糖尿病大血管病变少阴枢机不利探微
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摘要
糖尿病大血管病变属于中医"脉痹"范畴,基于《内经》开阖枢理论探讨糖尿病大血管病变。认为应当遵循《内经》原文以"少阴"为阴枢,且少阴枢机不利是糖尿病大血管病变的关键病机。少阴枢机不利,使"脉有所结而不通",并可影响太阴、厥阴之开阖从而导致"脉痹",治疗当将"和畅少阴枢机"的理念应用到糖尿病大血管病变的防治中。
Diabetic macrovascular disease belongs to vascular arthralgia in traditional Chinese medicine. This article studies diabetic macrovascular disease based on the opening and closing theory in the Internal Classics. It is believed that Shaoyin should be followed as the pivot in the Internal Classics, and the dysfunction of Shaoyin pivot is the key pathogenesis of diabetic macrovascular disease. The dysfunction of Shaoyin pivot can lead to vascular arthralgia, and finally affects the opening and closing of Fusuma. Therefore, regulating the function of Shaoyin pivot is highly recommended in the clinical treatment of diabetic macrovascular disease.
Diabetic macrovascular disease belongs to vascular arthralgia in traditional Chinese medicine. This article studies diabetic macrovascular disease based on the opening and closing theory in the Internal Classics. It is believed that Shaoyin should be followed as the pivot in the Internal Classics, and the dysfunction of Shaoyin pivot is the key pathogenesis of diabetic macrovascular disease. The dysfunction of Shaoyin pivot can lead to vascular arthralgia, and finally affects the opening and closing of Fusuma. Therefore, regulating the function of Shaoyin pivot is highly recommended in the clinical treatment of diabetic macrovascular disease.
引文
[1] Maruthur NM. The growing prevalence of type 2 diabetes: increased incidence or improved survival?[J]. Current diabetes reports, 2013, 13(6): 786-794.
[2] Kannel WB, McGee DL. Diabetes and cardiovascular disease: the Framingham study[J]. Jama, 1979, 241(19): 2035-2038.
[3] Scognamiglio R, Negut C, Ramondo A, et al. Detection of coronary artery disease in asymptomatic patients with type 2 diabetes mellitus[J]. Journal of the American College of Cardiology, 2006, 47(1): 65-71.
[4] Nathan DM, Bayless M, Cleary P, et al. Diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: advances and contributions[J]. Diabetes, 2013, 62(12): 3976-3986.
[5] Ratzmann KP. Therapeutic strategy for type 2 diabetes--clear outcome. Results of the United Kingdom Prospective Diabetes Study (UKPDS)[J]. Fortschritte der Medizin, 1999, 117(5): 45.
[6] 张效科, 田正良. 张学文运用三阳经开阖枢理论辨治疑难杂症经验[J]. 中医杂志, 2014, 55(15): 1275-1277.
[7] 庞军, 李建敏, 唐宏亮, 等. 试探 “开阖枢” 与 “枢” 之关系内涵[J]. 辽宁中医杂志, 2011, 38(6): 1074-1076.
[8] Colwell JA. Pharmacological strategies to prevent macrovascular disease in NIDDM[J]. Diabetes, 1997, 46(Supplement 2): S131-S134.
[9] Ceriello A, Ihnat MA, Thorpe JE. The “metabolic memory”: is more than just tight glucose control necessary to prevent diabetic complications?[J]. The Journal of Clinical Endocrinology & Metabolism, 2009, 94(2): 410-415.
[10] Yamagishi S, Fukami K, Matsui T. Crosstalk between advanced glycation end products (AGEs)-receptor RAGE axis and dipeptidyl peptidase-4-incretin system in diabetic vascular complications[J]. Cardiovascular diabetology, 2015, 14(1): 2.
