 吴志平; 齐国卿; 谢瑞霞; 杭卫红; 阎俊; 张德奎

doi:10.16016/j.1000-5404.201607166

您当前的位置：

首页 >

文章列表页 >

二氢杨梅素对小鼠葡聚糖硫酸钠结肠炎的疗效

基础医学 | 更新时间：2020-08-05

- 二氢杨梅素对小鼠葡聚糖硫酸钠结肠炎的疗效
- Efficacy of dihydromyricetin in treatment of dextran sulfate induced colitis in mice
- 第三军医大学学报 2017年39卷第2期页码：169-174
- 作者机构：
  
  1.730030 兰州, 兰州大学第二医院消化科
  2.730030 兰州, 甘肃省人民医院西院消化科
  3.730030 兰州, 甘肃省消化系肿瘤重点实验室
- 作者简介：
  
  张德奎, E-mail: sczdk1972@163.com Zhang Dekui, E-mail: sczdk1972@163.com
- 基金信息：
  
  国家自然科学基金面上项目(81272661);甘肃省自然科学基金(1506RJZA204)
- DOI：10.16016/j.1000-5404.201607166
  中图分类号： R284.1;R285.6;R574.62
- 纸质出版日期：2017-1-30，
  
  收稿日期：2016-7-24，
  
  录用日期：2016-10-14
扫描看全文
危蓉, 李佩容, 吴志平, 等. 二氢杨梅素对小鼠葡聚糖硫酸钠结肠炎的疗效[J]. 第三军医大学学报, 2017,39(2):169-174.

Rong Wei, Peirong Li, Zhiping Wu, et al. Efficacy of dihydromyricetin in treatment of dextran sulfate induced colitis in mice[J]. J Third Mil Med Univ, 2017,39(2):169-174.
危蓉, 李佩容, 吴志平, 等. 二氢杨梅素对小鼠葡聚糖硫酸钠结肠炎的疗效[J]. 第三军医大学学报, 2017,39(2):169-174. DOI： 10.16016/j.1000-5404.201607166.

Rong Wei, Peirong Li, Zhiping Wu, et al. Efficacy of dihydromyricetin in treatment of dextran sulfate induced colitis in mice[J]. J Third Mil Med Univ, 2017,39(2):169-174. DOI： 10.16016/j.1000-5404.201607166.

摘要

目的

观察二氢杨梅素(dihydromyricetin， DHM)治疗溃疡性结肠炎(ulcerative colitis， UC)的效果并探讨其机制。

方法

60只BALB/c小鼠采用随机数字表法分为正常组，模型组，DHM低剂量、中剂量、高剂量组，5-氨基水杨酸组。分组当日给予正常组小鼠蒸馏水自行饮用，其余组小鼠给予4%葡聚糖硫酸钠(DSS)水溶液7 d诱导急性UC模型。于饮用DSS当日开始，用DHM各剂量组及5-氨基水杨酸组按各组拟定剂量分别进行灌胃处理，连续给药14 d。对比各组疾病活动指数(DAI)、结肠长度、脾脏指数的变化、结肠组织学评分，肠组织TLR2、TLR4和NF-κB 的活性以及炎性细胞因子IL-1β、TNF-α、IL-6表达及MPO、NO、SOD的活性变化。

结果

与模型组比较，DHM可显著降低结肠组织中TLR2、TLR4、NF-κB的表达，减少炎性因子如IL-1β、TNF-α、IL-6水平，同时还能够减少肠组织中MPO、NO活性及增加SOD的活性。其中DHM高剂量组优于低、中剂量组，差异有统计学意义(

＜0.05)，治疗效果最明显，其与5-氨基水杨酸组相比差异无统计学意义(

＞0.05)，治疗效果相当。

结论

DHM可显著缓解DSS诱导的小鼠结肠炎症，其作用机制可能与抗炎、抗氧化有关。

Abstract

Objective

To observe the curative effect of dihydromyricetin(DHM) in treating ulcerative colitis (UC) and to explore its mechanism.

Methods

Sixty BALB/c mice were randomly divided into normal group

model group

low-

middle-

and high-dosed DHM treatment groups and 5- ASA control group

with 10 mice in each group. The normal group was given distilled water to drink

and the other groups were given 4% dextran sodium sulfate (DSS) solution for 7 d to induce the acute UC model. At the beginning of the day of drinking DSS

the drugs were given to the mice of DHM and 5-ASA treatment groups respectively through intragastric continuous administration for 14 d. Disease activity index (DAI)

colon length

spleen index changes

histological scores

activities of TLR2

TLR4 and NF-kappa B

expression levels of inflammatory cytokines IL-1β

TNF-α

IL-6 and activities of MPO

SOD in intestinal tissue were compared among the groups.

