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中国精品科技期刊2020
肖爱爱,王雪艳,温敏,等. D-核糖对阿霉素诱导心脏毒性的保护作用及机制研究[J]. 食品工业科技,2022,43(13):359−366. doi: 10.13386/j.issn1002-0306.2021100074.
引用本文: 肖爱爱,王雪艳,温敏,等. D-核糖对阿霉素诱导心脏毒性的保护作用及机制研究[J]. 食品工业科技,2022,43(13):359−366. doi: 10.13386/j.issn1002-0306.2021100074.
XIAO Aiai, WANG Xueyan, WEN Min, et al. Protective Effect and Mechanism of D-ribose on Doxorubicin-induced Cardiotoxicity[J]. Science and Technology of Food Industry, 2022, 43(13): 359−366. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021100074.
Citation: XIAO Aiai, WANG Xueyan, WEN Min, et al. Protective Effect and Mechanism of D-ribose on Doxorubicin-induced Cardiotoxicity[J]. Science and Technology of Food Industry, 2022, 43(13): 359−366. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021100074.

D-核糖对阿霉素诱导心脏毒性的保护作用及机制研究

Protective Effect and Mechanism of D-ribose on Doxorubicin-induced Cardiotoxicity

  • 摘要: 目的:研究D-核糖对阿霉素(Doxorubicin,DOX)诱导的小鼠心脏毒性保护作用及机制。方法:8周龄雄性ICR小鼠随机分为对照组(Con),模型组(DOX)组,D-核糖低剂量组(LDR),D-核糖高剂量组(HDR),每组10只。采用单次腹腔注射大剂量阿霉素(15 mg/kg)建立DOX急性心脏毒性小鼠模型,检测血清中乳酸脱氢酶(lactate dehydrogenase,LDH)活性和心脏组织三磷酸腺苷(adenosine triphosphate,ATP)含量;通过苏木素-伊红(hematoxylin-eosin stain,HE)染色观察心肌组织病理变化;通过检测心肌组织内总超氧化物歧化酶(Total superoxide dismutase,T-SOD)、过氧化氢酶(Catalase,CAT)活性以及丙二醛(Malondialdehyde,MDA)含量,评价心脏氧化应激水平;采用蛋白免疫印迹法(Western blot)检测沉默信息调节因子2相关酶类1(silent mating type information regulation 2 homolog 1,Sirt1)、过氧化物酶体增殖物激活受体γ共激活因子1α(peroxisome proliferator-activated receptor γ coactivator-1α,PGC-1α)、B淋巴细胞瘤-2(B-cell lymphoma 2,Bcl-2)、Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)、半胱氨酸天冬氨酸蛋白酶3(cysteine-containing aspartate specific protease 3,Caspase-3)的表达。结果:DOX可引起小鼠体质量显著降低(P<0.05),血清LDH活性显著升高(P<0.05),心肌抗氧化酶活力显著降低(P<0.05);与DOX组相比,高剂量D-核糖可以显著降低血清LDH水平(P<0.05),提高心肌抗氧化酶活力(P<0.05),提高Sirt1、PGC-1α、Bcl-2蛋白表达水平(P<0.05),降低Caspase-3、Bax蛋白表达水平(P<0.05)。结论:高剂量D-核糖可以通过激活Sirt1/PGC-1α通路,缓解氧化应激,抑制心肌细胞凋亡,降低阿霉素诱导的急性心脏毒性。

     

    Abstract: Objective: To study the protective effect and mechanism of D-ribose on Doxorubicin (DOX)-induced cardiotoxicity in mice. Methods: Eight-week-old male ICR mice were randomly divided into normal group (Con), model (DOX) group, D-ribose low-dose group (LDR) and D-ribose high-dose group (HDR), with 10 mice in each group. DOX acute cardiotoxicity mouse model was established by a single intraperitoneal injection of high dose doxorubicin (15 mg/kg). Lactate dehydrogenase (LDH) activity levels in serum and adenosine triphosphate (ATP) content in heart tissue were detected by the commercial kits. The pathological changes of myocardial tissue were observed by hematoxylin-eosin stain (HE) staining. Cardiac oxidative stress was assessed by measuring the activities of total superoxide dismutase (T-SOD), catalase (CAT) and malondialdehyde (MDA) in myocardial tissue. The levels of silent mating type information regulation 2 homolog 1 (Sirt1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax) and cysteine-containing aspartate specific protease 3 (Caspase-3) were detected by Western blotting. Results: DOX could significantly reduce the body weight of mice (P<0.05), serum LDH activity was significantly increased (P<0.05), antioxidant enzyme activity significantly decreased (P<0.05); Oral D-ribose significantly decreased LDH levels (P<0.05) and increased antioxidant enzyme activity (P<0.05), increased Sirt1, PGC-1α, Bcl-2 protein expression levels (P<0.05), decreased Caspase-3, Bax protein expression levels (P<0.05). Conclusion: D-ribose could alleviate the DOX-induced acute cardiotoxicity by activating Sirt1/PGC-1α pathway, inhibiting oxidative stress and apoptosis.

     

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