[11] Lupachyk S, Shevalye H, Maksimchyk Y, et al. PARP inhibition alleviates diabetes-induced systemic oxidative stress and neural tissue 4-hydroxynonenal adduct accumulation: correlation with peripheral nerve function[J]. Free Radical Biology and Medicine, 2011, 50(10): 1400-1409.
[12] Chalmers J, Cooper ME. UKPDS and the legacy effect[J]. New England Journal of Medicine, 2008, 359(15): 1618.
[13] Reddy MA, Jin W, Villeneuve L, et al. Pro-inflammatory role of microrna-200 in vascular smooth muscle cells from diabetic mice[J]. Arteriosclerosis, thrombosis, and vascular biology, 2012, 32(3): 721-729.
[14] Pirola L, Balcerczyk A, Tothill R W, et al. Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells[J]. Genome research, 2011,21(10):1601-1615.
[15] Genuth S, Sun W, Cleary P, et al. Skin advanced glycation endproducts (AGEs) glucosepane and methylglyoxal hydroimidazolone are independently associated with long-term microvascular complication progression of type 1 diabetes[J]. Diabetes, 2015, 64(1): 266-278.
[16] Guarner V, Rubio-Ruiz ME. Low-grade systemic inflammation connects aging, metabolic syndrome and cardiovascular disease[M]//Aging and Health-A Systems Biology Perspective. Karger Publishers, 2015, 40: 99-106.
[17] Kato M, Natarajan R. Diabetic nephropathy—emerging epigenetic mechanisms[J]. Nature Reviews Nephrology, 2014, 10(9): 517.
[18] Forbes JM, Cooper ME. Mechanisms of diabetic complications[J]. Physiological reviews, 2013, 93(1): 137-188.
[19] Zhong X, Liao Y, Chen L, et al. The microRNAs in the pathogenesis of metabolic memory[J]. Endocrinology, 2015, 156(9): 3157-3168.
[20] Zhao S, Li T, Li J, et al. miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway[J]. Diabetologia, 2016, 59(3): 644-654.
[21] Prattichizzo F, Giuliani A, Ceka A, et al. Epigenetic mechanisms of endothelial dysfunction in type 2 diabetes[J]. Clinical epigenetics, 2015, 7(1): 56.
[22] Cai J, Wu G, Jose P A, et al. Functional transferred DNA within extracellular vesicles[J]. Experimental cell research, 2016, 349(1): 179-183.
[23] Lakhter AJ, Sims EK. Minireview: emerging roles for extracellular vesicles in diabetes and related metabolic disorders[J]. Molecular Endocrinology, 2015, 29(11): 1535-1548.
[24] Garcia-Contreras M, Brooks RW, Boccuzzi L, et al. Exosomes as biomarkers and therapeutic tools for type 1 diabetes mellitus[J]. Eur Rev Med Pharmacol Sci, 2017, 21(12): 2940-2956.
[25] Figliolini F, Cantaluppi V, De Lena M, et al. Isolation, characterization and potential role in beta cell-endothelium cross-talk of extracellular vesicles released from human pancreatic islets[J]. PloS one, 2014, 9(7): e102521.
[26] Cianciaruso C, Phelps EA, Pasquier M, et al. Primary human and rat beta cells release the intracellular autoantigens GAD65, IA-2 and proinsulin in exosomes together with cytokine-induced enhancers of immunity[J]. Diabetes, 2017, 66(2): 460-473.
[27] 田佳星, 赵林华, 连凤梅, 等. 中医药防治糖尿病研究进展述评[J]. 中医杂志, 2015, 56(24): 2093-2097.
[28] 刘桠, 康健, 高泓. 从 “脾胰同源” 论血糖波动的中医辨治思路[J]. 辽宁中医杂志, 2015, 42(7): 1246-1247.
[29] Guay C, Menoud V, Rome S, et al. Horizontal transfer of exosomal microRNAs transduce apoptotic signals between pancreatic beta-cells[J]. Cell Communication and Signaling, 2015, 13(1): 17.