Results

Compared with model group

DHM could significantly reduce the expression of TLR2

TLR4

NF-κB in colon tissue

reduce the levels of inflammatory cytokines such as IL-1β

TNF-α and IL-6

and also reduce the production of MPO and NO and increase SOD activity in intestinal tissue. The high-dosed treatment group had better results than low- and middle-dosed treatment groups

with significant with differences (

＜0.05)

and the treatment effect was most obvious and was equivalent to the action of 5-ASA (

0.05).

Conclusion

DHM can significantly alleviate the DSS induced colitis in mice

and its mechanism may be related to its anti-inflammatory and antioxidant activities.

关键词

二氢杨梅素葡聚糖硫酸钠结肠炎TLR2TLR4

Keywords

dihydromyricetindextran sulphate sodium saltulcerative colitisToll-like receptor 2Toll-like receptor 4

references

Korzenik J R, Podolsky D K. Evolving knowledge and therapy of inflammatory bowel disease[J].Nat Rev Drug Discov, 2006, 5(3): 197-209. DOI: 10.1038/nrd1986

陈夏静, 姚汉玲, 张秋琼, 等.大叶蛇葡萄中蛇葡萄素含量的高效液相色谱法测定 [J]. 时珍国医国药, 2010, 21(5): 1053-1054. DOI: 10.3969/j.issn.1008-0805.2010.05.010

Deng X, Tolstanova G, Khomenko T, et al. Mesalamine restores angiogenic balance in experimental ulcerative colitis by reducing expression of endostatin and angiostatin: novel molecular mechanism for therapeutic action of mesalamine[J]. J Pharmacol Exp Ther, 2009, 331(3): 1071-1078. DOI: 10.1124/jpet.109.158022

Kruis W, Kiudelis G, Racz I, et al. Once daily versus three times daily mesalazine granules in active ulcerative colitis: adoube-blind, double-dummy, randomised, non-inferiority trial[J]. Gut, 2009, 58(2): 233-240. DOI: 10.1136/gut.2008.154302

农辉, 黄雪. 葡聚糖硫酸钠诱导结肠炎模型的研究进展[J]. 世界华人消化杂志, 2014, 22(22): 3245-3250.

Wirtz S, Neurath MF. Mouse models of inflammatory bowel disease[J]. Adv Drug Deliv Rev, 2007, 59 (11): 1073-1083. DOI: 10.1016/j.addr.2007.07.003

甘华田, 欧阳钦, 贾道全, 等.溃疡性结肠炎患者核因子NF-κB活化与细胞因子基因表达[J].中华内科杂志, 2002, 41(4): 252-255.

Grivennikov S I, Karin M. Dangerous liaisons: STAT3 and NFKB collaboration and crosstalk in cancer [J]. Cytok Growth Factor Rev, 2010, 21(1): 11-19. DOI: 10.1016/j.cytogfr.2009.11.005

Muzio M, Mantovani A. Toll-like receptors. Microbes Infect, 2000, 2(3): 251-255. DOI: 10.1016/s1286-4579(00)00303-8

Dogi C A, Galdeano C M, Perdigón G. Gut immune stimulation by non pathogenic Gram(+ )and Gram(-)bacteria. Comparison with a probiotic strain[J]. Cytokine, 2008, 41(3): 223-231. DOI: 10.1016/j.cyto.2007.11.014

Szebeni B, Veres G, Dezsfi A, et al. Increased expression of Toll-like receptor(TLR) 2 and TLR4 in the colonic mucosa of children with inflammatory bowel disease [J]. Clin Exp Immunol, 2008, 151(1): 34-41. DOI: 10.1111/j.1365-2249.2007.03531.x

Mylonas C, Kouretas D. Lipid peroxidation and tissue damage[J].In Vivo, 1999, 13( 3): 295-309.

游宇, 刘玉晖, 卢放根, 等.N-乙酰半胱氨酸对葡聚糖硫酸钠诱导的小鼠溃疡性结肠炎的保护作用[J]. 中南药学. 2007, 5(4): 295-299. DOI: 10.3969/j.issn.1672-2981.2007.04.003

Fakhfouri G, Rahimian R, Daneshmand A. et al Granisetron ameliorates acetic acid-induced colitis in rats[J]. Hum Exp Toxicol, 2010, 29(4): 321-328. DOI: 10.1177/0960327110362702

金惠铭. 病理生理学[M]. 5 版. 北京: 人民卫生出版社, 2000: 150.

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

二氢杨梅素通过Sirt3抑制NLRP3炎性小体活性改善血管内皮细胞损伤

二氢杨梅素对代谢相关脂肪性肝病小鼠结肠黏膜屏障功能改善作用研究

二氢杨梅素通过SIRT3调节2型糖尿病小鼠肠上皮屏障功能作用

二氢杨梅素改善糖尿病心肌病小鼠心肌糖吸收与糖酵解作用

低剂量LPS通过上调巨噬细胞TLR4表达促进非酒精性脂肪性肝炎进展