ارزیابی تغییرات شاخص‌های سرمی آسیب قلبی در موش‌های صحرایی‌دیابتی شده با آلوکسان
محورهای موضوعی :
آسیب شناسی درمانگاهی دامپزشکی
یعقوب حاجی صادقی
1
,
مجید فرتاش وند
2
1 - عضو انجمن علمی دامپزشکی، واحد تبریز، دانشگاه آزاد اسلامی، تبریز، ایران.
2 - استادیار گروه علوم درمانگاهی، دانشکده دامپزشکی، واحد تبریز، دانشگاه آزاد اسلامی، تبریز، ایران.
تاریخ دریافت : 1395/11/27
تاریخ پذیرش : 1395/11/27
تاریخ انتشار : 1396/09/01
کلید واژه:
موش صحرایی,
دیابت,
آلوکسان,
تروپونین قلبی,
چکیده مقاله :
دیابت ملیتوس اختلالی متابولیکی است که از شیوع بالایی در سراسر جهان برخوردار می‌باشد و افزایش سطح قند خون و در پی آن آسیب‌های جدی را در عروق و بافت های مختلف بدن سبب می‌گردد. هدف از این مطالعه ارزیابی تغییرات میزان شاخص های سرمی آسیب قلبی در موش های صحرایی دچار دیابت تجربی بود. بدین منظور تعداد 30 سر موش صحرایی نر ویستار به طور تصادفی در 2 گروه 15 تایی شاهد سالم و تیمار دیابتی تقسیم شدند. دیابت ملیتوس تجربی نیز با تزریق داخل صفاقی تک دز آلوکسان (mg/kg 120) ایجاد گردید. چهار هفته پس از القاء دیابت، شاخص های سرمی آسیب قلبی در موش های مورد مطالعه اندازه گیری شد. متوسط قند خون گروه دیابتی mg/dl 36±1/263 و گروه شاهد mg/dl 12±7/96 بود که حاکی از وجود اختلاف آماری معنی دار بین دو گروه بود (000/0=p). میزان سرمی cTnI (تروپونین I قلبی) در موش های صحرایی مبتلا به دیابت تجربی به طور معنی داری بیشتر از موش های صحرایی گروه شاهد بود (002/0=p). هم چنین فعالیت سرمی آنزیم های AST (آسپارتات آمینوترانسفراز)، LDH (لاکتات دهیدروژناز) و CK-MB (کراتین کیناز قلبی- مغزی) در گروه دیابت تجربی در مقایسه با گروه شاهد به طور معنی داری بیشتر بود. در این مطالعه از لحاظ ارتباط بین مقدار قند خون و میزان تروپونین I قلبی سرم (685/0=r، 010/0=p) و نیز سطح فعالیت سرمی آنزیم ها شامل AST (862/0=r، 000/0=p)، LDH (760/0=r، 008/0=p) و CK-MB (590/0=r، 014/0=p) همبستگی مستقیم و معنی دار برآورد گردید.در این مطالعه افزایش میزان cTnI سرم همراه با بالا رفتن میزان فعالیت آنزیم های سرمی شاخص قلب در موش های صحرایی دچار دیابت در مقایسه با گروه شاهد موید بروز درجاتی از آسیب عضله قلب است.
چکیده انگلیسی:
Diabetes mellitus is a metabolic disorder and its incidence is considered to be high all over the world. It causes increase in blood glucose levels and subsequent damage to various tissues and blood vessels. The aim of the present study was to evaluate cardiac injury biomarkers of serum in rats with experimental diabetes. Thirty male Wistar rats were randomly assigned into 2 groups including healthy control and diabetic rats. Diabetes was induced with a single injection of alloxan (120 mg/kg IP). Four weeks after induction of diabetes, levels of cTnI (cardiac troponin I), AST (Aspartate aminotransferase), LDH (lactate dehydrogenase) and CK-MB (keratin kinase) were measured in serum. At the end of the experiment, mean blood sugar levels were 263.1 ± 36 and 96.7 ± 12 mg/dl in diabetic and control groups respectively that reveals a statistically significant difference between the two groups (p=0.000). Serum cTnI level in diabetic rats was significantly higher than healthy control group (p=0.002). Other cardiac biomarkers of serum in experimentally induced diabetic rats were significantly higher than control group. There were significant correlation between blood glucose levels and serum cTnI (r=0.685; p=0.010), and with serum activities of enzymes, including AST (r=0.862; p=0.000), LDH (r=0.760; p=0.008) and CK-MB (r=0.590; p=0.014). In conclusion, elevated level of serum cTnI and enzyme activities in diabetic rats in comparison to the control group suggests some degree of cardiac muscle damages.