[30] Palmisano G, Jensen SS, Le Bihan MC, et al. Characterization of membrane-shed microvesicles from cytokine-stimulated β-cells using proteomics strategies[J]. Molecular & cellular proteomics, 2012, 11(8): 230-243.
[31] 张敬文, 章文春. 论中医整体观之形成渊源和科学内涵[J]. 中华中医药学刊, 2012, 30(5): 1024-1025.
[32] 高泓, 谢春光, 郭宝根, 等. 从伏邪理论对糖尿病大血管病变代谢记忆的理论探讨[J]. 时珍国医国药, 2013, 24(9): 2203-2204.
[33] 郭仪, 石岩. 中药复方治疗糖尿病大血管病变临床疗效及对血糖, 血脂影响的系统评价[J]. 中华中医药学刊, 2017, 35(6): 1369-1375.
[34] 张翕宇, 王鹤亭, 富晓旭, 等. 养阴益气活血法对糖尿病 GK 大鼠氧化应激和硝化应激损伤的影响[J]. 中华中医药学刊, 2017, 35(8): 2066-2069.
[35] 邓远雄, 何丽华, 万思婷, 等. 黄连解毒汤对体内外晚期糖基化终产物形成的影响[J]. 中草药, 2011, 42(1): 130-133.
[36] 聂绪强, 张丹丹, 张涵. 炎症, 胰岛素抵抗与糖尿病的中药治疗[J]. 中国药学杂志, 2017, 52(1): 1-7.
[37] 李俊贤. 基于DNA甲基化探讨益气养阴活血法阻断大血管病变KKay小鼠高血糖 “代谢记忆” 效应的表观遗传学机制[D]. 成都:成都中医药大学, 2014.
[38] 辞海委员会. 辞海[M]. 6版. 上海: 上海辞书出版社, 2009: 2009, 2958.
[39] 韩永刚. 以开阖枢理论为指导使用柴胡调枢汤治疗2型糖尿病的研究[D]. 北京: 中国中医科学院, 2008.
[40] 岳小强, 杨学. 三阴三阳的位序与《伤寒论》六经 “开, 阖, 枢”[J]. 中西医结合学报, 2008, 6(12): 1294-1296.
[41] 孙云松. 论 “厥阴为枢”[J]. 中华中医药杂志, 2010, 25(7): 982-984.
[42] 庞军, 唐宏亮, 王开龙, 等. “枢经”学说与张景岳学术思想[J]. 中华中医药学刊, 2012, 30(9): 1941-1942.
[43] 谢胜, 刘园园. 四象脾土四时六气和五脏的理论渊源及其在中医治未病实践中的意义[J]. 中华中医药学刊, 2016, 34(11): 2785-2790.
[44] 唐咸玉, 周泉. 糖尿病阳虚枢机不利探微[J]. 中医杂志, 2006, 47(12): 886-887.
[2] Kannel WB, McGee DL. Diabetes and cardiovascular disease: the Framingham study[J]. Jama, 1979, 241(19): 2035-2038.
[3] Scognamiglio R, Negut C, Ramondo A, et al. Detection of coronary artery disease in asymptomatic patients with type 2 diabetes mellitus[J]. Journal of the American College of Cardiology, 2006, 47(1): 65-71.
[4] Nathan DM, Bayless M, Cleary P, et al. Diabetes control and complications trial/epidemiology of diabetes interventions and complications study at 30 years: advances and contributions[J]. Diabetes, 2013, 62(12): 3976-3986.
[5] Ratzmann KP. Therapeutic strategy for type 2 diabetes--clear outcome. Results of the United Kingdom Prospective Diabetes Study (UKPDS)[J]. Fortschritte der Medizin, 1999, 117(5): 45.
[6] 张效科, 田正良. 张学文运用三阳经开阖枢理论辨治疑难杂症经验[J]. 中医杂志, 2014, 55(15): 1275-1277.
