岩藻聚糖硫酸酯对大鼠缺血再灌注心肌损伤的保护作用及抗氧化应激机制研究
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摘要
目的研究岩藻聚糖硫酸酯对大鼠缺血再灌注心肌损伤的保护作用及抗氧化应激机制。方法按照体重将大鼠随机分为5组:假手术组、模型组和低、中、高3个剂量实验组,每组10只。于再灌注开始时,实验组给予低、中、高3个剂量(50,100,200 mg·kg~(-1))稀释岩藻聚糖硫酸酯10 m L,假手术组和模型组给予等量0. 9%Na Cl。以蛋白印记检测心肌肌钙蛋白I (c Tn I)、肌红蛋白(Mb)、肌酸激酶同工酶(CK-MB)表达;以酶联免疫吸附法测定丙二醛(MDA)和谷胱甘肽(GSH)的水平。结果假手术组、模型组和低、中、高3个剂量实验组的c Tn I相对表达量分别为0. 20±0. 04,2. 10±0. 10,1. 47±0. 15,0. 90±0. 09和0. 26±0. 04;这5组的Mb相对表达量分别为0. 15±0. 03,2. 30±0. 13,1. 90±0. 12,0. 60±0. 07和0. 24±0. 05;这5组的CK-MB相对表达量分别为0. 26±0. 05,2. 60±0. 20,1. 36±0. 15,0. 82±0. 09和0. 36±0. 03;这5组的MDA水平分别为(2. 41±0. 32),(5. 91±0. 52),(5. 62±0. 43),(4. 11±0. 64)和(2. 81±0. 31) U·m L~(-1);这5组的GSH水平分别为(28. 21±4. 31),(5. 13±1. 02),(7. 04±2. 01),(18. 21±2. 62)和(23. 01±3. 03) U·mL~(-1);模型组与假手术组相比或者低、中、高剂量3个实验组与模型组相比,上述指标的差异均有统计学意义(均P <0. 05)。结论岩藻聚糖硫酸酯可减轻缺血再灌注大鼠心肌损伤和氧化应激。
Objective To investigate the protective effect of fucoidan on ischemia reperfusion injury and the mechanism of anti-oxidative stress in rats. Methods Rats were randomly divided into five groups: sham operation group,model group,experimental-L,experimental-M,experimental-H group,each group had ten rats. At the beginning of reperfusion,the experimental-L,-M,-H groups were added with 10 m L of diluted fucosan sulfate at the dose of 50,100,200 mg·kg~(-1) in the blood reservoir,and the sham operation group and the model group were added with the same amount of normal saline. The expression of cardiac troponin I( c Tn I),myoglobin( Mb),creatine phosphokinase isoenzyme( CK-MB) was detected by Western blot. The levels of malonaldehyde( MDA) and glutathione( GSH) were tested by enzyme linked immunosorbent assay. Results The relative expression levels of cTn I in sham operation group,model group and experimental-L,-M,-H groups were 0. 20 ± 0. 04,2. 10 ± 0. 10,1. 47 ± 0. 15,0. 90 ± 0. 09,0. 26 ± 0. 04,respectively; the expression levels in the five groups were 0. 15 ± 0. 03,2. 30 ± 0. 13,1. 90 ± 0. 12,0. 60 ± 0. 07,0. 24 ± 0. 05; the relative expression of CK-MB in the five groups were 0. 26 ± 0. 05,2. 60 ± 0. 20,1. 36 ± 0. 15,0. 82 ± 0. 09. 0. 36 ± 0. 03,respectively; the MDA levels in the five groups were( 2. 41 ± 0. 32),( 5. 91 ± 0. 52),( 5. 62 ± 0. 43),( 4. 11 ± 0. 64),( 2. 81 ± 0. 31) U·m L~(-1),respectively; the GSH levels in the five groups were( 28. 21 ± 4. 31),( 5. 13 ± 1. 02),( 7. 04 ± 2. 01),( 18. 21 ± 2. 62),( 23. 01 ± 3. 03) U·m L~(-1),respectively. Comparison between model group and sham operation group,the difference of the factors were significantly( all P < 0. 05); comparison between three doses experimental groups and model group,the difference of the factors were significantly( all P < 0. 05). Conlusion Fucoidan alleviates the myocardial injury and oxidative stress in ischemia-reperfusion rats.
