五参口服液治疗糖尿病性冠心病心绞痛的研究
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摘要
糖尿病性冠心病是糖尿病重要、常见的并发症之一。由于糖尿病对心脏的影响是多方面的,目前国内外还没有早期诊断糖尿病性冠心病的方法及指标,还没有治疗糖尿病性冠心病的理想药物,进一步开展对糖尿病性冠心病的深入研究,以期探讨其证治规律,开发研制出防治糖尿病性冠心病,延缓其病情进展的有效方剂,具有重大意义。
目的：探讨五参口服液治疗糖尿病性冠心病心绞痛的临床疗效及作用机制。
方法：1.临床研究：采用前瞻性随机对照的方法,将符合诊断标准的60例糖尿病性冠心病心绞痛患者,分为治疗组和对照组,每组30例患者,在糖尿病基础治疗上,治疗组予五参口服液,对照组予西药拜新同,治疗观察8周,将治疗前后的临床症状评分及主要实验室指标进行统计学处理、分析。2.动物实验研究：将80只Wistar大鼠随机分为正常对照组、模型对照组、消心痛组、格列美脲组、五参口服液大剂量组、五参口服液小剂量组6组。除正常对照组外,其余各组大鼠均予腹腔注射链脲佐菌素(STZ),造成大鼠糖尿病模型,再以食饵造成大鼠高脂血症及动脉粥样硬化症模型,最后予腹腔注射垂体后叶素,诱发急性心肌缺血损伤模型。在此过程中分别施以不同处理,心肌缺血造模后随即取样,从生化、病理组织学等方面观察,探讨五参口服液对糖尿病性冠心病动脉粥样硬化改变的作用机理及特点。
结果：1.临床研究：治疗组总有效率(86.7%)高于对照组(56.7%),治疗组在改善临床症状、降低血糖、改善血液流变学指标及改善脂质代谢紊乱等方面均优于对照组(P<0.05)。
2.实验研究：①五参口服液能调节血脂代谢,与模型组比较,差异有显著性意义(p<0.05)；格列美脲亦有此作用,与模型组比较,差异有非常显著性意义(p<0.01)；五参口服液组与格列美脲组差异无显著性意义(p>0.05),消心痛无上述作用。②五参口服液能调节血糖代谢,改善胰岛素抵抗,与模型组比较,差异有显著性意义(p<0.05)；格列美脲亦有此作用,与模型组比较,差异有非常显著性意义(p<0.01)；五参口服液组与格列美脲组差异无显著性意义(p>0.05),消心痛无上述作用。③五参口服液能改善ET/NO失衡,保护血管内皮功能,消心痛、格列美脲也有类似作用,但作用机理与五参口服液不同。④五参口服液能调节脂肪细胞因子功能,抑制大血管炎性反应,从而保护血管内皮。格列美脲及消心痛亦有类似作用。⑤五参口服液对垂体后叶素所致的急性心肌缺血有明显的预防作用。⑥五参口服液对动脉硬化脂质斑块具有一定的消退作用,经病理组织学观察,与模型组比较差异有显著性(p<0.05)。与空白组比较差异无显著性(p>0.05)
结论：五参口服液在减轻症状、改善心肌缺血、降低血糖、改善血液流变学指标及改善脂质代谢紊乱等方面均有良好疗效。其可能作用机理：1.通过抑制胰岛素抵抗,调节糖代谢,达到降低血糖,减轻内皮细胞损伤,保护心肌组织的作用；2.通过调节脂质代谢,保护大血管,减轻动脉粥样硬化性损伤,保护心肌组织；3.通过抑制TNF-α、IL-6、CRP等炎性细胞因子,抑制血管炎性反应,保护血管内皮功能。另外,可能通过抑制脂肪细胞因子紊乱,达到促进细胞内脂联素基因的表达、抑制瘦素抵抗的作用,从而调节脂质代谢,对大血管及心肌组织有一定的保护作用。
Diabetic coronary heart disease is one of the major and common diabetes complications. As diabetes has various impacts on human heart, and currently no method or index can help diagnose diabetic coronary disease at an early stage whether in home or abroad, plus no effective medication for diabetic coronary disease has been developed yet, it bares great importance to carry out further studies on this disease, aiming at exploring the rules for its diagnosis and cure, so as to develop effective formula to prevent diabetic coronary disease and ease the severity of the conditions.
Objective:To find out the mechanism of the stenocardia to Diabetes mellitus and coronary heart disease by Wu-Shen oral liquid.