[7] 庞军, 李建敏, 唐宏亮, 等. 试探 “开阖枢” 与 “枢” 之关系内涵[J]. 辽宁中医杂志, 2011, 38(6): 1074-1076.
[8] Colwell JA. Pharmacological strategies to prevent macrovascular disease in NIDDM[J]. Diabetes, 1997, 46(Supplement 2): S131-S134.
[9] Ceriello A, Ihnat MA, Thorpe JE. The “metabolic memory”: is more than just tight glucose control necessary to prevent diabetic complications?[J]. The Journal of Clinical Endocrinology & Metabolism, 2009, 94(2): 410-415.
[10] Yamagishi S, Fukami K, Matsui T. Crosstalk between advanced glycation end products (AGEs)-receptor RAGE axis and dipeptidyl peptidase-4-incretin system in diabetic vascular complications[J]. Cardiovascular diabetology, 2015, 14(1): 2.
[11] Lupachyk S, Shevalye H, Maksimchyk Y, et al. PARP inhibition alleviates diabetes-induced systemic oxidative stress and neural tissue 4-hydroxynonenal adduct accumulation: correlation with peripheral nerve function[J]. Free Radical Biology and Medicine, 2011, 50(10): 1400-1409.
[12] Chalmers J, Cooper ME. UKPDS and the legacy effect[J]. New England Journal of Medicine, 2008, 359(15): 1618.
[13] Reddy MA, Jin W, Villeneuve L, et al. Pro-inflammatory role of microrna-200 in vascular smooth muscle cells from diabetic mice[J]. Arteriosclerosis, thrombosis, and vascular biology, 2012, 32(3): 721-729.
[14] Pirola L, Balcerczyk A, Tothill R W, et al. Genome-wide analysis distinguishes hyperglycemia regulated epigenetic signatures of primary vascular cells[J]. Genome research, 2011,21(10):1601-1615.
[15] Genuth S, Sun W, Cleary P, et al. Skin advanced glycation endproducts (AGEs) glucosepane and methylglyoxal hydroimidazolone are independently associated with long-term microvascular complication progression of type 1 diabetes[J]. Diabetes, 2015, 64(1): 266-278.
[16] Guarner V, Rubio-Ruiz ME. Low-grade systemic inflammation connects aging, metabolic syndrome and cardiovascular disease[M]//Aging and Health-A Systems Biology Perspective. Karger Publishers, 2015, 40: 99-106.
[17] Kato M, Natarajan R. Diabetic nephropathy—emerging epigenetic mechanisms[J]. Nature Reviews Nephrology, 2014, 10(9): 517.
[18] Forbes JM, Cooper ME. Mechanisms of diabetic complications[J]. Physiological reviews, 2013, 93(1): 137-188.
[19] Zhong X, Liao Y, Chen L, et al. The microRNAs in the pathogenesis of metabolic memory[J]. Endocrinology, 2015, 156(9): 3157-3168.
[20] Zhao S, Li T, Li J, et al. miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway[J]. Diabetologia, 2016, 59(3): 644-654.
[21] Prattichizzo F, Giuliani A, Ceka A, et al. Epigenetic mechanisms of endothelial dysfunction in type 2 diabetes[J]. Clinical epigenetics, 2015, 7(1): 56.
[22] Cai J, Wu G, Jose P A, et al. Functional transferred DNA within extracellular vesicles[J]. Experimental cell research, 2016, 349(1): 179-183.
[23] Lakhter AJ, Sims EK. Minireview: emerging roles for extracellular vesicles in diabetes and related metabolic disorders[J]. Molecular Endocrinology, 2015, 29(11): 1535-1548.
[24] Garcia-Contreras M, Brooks RW, Boccuzzi L, et al. Exosomes as biomarkers and therapeutic tools for type 1 diabetes mellitus[J]. Eur Rev Med Pharmacol Sci, 2017, 21(12): 2940-2956.
