Effect of  Polysaccharide on Thymocyte Apoptosis and Mitochondrial Membrane Potential in Rats

HUANG Qing-song; LI Hong-zhi; CHEN Ai-kui

doi:10.11653/syfj2013100232

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Effect of Polysaccharide on Thymocyte Apoptosis and Mitochondrial Membrane Potential in Rats

更新时间：2024-01-04

- Effect of Polysaccharide on Thymocyte Apoptosis and Mitochondrial Membrane Potential in Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 19, Issue 10, Pages: 232-235(2013)
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- DOI：10.11653/syfj2013100232
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- Published：2013
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HUANG Qing-song, LI Hong-zhi, CHEN Ai-kui. Effect of Polysaccharide on Thymocyte Apoptosis and Mitochondrial Membrane Potential in Rats[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(10): 232-235.
DOI：

HUANG Qing-song, LI Hong-zhi, CHEN Ai-kui. Effect of Polysaccharide on Thymocyte Apoptosis and Mitochondrial Membrane Potential in Rats[J]. Chinese journal of experimental traditional medical formulae, 2013, 19(10): 232-235. DOI： 10.11653/syfj2013100232.

摘要

目的: 观察姬松茸多糖对地塞米松(dexamethasone

DEX)诱发大鼠胸腺细胞凋亡和线粒体膜电位的影响。方法: Wistar大鼠随机分为4组:正常组

模型组

姬松茸多糖低、高剂量组

每组10只。正常组和模型组灌胃(ig)生理盐水

姬松茸多糖低、高剂量组ig姬松茸多糖溶液(60

120 mg·kg-1)

1次/d

连续7 d。模型组和姬松茸多糖低、高剂量于第7日腹腔注射DEX(0.02 g·kg-1)。3 h后处死各组动物

迅速无菌取胸腺

采用显微观察、流式细胞技术观察胸腺细胞形态学改变

胸腺细胞凋亡、脱氧核糖核酸(DNA)断裂百分率及线粒体膜电位变化

胸腺组织超氧化物歧化酶(SOD)、丙二醛(MDA)的变化。结果: 与模型组比较

姬松茸多糖组大鼠胸腺细胞线粒体嵴肿胀明显减轻;姬松茸多糖组大鼠胸腺细胞凋亡率[低、高剂量(5.96±1.14)%

(5.07±1.02)%]

DNA断裂率[低、高剂量(3.67±0.49)%

(3.24±0.45)%]及胸腺组织MDA含量[低、高剂量(1.87±0.25)

(1.72±0.23)μg·mg-1]均明显低于模型组[(7.14±1.62)%

(4.25±0.86)%

(2.16±0.38)μg·mg-1];姬松茸多糖组大鼠胸腺细胞线粒体膜电位(荧光指数:低剂量38.57±6.29

高剂量41.36±7.18)及胸腺组织SOD活性量[低、高剂量(25.78±3.94)

(27.36±4.21)U·mg-1]明显高于模型组(32.76±5.48)荧光指数

(21.45±3.52)μg·mg-1。结论: 姬松茸多糖可阻断胸腺细胞DNA断裂和线粒体膜电位的下降

有效抑制DEX诱导的胸腺细胞凋亡

其作用机制与姬松茸多糖提高胸腺组织抗氧化功能有关。

Abstract

Objective: To investigate effects of Agaricus blazei polysaccharide (ABP) on rat thymocyte apoptosis and mitochondrial membrane potential which were induced by dexamethasone (DEX). Method: Forty Wistar rats were divided into four groups randomly with 10 in each group. The four groups were as follows: normal group

model group

low dose ABP group and high dose ABP group.Normal group and model group were prepared by normal saline solution; low dose ABP group and high dose ABP group were prepared by ABP solution(60

120 mg·kg-1)

once a day for seven days continuously. Model group and low dose ABP group were injected through belly by DEX(0.02 g·kg-1). All groups were killed three hours later and rat thymocyte was taken out clenly. Mcroscopic observation and flow cytometry were used to observe morph ological changes and apoptosis of rat thymocyte

percentage of deoxyribonucleic acid(DNA) strand breakage

mitochondrial membrane potential changes and contents of superoxide dismutase (SOD) in rat thymocyte and malomialdehvde (MDA). Result: Mitochondria cristal dilatation of thyocyte obviously released in ABP group compared with model group. Rate of rat thymocyte apoptosis in ABP group [low dose(5.96±1.14)%

high dose(5.07±1.02)%]

DNA breakage rate[low dose(3.67±0.49)%

high dose(3.24±0.45)%]and MDA content in rat thymocyte [low dose(1.87±0.25)μg·mg-1

high dose(1.72±0.23)μg·mg-1] were obviously lower than model group[(7.14±1.62)%

(4.25±0.86)%

(2.16±0.38)μg·mg-1]; mitochondrial membrane potential in rat thymocyte (fluorescence index:low dose 38.57±6.29

high dose 41.36±7.18)and SOD conten in rat thymocyte [low dose(25.78±3.94)μg·mg-1

high dose(27.36±4.21)μg·mg-1]; mitochondrial membrane potential in rat thymocyte (fluorescence index:low dose 38.57±6.29

high dose 41.36±7.18)and SOD conten in rat thymocyte·mg-1

high dose(27.36±4.21)μg·mg-1]were significantly higher than model group(32.76±5.48) fluorescence index

(21.45±3.52)μg·mg-1. Conclusion: ABP prevent DNA strand breakage and the decreasing of mitochondrial membrane potential which can inhibit rat thymocyte apoptosis induced by DEX. The mechanism may be that ABP strengthen antioxidan function of thymus.

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