Methods:80 Wistar rats only randomly divided into normal controls, model control group, Isoket group, Glimepiride group, Wu-Shen oral liquid small dose group, Wu-Shen oral liquid large dose group. In addition to the normal control group, Make the rest of the group diabetes mellitus and HyPerliPemia model With the Phago-source, and give the Pituitrin by vein injection to evoke the acute Myoeardial ischemia model。Then give different treatment, observe the mechanism of Wu-Shen oral liquid on biochemistry and Pathological histology. The Experimental rats diabetes mellitus and HyPerliPemia model With the Phago-source,and give the Pituitrin by vein injeeion to evoke the acute Myoeardial ischemia model。Then give different treatment,observe the mechanism of Wu-Shen oral liquid on biochemistry and Pathological histology.
Results:1.Wu-Shen oral liquid and Glimepiride can regulate the blood lipid, decrease the TG, TC, LDL-c level, and increase the HDL-c level.
2. Wu-Shen oral liquid and Glimepiride can regulate blood sugar metabolism, improve insulin resistance.Have the sigbificantly difference than model group (p< 0.05).
3. There is no difference of regulating the balance of ET/NO between the Wu-Shen oral liquid and Isoket
4. Wu-Shen oral liquid can adjust fat cells factor function and restrain the inflammatory response vessels to protect endothelial. Isoket group and Glimepiride group also have a similar effect.
5. Wu-Shen oral liquid have the remarkable effect on preventing the acute myocardial ischemic induced by Pituitrin.
6. Wu-Shen oral liquid extinct atherosclerosis lipid plaque. Have the significantly difference than model group(p<0.05)
Conclusion: Wu-Shen oral liquid canremission angina pectoris.Its mechanism perhaps is by regulating the blood lipid, adjusting sugar metabolism, inhibiting vascular inflammatory reaction and Wu-Shen oral liquid canremission angina pectoris. its mechanism perhaps is by regulating the blood lipid, adjusting sugar metabolism, inhibiting vascular inflammatory reaction and protecting endothelial function to protect myocardial tissue.
目的：探讨五参口服液治疗糖尿病性冠心病心绞痛的临床疗效及作用机制。
方法：1.临床研究：采用前瞻性随机对照的方法,将符合诊断标准的60例糖尿病性冠心病心绞痛患者,分为治疗组和对照组,每组30例患者,在糖尿病基础治疗上,治疗组予五参口服液,对照组予西药拜新同,治疗观察8周,将治疗前后的临床症状评分及主要实验室指标进行统计学处理、分析。2.动物实验研究：将80只Wistar大鼠随机分为正常对照组、模型对照组、消心痛组、格列美脲组、五参口服液大剂量组、五参口服液小剂量组6组。除正常对照组外,其余各组大鼠均予腹腔注射链脲佐菌素(STZ),造成大鼠糖尿病模型,再以食饵造成大鼠高脂血症及动脉粥样硬化症模型,最后予腹腔注射垂体后叶素,诱发急性心肌缺血损伤模型。在此过程中分别施以不同处理,心肌缺血造模后随即取样,从生化、病理组织学等方面观察,探讨五参口服液对糖尿病性冠心病动脉粥样硬化改变的作用机理及特点。
结果：1.临床研究：治疗组总有效率(86.7%)高于对照组(56.7%),治疗组在改善临床症状、降低血糖、改善血液流变学指标及改善脂质代谢紊乱等方面均优于对照组(P<0.05)。
2.实验研究：①五参口服液能调节血脂代谢,与模型组比较,差异有显著性意义(p<0.05)；格列美脲亦有此作用,与模型组比较,差异有非常显著性意义(p<0.01)；五参口服液组与格列美脲组差异无显著性意义(p>0.05),消心痛无上述作用。②五参口服液能调节血糖代谢,改善胰岛素抵抗,与模型组比较,差异有显著性意义(p<0.05)；格列美脲亦有此作用,与模型组比较,差异有非常显著性意义(p<0.01)；五参口服液组与格列美脲组差异无显著性意义(p>0.05),消心痛无上述作用。③五参口服液能改善ET/NO失衡,保护血管内皮功能,消心痛、格列美脲也有类似作用,但作用机理与五参口服液不同。④五参口服液能调节脂肪细胞因子功能,抑制大血管炎性反应,从而保护血管内皮。格列美脲及消心痛亦有类似作用。⑤五参口服液对垂体后叶素所致的急性心肌缺血有明显的预防作用。⑥五参口服液对动脉硬化脂质斑块具有一定的消退作用,经病理组织学观察,与模型组比较差异有显著性(p<0.05)。与空白组比较差异无显著性(p>0.05)
结论：五参口服液在减轻症状、改善心肌缺血、降低血糖、改善血液流变学指标及改善脂质代谢紊乱等方面均有良好疗效。其可能作用机理：1.通过抑制胰岛素抵抗,调节糖代谢,达到降低血糖,减轻内皮细胞损伤,保护心肌组织的作用；2.通过调节脂质代谢,保护大血管,减轻动脉粥样硬化性损伤,保护心肌组织；3.通过抑制TNF-α、IL-6、CRP等炎性细胞因子,抑制血管炎性反应,保护血管内皮功能。另外,可能通过抑制脂肪细胞因子紊乱,达到促进细胞内脂联素基因的表达、抑制瘦素抵抗的作用,从而调节脂质代谢,对大血管及心肌组织有一定的保护作用。
Diabetic coronary heart disease is one of the major and common diabetes complications. As diabetes has various impacts on human heart, and currently no method or index can help diagnose diabetic coronary disease at an early stage whether in home or abroad, plus no effective medication for diabetic coronary disease has been developed yet, it bares great importance to carry out further studies on this disease, aiming at exploring the rules for its diagnosis and cure, so as to develop effective formula to prevent diabetic coronary disease and ease the severity of the conditions.