[25] Figliolini F, Cantaluppi V, De Lena M, et al. Isolation, characterization and potential role in beta cell-endothelium cross-talk of extracellular vesicles released from human pancreatic islets[J]. PloS one, 2014, 9(7): e102521.
[26] Cianciaruso C, Phelps EA, Pasquier M, et al. Primary human and rat beta cells release the intracellular autoantigens GAD65, IA-2 and proinsulin in exosomes together with cytokine-induced enhancers of immunity[J]. Diabetes, 2017, 66(2): 460-473.
[27] 田佳星, 赵林华, 连凤梅, 等. 中医药防治糖尿病研究进展述评[J]. 中医杂志, 2015, 56(24): 2093-2097.
[28] 刘桠, 康健, 高泓. 从 “脾胰同源” 论血糖波动的中医辨治思路[J]. 辽宁中医杂志, 2015, 42(7): 1246-1247.
[29] Guay C, Menoud V, Rome S, et al. Horizontal transfer of exosomal microRNAs transduce apoptotic signals between pancreatic beta-cells[J]. Cell Communication and Signaling, 2015, 13(1): 17.
[30] Palmisano G, Jensen SS, Le Bihan MC, et al. Characterization of membrane-shed microvesicles from cytokine-stimulated β-cells using proteomics strategies[J]. Molecular & cellular proteomics, 2012, 11(8): 230-243.
[31] 张敬文, 章文春. 论中医整体观之形成渊源和科学内涵[J]. 中华中医药学刊, 2012, 30(5): 1024-1025.
[32] 高泓, 谢春光, 郭宝根, 等. 从伏邪理论对糖尿病大血管病变代谢记忆的理论探讨[J]. 时珍国医国药, 2013, 24(9): 2203-2204.
[33] 郭仪, 石岩. 中药复方治疗糖尿病大血管病变临床疗效及对血糖, 血脂影响的系统评价[J]. 中华中医药学刊, 2017, 35(6): 1369-1375.
[34] 张翕宇, 王鹤亭, 富晓旭, 等. 养阴益气活血法对糖尿病 GK 大鼠氧化应激和硝化应激损伤的影响[J]. 中华中医药学刊, 2017, 35(8): 2066-2069.
[35] 邓远雄, 何丽华, 万思婷, 等. 黄连解毒汤对体内外晚期糖基化终产物形成的影响[J]. 中草药, 2011, 42(1): 130-133.
[36] 聂绪强, 张丹丹, 张涵. 炎症, 胰岛素抵抗与糖尿病的中药治疗[J]. 中国药学杂志, 2017, 52(1): 1-7.
[37] 李俊贤. 基于DNA甲基化探讨益气养阴活血法阻断大血管病变KKay小鼠高血糖 “代谢记忆” 效应的表观遗传学机制[D]. 成都:成都中医药大学, 2014.
[38] 辞海委员会. 辞海[M]. 6版. 上海: 上海辞书出版社, 2009: 2009, 2958.
[39] 韩永刚. 以开阖枢理论为指导使用柴胡调枢汤治疗2型糖尿病的研究[D]. 北京: 中国中医科学院, 2008.
[40] 岳小强, 杨学. 三阴三阳的位序与《伤寒论》六经 “开, 阖, 枢”[J]. 中西医结合学报, 2008, 6(12): 1294-1296.
[41] 孙云松. 论 “厥阴为枢”[J]. 中华中医药杂志, 2010, 25(7): 982-984.
[42] 庞军, 唐宏亮, 王开龙, 等. “枢经”学说与张景岳学术思想[J]. 中华中医药学刊, 2012, 30(9): 1941-1942.
[43] 谢胜, 刘园园. 四象脾土四时六气和五脏的理论渊源及其在中医治未病实践中的意义[J]. 中华中医药学刊, 2016, 34(11): 2785-2790.
[44] 唐咸玉, 周泉. 糖尿病阳虚枢机不利探微[J]. 中医杂志, 2006, 47(12): 886-887.