实验方法与实验动物 EXPERIMENTAL METHOD AND ANIMAL

紫云英苷对急性力竭运动小鼠肝脏组织中miR-155表达的影响

  • 祝锴烨 ,
  • 吴秋雪 ,
  • 罗海静 ,
  • 张伟伟 ,
  • 邵淑丽
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  • 1. 齐齐哈尔大学生命科学与农林学院, 齐齐哈尔 161006;
    2. 抗性基因工程与寒地生物多样性保护黑龙江省重点实验室, 齐齐哈尔 161006
祝锴烨(1996-),男,黑龙江齐齐哈尔人,硕士研究生,从事分子生物学研究。E-mail:939721695@qq.com

收稿日期: 2021-05-06

  网络出版日期: 2021-12-16

基金资助

国家青年科学基金项目(31801148);黑龙江省自然科学基金项目(C2016057);黑龙江省教育厅基本业务专项(135209260);黑龙江省省属高等学校基本科研业务费科研项目(植物性食品加工技术特色学科专项)(YSTSXK201874);齐齐哈尔大学研究生创新科研项目(YJSCX2020045)

Effects of Astragalin on Expression of miR-155 in Liver Tissue of Mice after Acute Exhaustive Exercise

  • ZHU Kaiye ,
  • WU Qiuxue ,
  • LUO Haijing ,
  • ZHANG Weiwei ,
  • SHAO Shuli
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  • 1. School of Life Science and Agriculture and Forestry, Qiqihar University, Qiqihar 161006, China;
    2. Key Laboratory of Resistant Genetic Engineering and Cold Biodiversity Conservation of Heilongjiang Province, Qiqihar 161006, China

Received date: 2021-05-06

  Online published: 2021-12-16

摘要

为探讨紫云英苷对急性力竭运动小鼠肝脏组织中miR-155表达的影响,试验将48只8周龄无特定病原体(SPF)级C57BL/6J雄性小鼠随机分成4组:二甲基亚砜(DMSO)组、力竭运动组、50 mg/kg紫云英苷组、100 mg/kg紫云英苷组,除DMSO组外,其余3组小鼠进行一次性力竭运动4 h;紫云英苷组在力竭运动后分别灌胃50和100 mg/kg的紫云英苷,力竭运动组在力竭运动后灌胃等量生理盐水,DMSO组灌胃等量由生理盐水配制的0.1% DMSO。在灌注1 h后处死小鼠,测定小鼠血清中谷丙转氨酶(ALT)活性、肝脏组织中抗超氧阴离子自由基(ASAFR)活力和氧化相关miRNAs的表达。结果表明:与DMSO组相比,急性力竭运动后小鼠血清中谷丙转氨酶(ALT)活性提高16.03倍(P<0.05),肝脏组织中抗超氧阴离子自由基(ASAFR)活力降低43%(P<0.05),说明急性力竭运动导致了小鼠肝脏氧化损伤。与DMSO组相比,急性力竭运动后小鼠肝脏组织中miR-155的相对表达量升高6.29倍(P<0.01)。与力竭运动组相比,50 mg/kg紫云英苷组血清中ALT活性降低77%(P<0.05),肝脏组织中ASAFR活力升高1.77倍(P<0.05),肝脏组织中miR-155的相对表达量降低66%(P<0.01);100 mg/kg紫云英苷组血清中ALT活性降低91%(P<0.05),肝脏组织中ASAFR活力升高1.95倍(P<0.05),肝脏组织中miR-155的相对表达量降低60%(P<0.01)。上述结果说明紫云英苷可以部分修复急性力竭运动引起的小鼠肝脏氧化损伤。

本文引用格式

祝锴烨 , 吴秋雪 , 罗海静 , 张伟伟 , 邵淑丽 . 紫云英苷对急性力竭运动小鼠肝脏组织中miR-155表达的影响[J]. 动物营养学报, 2021 , 33(12) : 7062 -7069 . DOI: 10.3969/j.issn.1006-267x.2021.12.046

Abstract

In order to study the effects of astragalin on the expression of miR-155 in liver tissue of mice after acute exhaustive exercise. Forty specific pathogen free (SPF) 8-week-old c57BL/6J male mice were randomly divided into 4 groups:DMSO group, exhaustion exercise group, 50 mg/kg astragalin group and 100 mg/kg astragalin group. In addition to the DMSO group, the mice of other three groups received exhaustive exercise for 4 h. The mice of the astragalin group were given 50 and 100 mg/kg astragalin after exhaustive exercise, respectively, those in the exhaustion exercise group were given the same amount of normal saline after exhaustive exercise, and those in the DMSO group were given the same amount of 0.1% DMSO which prepared with normal saline, and the animals were sacrificed for 1 hour. The serum and liver tissue were collected, the activity of alanine aminotransferase (ALT) in serum and the activity of anti-superoxide anion free radical (ASAFR) in liver tissue were determined. The expression of oxidation-related miRNAs in liver tissue were detected by real-time quantitative fluorescence PCR (qRT-PCR). The results showed that, compared with the DMSO group, the activity of ALT in serum of mice after acute exhaustive exercise was increased by16.03 times (P<0.05), the activity of ASAFR in liver tissue of mice was decreased by 43% (P<0.05), which indicated that acute exhaustive exercise caused oxidative damage to the liver of mice. Compared with the DMSO group, the relative expression level of miR-155 was increased by 6.29 times in liver tissue of mice after acute exhaustive exercise (P<0.01). After gavage 50 mg/kg of astragalin, compared with the exhaustive exercise group, the activity of ALT in serum was decreased by 77% (P<0.05), the activity of ASAFR in liver tissue was increased by 1.77 times (P<0.05), and the relative expression level of miR-155 was decreased by 66% (P<0.05). After gavage 100 mg/kg astragalin, compared with the exhaustive exercise group, the activity of ALT in serum was decreased by 91% (P<0.05), the activity of ASAFR in liver tissue was increased by 1.95 times (P<0.05), and the relative expression level of miR-155 was decreased by 60% (P<0.05). These results indicate that the hepatic oxidative damage induced by acute exhaustive exercise in mice can be partially repaired by astragalin.

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