منابع و مأخذ:
· منابع
Al-Mallah, M., Zuberi, O., Arida, M. and Kim, H.E., (2008). Positive troponin in diabetic ketoacidosis without evident acute coronary syndrome predicts adverse cardiac events. Clinical Cardiology, 31(2): 67-71.
Cosson, S. and Kevorkian, J.P. (2003). Left ventricular diastolic dysfunction: an early sign of diabetic cardiomyopathy? Diabetes Metabolism, 29: 455-466.
Fang, Z.Y., Yuda, S., Anderson, V., Anderson, V., Short, L., Case, C., et al. (2003). Echocardiographic detection of early diastolic myocardial disease, Journal of the American College of Cardiology, 41: 611-617.
Fein, F.S., Strobeck, J.E., Malhotra, A., Scheuer, J. and Sonnenblick, E.H. (1981). Reversibility of diabetic cardiomyopathy with insulin in rats. Circulation Research, 49(6): 1251-1261.
Gupta, R.K., Kesari, A.N., Murthy, P.S., Chandra, R., Tandon, V. and Watal, G. (2005). Hypoglycemic and antidiabetic effect of ethanolic extract of leaves of Annona squamosa L. in experimental animals. Journal of Ethnopharmacology, 99(1): 75-81.
Heshmati, H., Behnampour, N., Khorasani, F. and Moghadam, Z. (2014). Prevalence of chronic complications of diabete and its related factors in referred type 2 diabetes patients in Freydonkenar diabetes center. Journal of Neyshabur University of Medical Sciences, 1(1): 36-43. [In Persian]
Joseph, T., Coirault, C., Dubourg, O. and Lecarpentier, Y., (2005). Changes in crossbridge mechanical properties in diabetic rat cardiomyopathy. Basic Research in Cardiology, 100(3): 231-239.
· Kesari, A.N., Gupta, R.K., Singh, S.K., Diwakar, S. and Watal,G. (2006). Hypoglycemic and antihyperglycemic activity of Aegle marmelos seed extract in normal and diabetic rats. Journal of Ethnopharmacology, 107(3): 374-379.
Kita, Y., Shimizu, M., Sugihara, N., Yoshio, H., Shibayama, S. and Takeda, R. (1991). Correlation between histological changes and mechanical dysfunction in diabetic rat hearts. Diabetes Research and Clinical Practice, 11: 177-188.
Laakso, M. (2001). Cardiovascular disease in type 2 diabetes: challenge for treatment and prevention, Journal of Internal Medicine, 249: 225-235.
Lachin, T. and Reza, H. (2012). Anti diabetic effect of cherries in alloxan induced diabetic rats. Recent Patents on Endocrine, Metabolic and Immune Drug Discovery, 6(1): 67-72.
Ligeti, L., Szenczi, O., Prestia, C.M., Szabó, C., Horváth, K., Marcsek, Z.L., et al. (2006). Altered calcium handling is an early sign of streptozotocin-induced diabetic cardiomyopathy. International Journal of Molecular Medicine, 17(6): 1035-1043.
Liu, X., Takeda, N. and Dhalla, N.S. (1996). Troponin I phosphorylation in heart homogenate from diabetic rat. Biochimica et Biophysica Acta, 1316(2): 78-84.
Mandavia, C.H., Pulakat, L., DeMarco, V. and Sowers, J.R. (2012). Over-nutrition, obesity and metabolic cardiomyopathy. Metabolism, 61(9): 1205-1210.
Mongeon, F.P., Dorais, M., Lorier, J.L., Froment, D., Letendre, E. and Rinfret, S. (2009). Effect of hemodialysis, coronary artery disease and diabetes on cardiac troponin-I: a prospective survey over one year. The Open Cardiovascular Medicine Journal, 3: 69-77.
Oran, B., Cam, L., Başpinar, O., Baysal, T., Reisli, I., Peru, H., et al. (2003). Cardiac troponin-I in the serum of infants of diabetic mothers. Cardiology in the Young, 13: 248-252.
Pourmoghaddas, A. and Hekmatnia, A. (2003). The relationship between QTc interval and cardiac autonomic neuropathy in diabetes mellitus. Molecular and Cellular Biochemistry, 249: 125-128.
Rodrigues, B., Cam, M.C. and McNeill, J.H. (1995). Myocardial substrate metabolism: implications for diabetic cardiomyopathy. Journal of Molecular and Cellular Cardiology, 27: 169-179.
· Takeda, N. (2010). Cardiac disturbances in diabetes mellitus. Pathophysiology, 17: 83-88.
Turner, R.C., Millns, H., Neil, H.A., Stratton, I.M., Manley, S.E., Matthews, D.R., et al. (1998). Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus United Kingdom Prospective Diabetes Study (UKPDS: 23). British Medical Journal, 317: 693-694.
Vasiliadis, I., Kolovou, G., Mavrogeni, S., Nair, D.R. and Mikhailidis, D.P. (2014). Sudden cardiac death and diabetes mellitus. Journal of Diabetes and Its Complications 28: 573-579.