Objective:To find out the mechanism of the stenocardia to Diabetes mellitus and coronary heart disease by Wu-Shen oral liquid.
Methods:80 Wistar rats only randomly divided into normal controls, model control group, Isoket group, Glimepiride group, Wu-Shen oral liquid small dose group, Wu-Shen oral liquid large dose group. In addition to the normal control group, Make the rest of the group diabetes mellitus and HyPerliPemia model With the Phago-source, and give the Pituitrin by vein injection to evoke the acute Myoeardial ischemia model。Then give different treatment, observe the mechanism of Wu-Shen oral liquid on biochemistry and Pathological histology. The Experimental rats diabetes mellitus and HyPerliPemia model With the Phago-source,and give the Pituitrin by vein injeeion to evoke the acute Myoeardial ischemia model。Then give different treatment,observe the mechanism of Wu-Shen oral liquid on biochemistry and Pathological histology.
Results:1.Wu-Shen oral liquid and Glimepiride can regulate the blood lipid, decrease the TG, TC, LDL-c level, and increase the HDL-c level.
2. Wu-Shen oral liquid and Glimepiride can regulate blood sugar metabolism, improve insulin resistance.Have the sigbificantly difference than model group (p< 0.05).
3. There is no difference of regulating the balance of ET/NO between the Wu-Shen oral liquid and Isoket
4. Wu-Shen oral liquid can adjust fat cells factor function and restrain the inflammatory response vessels to protect endothelial. Isoket group and Glimepiride group also have a similar effect.
5. Wu-Shen oral liquid have the remarkable effect on preventing the acute myocardial ischemic induced by Pituitrin.
6. Wu-Shen oral liquid extinct atherosclerosis lipid plaque. Have the significantly difference than model group(p<0.05)
Conclusion: Wu-Shen oral liquid canremission angina pectoris.Its mechanism perhaps is by regulating the blood lipid, adjusting sugar metabolism, inhibiting vascular inflammatory reaction and Wu-Shen oral liquid canremission angina pectoris. its mechanism perhaps is by regulating the blood lipid, adjusting sugar metabolism, inhibiting vascular inflammatory reaction and protecting endothelial function to protect myocardial tissue.
引文
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[4]Iooker HC,Krakoff J,Funahashi T,et al. Adiponectin concentrations are influenced by renal function and diabetes duration in Pima Indian with Type 2 diabetes [J]. J Clin Endocrinol Metab,2004,89 (8):4010.
[5]Matsuda M, Shimomura I.Adipocytokies and metabolic syndromemolecular mechanism and clinical imp lication[J]. Nippon Rinsho,2004,62 (6):1085.
[6]Matsuzawa Y, Funahashi T,Kihara S, et al. Adiponectin and metabolic syndrome [J]. Arterioseler Thromb Vase Biol,2004,24 (1):29.
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[1]Yamauchi T, Kamon J,Waki H, et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity [J]. Nat Med,2001,7(8):941.
[2]Pellme F,Smith U,Funahashi T,et al.Circulating adiponectin levels are reduced in nonobese but insulin-resistant first-degree relatives of type 2 diabetic patients [J]. Diabetes, 2003,52 (5):1182.
