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高脂血症对胰岛素抵抗犬多脏器损伤机理的研究

The role of hyperlipidemia in insulin resistant beagle dog multi-organ injury
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摘要 目的探讨高脂血症对胰岛素抵抗时多脏器损伤机理及防治措施。方法采用高脂饮食诱发高脂血症复制胰岛素抵抗Beagle犬模型,随机分为高脂组(n=4)、复方丹参滴丸组(n=4)和对照组(n=4)。饲养40周后取肾、肝、脑、心肌、胰腺等组织标本,通过H-E、甲苯胺蓝、丙二醛等免疫组化,苏丹和锇酸脂肪染色等多种染色,观察组织病理改变和脂质氧化、脂质沉积。结果高脂组,肝、脑尤其肾的病理损伤较其他脏器重。肾小球硬化,髓质肾小管上皮细胞内和管腔内大量脂质沉积并脂质氧化。肝细胞、小叶间胆管上皮细胞和脑神经元内发生脂质沉积和氧化,胶质细胞增生,微动脉硬化。复方丹参滴丸明显减轻脂质沉积和脂质氧化。结论犬胰岛素抵抗模型的组织和细胞内脂毒性作用可能是引起肾、肝、脑、血管等脏器损伤的重要机制。复方丹参滴丸通过调脂和抗氧化作用保护脏器。 Objective To investigate the role hyperlipidemia in multi-organ injury in insulin resistant Beagle dog. Methods Insulin resistant Beagle dog model was established with high dietary lipid. The dogs were divided into high diet lipid group (n= 4), Danshen dripping pill group and control group. Liver, brain, kidney were taken after 40 weeks. Hematoxylin-Eosin staining, Toluidine Blue staining and MDA immunostaining, Sudan Ⅲ- Ⅳ staining, OsO staining was performed to observe the pathological changes, lipid accumulation and oxidation in tissues. Results The pathologic injury in liver, brain, especially kidney tissues was much more obvious in high diet lipid group. Sclerosis of glomerulus was observed with massive lipid accumulation and oxidation in both cells and nephric tubules. Lipid accumulation and oxidation were also observed in hepatocytes, interlobule bile duct epithelia, neuron, and neuroglia cells. The arteriosclerosis of tiny arteries was typical. Danshen dripping pill treatment can obviously decrease lipid accumulation and oxidization. Conclusion Insulin resistance caused multi-organ injury in Beagle dogs, especialy in kidney, liver, brain and vessels. Lipid toxicity in tissues and cells may play a very important role in multi-organ injury induced by insulin resistant Beagle dog. Danshen dropping pills obviously protect the organs via regulating lipid metabolism and protect against oxidation.
出处 《中国心血管病研究》 CAS 2006年第4期292-294,共3页 Chinese Journal of Cardiovascular Research
基金 南开大学"百项工程"项目资助
关键词 胰岛素抗药性 多器官功能衰竭 脂质贮积病 脂蛋白类 LDL Insulin resistance Multiple organ failure lipoidosis Lipoproteins, LDL Cogs
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