Objective To investigate the protective effect of fucoidan on ischemia reperfusion injury and the mechanism of anti-oxidative stress in rats. Methods Rats were randomly divided into five groups: sham operation group,model group,experimental-L,experimental-M,experimental-H group,each group had ten rats. At the beginning of reperfusion,the experimental-L,-M,-H groups were added with 10 m L of diluted fucosan sulfate at the dose of 50,100,200 mg·kg~(-1) in the blood reservoir,and the sham operation group and the model group were added with the same amount of normal saline. The expression of cardiac troponin I( c Tn I),myoglobin( Mb),creatine phosphokinase isoenzyme( CK-MB) was detected by Western blot. The levels of malonaldehyde( MDA) and glutathione( GSH) were tested by enzyme linked immunosorbent assay. Results The relative expression levels of cTn I in sham operation group,model group and experimental-L,-M,-H groups were 0. 20 ± 0. 04,2. 10 ± 0. 10,1. 47 ± 0. 15,0. 90 ± 0. 09,0. 26 ± 0. 04,respectively; the expression levels in the five groups were 0. 15 ± 0. 03,2. 30 ± 0. 13,1. 90 ± 0. 12,0. 60 ± 0. 07,0. 24 ± 0. 05; the relative expression of CK-MB in the five groups were 0. 26 ± 0. 05,2. 60 ± 0. 20,1. 36 ± 0. 15,0. 82 ± 0. 09. 0. 36 ± 0. 03,respectively; the MDA levels in the five groups were( 2. 41 ± 0. 32),( 5. 91 ± 0. 52),( 5. 62 ± 0. 43),( 4. 11 ± 0. 64),( 2. 81 ± 0. 31) U·m L~(-1),respectively; the GSH levels in the five groups were( 28. 21 ± 4. 31),( 5. 13 ± 1. 02),( 7. 04 ± 2. 01),( 18. 21 ± 2. 62),( 23. 01 ± 3. 03) U·m L~(-1),respectively. Comparison between model group and sham operation group,the difference of the factors were significantly( all P < 0. 05); comparison between three doses experimental groups and model group,the difference of the factors were significantly( all P < 0. 05). Conlusion Fucoidan alleviates the myocardial injury and oxidative stress in ischemia-reperfusion rats.
引文
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[2]ALEXA K.Fucoidan as a potential therapeutic for major blinding diseases-a hypothesis[J].Mar Drugs,2016,14(2):31.
[3]JANET F,DAMIEN S,SAMUEL K.Therapies from fucoidan:an update[J].Mar Drugs,2015,13(9):5920-5946.
[4]YU Q,LI X,CAO X.Cardioprotective effects of phenylethanoid glycoside-rich extract from cistanche deserticola in ischemia-reperfusion-induced myocardial infarction in rats[J].Ann Vasc Surg,2016,7(34):234-242.
[5]CHAO T,CHUAN P,LIANLIAN W,et al.Intravenous administration of lycopene,a tomato extract,protects against myocardial ischemia-reperfusion injury[J].Nutrients,2016,8(3):138.
[6]NATALIE LVLAND HALLADIN.Oxidative and inflammatory biomarkers of ischemia and reperfusion injuries[J].Dan Medi J,2014,62(4):5054.
[7]LIANG Z,ZHENG Y,WANG J,et al.Low molecular weight fucoidan ameliorates streptozotocin-induced hyper-responsiveness of aortic smooth muscles in type 1 diabetes rats[J].J Ethnopharmacol,2016,9(191):341-349.
[8]LI J,ZHANG Q H,LI S,et al.The natural product fucoidan ameliorates hepatic ischemia-reperfusion injury in mice[J].Biomed Pharmacother,2017,10(94):687-696.