| 谭小田,张志敏,贾 磊,张彦海,谢柏梅.白藜芦醇甙对糖尿病小鼠心肌损伤的保护作用及机制研究[J].,2018,(9):1669-1673 |
| 白藜芦醇甙对糖尿病小鼠心肌损伤的保护作用及机制研究 |
| Effects of Polydatin on Heart Impairment in Diabetic Mice and Potential Mechanism |
| 投稿时间：2017-06-28 修订日期：2017-07-22 |
| DOI：10.13241/j.cnki.pmb.2018.09.014 |
| 中文关键词: 白藜芦醇甙 糖尿病心肌病 沉默信息调节因子3 腺苷酸活化蛋白激酶 |
| 英文关键词: Polydatin Diabetic Cardiomyopathy Sirtuin-3 5-AMP activated kinase |
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| 中文摘要: |
| 摘要 目的：探讨白藜芦醇甙对小鼠小鼠心肌损伤的影响及其可能的调控机制。方法：采用腹腔注射链脲霉素的方法建立1型糖尿病小鼠模型模型，随机将雄性C57/BL6J的正常小鼠和糖尿病小鼠分为3组（每组18只）：对照组、糖尿病组、糖尿病+白藜芦醇甙组。其中糖尿病+白藜芦醇甙组给予白藜芦醇甙7.5 mg/kg/d腹腔注射治疗，对照组和糖尿病组给予同体积盐水腹腔注射。药物治疗12周后，小动物心脏超声检测小鼠的心功能；天狼星红染色观察胶原变化并进一步计算胶原容积分数（collagen volume fraction，CVF)；柠檬酸合酶检测试剂盒和ATP生物荧光试剂盒分别检测检测心肌柠檬酸合酶活性和ATP含量；Western blot检测Sirt3和p-AMPK的蛋白表达情况。结果：与对照组相比，糖尿病组LVEDD和LVESD均明显增加（4.823±0.103 mm和3.701±0.121 mm，P<0.05），LVEF和LVFS值均明显降低（37.121±4.298 %和21.023±2.187 %，P<0.05），CVF显著增高（20.102±1.155 %，P<0.05），心肌柠檬酸合酶活性和ATP含量显著降低（5.267±0.202 nmol/g和105±7.638 U/g，P<0.05），Sirt3和p-AMPK蛋白表达显著降低（P<0.05）；与糖尿病组相比，糖尿病+白藜芦醇甙组LVEDD和LVESD均显著降低（4.354±0.113 mm 和3.056±0.130 mm，P<0.05），LVFS和LVEF值均显著增加（58.435±8.143 %和29.071±2.232 %，P<0.05），CVF显著降低（10.343±0.882 %，P<0.05），心肌柠檬酸合酶活性和ATP含量显著增加（6.233±0.176 nmol/g和132.7±5.774 U/g，P<0.05），Sirt3和p-AMPK蛋白表达显著增加（P<0.05）。结论：白藜芦醇甙可改善糖尿病小鼠心肌损伤，其机制可能与白藜芦醇甙激活Sirt3/AMPK信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the effects of polydatin on heart impairment in diabetic mice and potential mechanism. Methods: Diabetes was induced by a single intraperitoneal of streptozotocin. Male C57/BL6J mice were randomly divided to three groups（n=18）: Control group, diabetes group, diabetes+ polydatin group. Diabetes+ polydatin group were injected a dose of 7.5 mg/kg/d polydatin in- traperitoneally, while control group and diabetes group were injected normal saline intraperitoneally for 12 weeks. Echocardiography was used to measure the cardiac functions of mice in different groups. Sirius red staining was used to evaluate the changes of collagen and measure Collagen volume fraction (CVF). Citratesynthase activity was evaluated by citratesynthase activity assay kit. The ATP content of the myocardium was measured by using an adenosine triphosphate bioluminescent assay kit. Western blot was used to determine the ex- pressions of p-AMPK and Sirt3. Results: Compared with control group, the cardiac functions attenuated (P<0.05) and CVF increased (20.102±1.155 %, P<0.05) significantly in diabetes group. After polydatin treatment, the cardiac functions increased (P<0.05) and CVF decreased (10.343±0.882 %, P<0.05) significantly in diabetic mice. Compared with control group, citratesynthase activity of the myo- cardium decreased significantly (5.267±0.202 nmol/g, P<0.05), with reduced ATP content (105±7.638 U/g, P<0.05), and expressions of p-AMPK and Sirt3 decreased(P<0.05) in diabetes group. Compared with diabetes group, citratesynthase activity of the myocardium in- creased significantly (6.233±0.176 nmol/g, P<0.05), with enhanced ATP content (132.7±5.774 U/g, P<0.05), and the expressions of p-AMPK and Sirt3 were upregulated (P<0.05) by the treatment with polydatinin diabetes +polydatin group. Conclusion: Polydatin can significantly attenuate heart impairment in diabetic mice, possibly by activating Sirt3 /AMPK signaling. |
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