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肉桂醛对苯所致免疫和氧化应激损伤模型小鼠的保护作用研究OACSTPCD

Protective effects of cinnamaldehyde on benzene-induced immune and oxidative stress injury in mice

中文摘要英文摘要

目的 探究肉桂主要活性成分肉桂醛对苯所致小鼠免疫损伤的保护作用及其机制.方法 选用40只雄性BALB/c小鼠,随机分为对照组、模型组(苯500 mg/kg)、肉桂醛低、中、高剂量组(5、25、50 mg/kg),每组8只.除对照组外,其余各组小鼠每天通过灌胃苯的方式造成小鼠免疫和氧化应激损伤,同时治疗组灌胃给予肉桂醛,每周5d,连续3周.末次灌胃24h后取小鼠外周血进行血细胞计数,观察各组小鼠体重的变化,苏木素-伊红(HE)染色观察小鼠脾脏和胸腺的病理结构,提取小鼠外周血单个核细胞(PBMC)测定其线粒体活性氧(ROS)及三磷酸腺苷(ATP)的含量,使用硫代巴比妥酸法测定血浆中丙二醛(MDA)的含量、二硫代二硝基苯甲酸法测定血浆中谷胱甘肽过氧化物酶(GSH-Px)的活力、羟胺法测定血浆中总超氧化物歧化酶(SOD)的活力.结果 苯暴露后,与对照组相比,模型组小鼠体重减轻(P<0.05);脾脏和胸腺组织受损,脾脏和胸腺指数均降低(P<0.05);外周血白细胞和淋巴细胞计数降低(P<0.05);血浆中GSH和SOD活性降低(P<0.05)、MDA含量升高(P<0.05);PBMC中线粒体ROS水平升高,ATP含量降低(P<0.05).肉桂醛治疗后,小鼠体重升高;脾脏和胸腺组织恢复良好,脾脏和胸腺指数均升高(P<0.05);肉桂醛高剂量组白细胞和淋巴细胞水平升高(P<0.05);血浆中GSH和SOD活性升高、MDA含量降低(P<0.05);PBMC中线粒体ROS水平降低,ATP含量升高(P<0.05);肉桂醛的治疗可以缓解苯诱导的小鼠PBMC线粒体功能的损伤,其中以50 mg/kg剂量为最佳(P<0.05),肉桂醛的治疗作用具有剂量效应关系.结论 肉桂醛可通过抗氧化作用和提高PBMC线粒体功能改善苯所致小鼠免疫损伤和氧化应激损伤.

Objective To investigate the effects of cinnamaldehyde,the main active component of cinnamon,on benzene-induced immune injury in mice and the related mechanism.Methods Forty male BALB/c mice were randomly divided into the control group,model group(benzene 500 mg/kg),cinnamaldehyde low,medium and high dose groups(5,25,50 mg/kg),with 8 mice in each group.Except the control group,mice in each group were treated with benzene by intragastric administration daily to induce immune and oxidative stress damage,but the intervention group was treated with cinnamaldehyde 5 times/week for 3 weeks.After medication,peripheral blood was collected 24 h after the last gavage for blood cell count,and the changes in body weight of mice in each group were observed.The pathological structure of the spleen and thymus was observed via hematoxylin-eosin(HE)staining.Peripheral blood mononuclear cells(PBMCs)of mice were extracted and the amounts of reactive oxygen species(ROS)and ATP in mitochondria were measured.Plasma levels of malondialdehyde(MDA)were measured using the barbituric acid method,the activity of glutathione peroxidase(GSH-PX)in plasmawith the dithiodinitrobenzoic acid methodand the activity of total superoxide dismutase(SOD)in plasma using the hydroxylamine method.Results After exposure to benzene,the body weight of the model group became lower(P<0.05).The spleen and thymus were damaged,and the indexes of the spleen and thymus were decreased(P<0.05).Counts of peripheral white blood cells and lymphocyteswere decreased(P<0.05).The activities of GSH and SOD in plasma were decreased(P<0.05),but the content of MDA was increased(P<0.05).The amount of mitochondrial ROS in PBMC was increased,while the ATP content was decreased(P<0.05).The weight of mice increased after treatment with cinnamaldehyde.The spleen and thymus tissues recovered well,and the indexes of the spleen and thymus were increased(P<0.05).Counts of peripheral white blood cells and lymphocytesin the high dose cinnamaldehyde group were increased(P<0.05).The activities of GSH and SOD in plasma were increased,while the content of MDA was decreased(P<0.05).The amount of mitochondrial ROS in PBMC was decreased,but the ATP content was increased(P<0.05).Treatment with cinnamaldehyde could alleviate the damage to the mitochondrial function of PBMC induced by benzene in mice,and 50 mg/kg was the best dose(P<0.05).The therapeutic effect of cinnamaldehyde had a dose-response relationship.Conclusion Cinnamaldehyde can inhibit benzene-induced immune injury and oxidative stress injury in mice by delivering an antioxidant effect and improving mitochondrial enhancement of PBMC.

李梦洋;王贵;乔亚梅;王萍玉;金敏;杨栋;李君文

滨州医学院公共卫生与管理学院,山东烟台 264003||军事科学院军事医学研究院环境医学与作业医学研究所,天津 300050军事科学院军事医学研究院环境医学与作业医学研究所,天津 300050滨州医学院公共卫生与管理学院,山东烟台 264003

预防医学

肉桂醛免疫氧化应激线粒体外周血单个核细胞保护作用

benzenecinnamaldehydeimmuneoxidative stressmitochondriaperipheral blood mononuclear cellsprotective effect

《军事医学》 2024 (001)

44-51 / 8

国家自然科学基金面上项目(82073508)

10.7644/j.issn.1674-9960.2024.01.008

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