当归补血汤对药物介导小鼠氧化性溶血的疗效及作用机制

任德旺; 叶渟渟; 倪必辉; 许泽南; 陈嘉捷; 魏立豪; 林晓晖; 林凡

doi:10.13422/j.cnki.syfjx.2014160135

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当归补血汤对药物介导小鼠氧化性溶血的疗效及作用机制

药理 | 更新时间：2024-01-04

- 当归补血汤对药物介导小鼠氧化性溶血的疗效及作用机制
- Effects and Mechanisms of Danggui Buxue Decoction on Drug-induced Oxidative Hemolysis in Mice
- 中国实验方剂学杂志 2014年20卷第16期页码：135-137
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家自然科学基金项目（81102844）;福建省教育厅资助项目（JA11134）;福建省大学生创新创业训练计划项目（201310393040）
- DOI：10.13422/j.cnki.syfjx.2014160135
  中图分类号： R285.5
- 纸质出版日期：2014
- 稿件说明：
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任德旺, 叶渟渟, 倪必辉, 等. 当归补血汤对药物介导小鼠氧化性溶血的疗效及作用机制[J]. 中国实验方剂学杂志, 2014,20(16):135-137.

REN De-wang, YE Ting-ting, NI Bi-hui, et al. Effects and Mechanisms of Danggui Buxue Decoction on Drug-induced Oxidative Hemolysis in Mice[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(16): 135-137.
任德旺, 叶渟渟, 倪必辉, 等. 当归补血汤对药物介导小鼠氧化性溶血的疗效及作用机制[J]. 中国实验方剂学杂志, 2014,20(16):135-137. DOI： 10.13422/j.cnki.syfjx.2014160135.

REN De-wang, YE Ting-ting, NI Bi-hui, et al. Effects and Mechanisms of Danggui Buxue Decoction on Drug-induced Oxidative Hemolysis in Mice[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(16): 135-137. DOI： 10.13422/j.cnki.syfjx.2014160135.

摘要

目的：观察当归补血汤对盐酸苯肼介导的小鼠氧化性溶血的治疗效果，并探讨其对红细胞抗氧化能力的影响。方法：采用盐酸苯肼（60 mg·kg-1）分别于第1，4，7天ip ICR小鼠，诱导氧化性溶血模型。实验设正常对照组、模型组、当归补血汤高、中、低剂量组（10，5，2.5 g·kg-1·d-1）和泼尼松组（0.005 g·kg-1·d-1），每组10只。给药干预后，观察当归补血汤对模型小鼠体重、红细胞数量（RBC）、血红蛋白（Hb）含量、红细胞超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量的影响。结果：与正常对照组比较，模型组小鼠外周血红细胞的数量和Hb含量显著下降，MDA增加，SOD活性下降（P<0.01或P<0.05）。相对于模型组，当归补血汤可增加模型小鼠红细胞的数量、提高Hb含量、降低MDA水平以及增强SOD活性（P<0.01或P<0.05）。结论：当归补血汤对盐酸苯肼介导的氧化性溶血具有良好的疗效，其作用机制可能与促进机体造血机能，增强红细胞抗氧化能力和拮抗氧化剂对红细胞的损伤有关。

Abstract

Objective: To observe the effects of Danggui Buxue decoction (DGBXD) on phenylhydrazine hydrochloride-induced oxidative hemolysis and investigate its mechanism related to antioxidant capacity in mice. Method: The mouse model of oxidative hemolysis was established by intraperitoneal injection of phenylhydrazine hydrochloride. Mice were divided into normal group

model group

DGBXD high

medium and low dose groups (10

2.5 g· kg-1· d-1) and prednisone treatment group (0.005 g· kg-1· d-1). Then

the effects of DGBXD on model mice were observed. The contents of hemoglobin(Hb) and red cell malondialdehyde (MDA) were measured. The numbers of red blood cells (RBC) and activity of superoxide dismutase (SOD) was also determined and the body weight was analyzed. Result: Compared with the control group

the number of RBC

level of Hb and activity of SOD were significantly decreased in the model group (P<0.01 or P<0.05)

the content of MDA in RBC was markedly increased in mice model with oxidative hemolysis (P<0.05). Compared with the model group

DGBXD could increase the number of RBC and level of Hb

decrease the content of MDA and raise the activity of SOD in RBC (P<0.01 or P<0.05). Conclusion: DGBXD has good efficacy in treating drug-induced oxidative hemolysis in mice. Its mechanism might be related to the promotion of hematopoietic function

enhancing red cell antioxidant capacity and protection of erythrocytes against oxidative damage.

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