[3]Daimon M, Oizumi T,Saitoh T,et al.Decreased serum levels of adiponectin are a risk fartor for the progression to type 2 diabetes in the Japanese population [J]. Diabetes Care,2003,26 (7):2015.
[4]Iooker HC,Krakoff J,Funahashi T,et al. Adiponectin concentrations are influenced by renal function and diabetes duration in Pima Indian with Type 2 diabetes [J]. J Clin Endocrinol Metab,2004,89 (8):4010.
[5]Matsuda M, Shimomura I.Adipocytokies and metabolic syndromemolecular mechanism and clinical imp lication[J]. Nippon Rinsho,2004,62 (6):1085.
[6]Matsuzawa Y, Funahashi T,Kihara S, et al. Adiponectin and metabolic syndrome [J]. Arterioseler Thromb Vase Biol,2004,24 (1):29.
[7]Staiger H, Haring HU. Adipocytokines:fat-derived humeral mediators of metabolic homeostasis[J]. Exp Clin Endoerinol Diabetes,2005,113(2):67.
[8]Chan DC, Watts GF, Ng TW, et al. Adiponectin and other adipocytokines as predictors of triglyceride-rich lipoprotein metabolism[J].Clin Chem,2005,51 (3):578.
[9]Meigs JB, Panhuysen CI, Myers BH,et al. A genome-wide scan for loci linked to plasma levels of glucose and HbAlc in a community-based sample of caucasian pedigree:The Framingham offspring study [J]. Diabetes,2002,51:833-840.
[10]Duggirala R, Blangero J, Almasy L, et al. Linkage of type 2 diabetes mellitus and age at onset to a genetic location on chromosome 10q in Mexican Americans[J]. Am J Hum Genet,1999,64:1127-1140.
[11]Perseghin G, Lattuada G, De C, et al. Serum retinol-binding protein-4, leptin, and adiponectin concentrations are related to ectopic fat accumulation [J]. J Clin Endocrinol Metab,2007, 92(12):4883-4888.
[12]Broch M, Vendrell J, wifredo R, et al. Circulating, insulin sensitivity, insulin secretion, and insulin disposition index in obese and nonobese subjects [J]. Diabetes Care,2007,30(7): 1802-1806.
[13]吴海娅,贾伟平,魏丽,等.肥胖及2型糖尿病患者血清视黄醇结合蛋白4水平的变化及其临床意义[J].中华内分泌代谢杂志,2006,22(3)：290-293.
[14]Yang RZ, Shuldiner AR, Gong Dw, et al. Cloning of omentin, a new adipokine in human omental fat tissue. Unpublished. NCBI, nucleotide database, accession number; A Y549722.
[15]Yang RZ, Lee MJ, Hu H, et al. Identification of omentin as a novel depot-specific adipokine in human adipose tissue:possible role in modulating insulin action[J]. Am J Physiol Endocrinol Metab,2006,290:E1253-1261.
[16]de souza Batista CM, Yang RZ, Lee MJ, et al. Omentin plasma levels and gene expression are decreased in obesity [J]. diabetes,2007,56(6):1655-1661.
[17]wurm S, Neumeier M, weigert J, et al. Plasma levels of leptin, omentin, collagenous repeal-containing sequence of 26-kDa protein(CORs-26) and adiponectin before and after oral glucose uptake in slim adults [J]. Cardiovasc Diabetol,2007,6:7.
[18]庞翠军,肖常青,苏宏业,等.血糖与脂肪细胞因子的关系研究[J].广西医科大学学报,2008,25(4)：569-570.
[19]Rajala MW, Obici S, Scherer PE, et al. Adipose-de-rived resistin and gut-derived resistin-like molecule-beta selectively impair insulin action on glucose product ion [J]. J Clin Invest,2003, 111(2):225-230.
[20]Liu F, Yang T,Wang B,et al. Resistin induces insulin resistance, but does not affect glucose output in rat-derived hepatocytes[J]. Acta Pharmacol Sin,2008,29(1):98-104.
[21]Chen J, Wang L, Boeg YS, et al. Differential dimerization and association among resistin family proteins with implications for functional specificity[J]. J Endocrinol,2002,175(2): 499-504.
[22]Trayhurn P, Beattie JH. Physiological role of adipose tissue: white adipose tissue as an endocrine and secretory organ[J]. Proc Nutr Soc,2001,60(3):329-339.
[23]Steppan CM, Lazar MA. Resistin and obesity-associated insulin resistance[J]. Trends Endocrinol Metab,2002,13(1):18-23.