Zhang, L., Cannell, M.B., Phillips, A.R.J., Cooper, G.J.S. and Ward, M.L. (2008). Altered Calcium Homeostasis Does Not Explain the Contractile Deficit of Diabetic Cardiomyopathy. Diabetes, 57(8): 2158-2166.
_||_
· منابع
Al-Mallah, M., Zuberi, O., Arida, M. and Kim, H.E., (2008). Positive troponin in diabetic ketoacidosis without evident acute coronary syndrome predicts adverse cardiac events. Clinical Cardiology, 31(2): 67-71.
Cosson, S. and Kevorkian, J.P. (2003). Left ventricular diastolic dysfunction: an early sign of diabetic cardiomyopathy? Diabetes Metabolism, 29: 455-466.
Fang, Z.Y., Yuda, S., Anderson, V., Anderson, V., Short, L., Case, C., et al. (2003). Echocardiographic detection of early diastolic myocardial disease, Journal of the American College of Cardiology, 41: 611-617.
Fein, F.S., Strobeck, J.E., Malhotra, A., Scheuer, J. and Sonnenblick, E.H. (1981). Reversibility of diabetic cardiomyopathy with insulin in rats. Circulation Research, 49(6): 1251-1261.
Gupta, R.K., Kesari, A.N., Murthy, P.S., Chandra, R., Tandon, V. and Watal, G. (2005). Hypoglycemic and antidiabetic effect of ethanolic extract of leaves of Annona squamosa L. in experimental animals. Journal of Ethnopharmacology, 99(1): 75-81.
Heshmati, H., Behnampour, N., Khorasani, F. and Moghadam, Z. (2014). Prevalence of chronic complications of diabete and its related factors in referred type 2 diabetes patients in Freydonkenar diabetes center. Journal of Neyshabur University of Medical Sciences, 1(1): 36-43. [In Persian]
Joseph, T., Coirault, C., Dubourg, O. and Lecarpentier, Y., (2005). Changes in crossbridge mechanical properties in diabetic rat cardiomyopathy. Basic Research in Cardiology, 100(3): 231-239.
· Kesari, A.N., Gupta, R.K., Singh, S.K., Diwakar, S. and Watal,G. (2006). Hypoglycemic and antihyperglycemic activity of Aegle marmelos seed extract in normal and diabetic rats. Journal of Ethnopharmacology, 107(3): 374-379.
Kita, Y., Shimizu, M., Sugihara, N., Yoshio, H., Shibayama, S. and Takeda, R. (1991). Correlation between histological changes and mechanical dysfunction in diabetic rat hearts. Diabetes Research and Clinical Practice, 11: 177-188.
Laakso, M. (2001). Cardiovascular disease in type 2 diabetes: challenge for treatment and prevention, Journal of Internal Medicine, 249: 225-235.
Lachin, T. and Reza, H. (2012). Anti diabetic effect of cherries in alloxan induced diabetic rats. Recent Patents on Endocrine, Metabolic and Immune Drug Discovery, 6(1): 67-72.
Ligeti, L., Szenczi, O., Prestia, C.M., Szabó, C., Horváth, K., Marcsek, Z.L., et al. (2006). Altered calcium handling is an early sign of streptozotocin-induced diabetic cardiomyopathy. International Journal of Molecular Medicine, 17(6): 1035-1043.
Liu, X., Takeda, N. and Dhalla, N.S. (1996). Troponin I phosphorylation in heart homogenate from diabetic rat. Biochimica et Biophysica Acta, 1316(2): 78-84.
Mandavia, C.H., Pulakat, L., DeMarco, V. and Sowers, J.R. (2012). Over-nutrition, obesity and metabolic cardiomyopathy. Metabolism, 61(9): 1205-1210.
Mongeon, F.P., Dorais, M., Lorier, J.L., Froment, D., Letendre, E. and Rinfret, S. (2009). Effect of hemodialysis, coronary artery disease and diabetes on cardiac troponin-I: a prospective survey over one year. The Open Cardiovascular Medicine Journal, 3: 69-77.
Oran, B., Cam, L., Başpinar, O., Baysal, T., Reisli, I., Peru, H., et al. (2003). Cardiac troponin-I in the serum of infants of diabetic mothers. Cardiology in the Young, 13: 248-252.
Pourmoghaddas, A. and Hekmatnia, A. (2003). The relationship between QTc interval and cardiac autonomic neuropathy in diabetes mellitus. Molecular and Cellular Biochemistry, 249: 125-128.
Rodrigues, B., Cam, M.C. and McNeill, J.H. (1995). Myocardial substrate metabolism: implications for diabetic cardiomyopathy. Journal of Molecular and Cellular Cardiology, 27: 169-179.
· Takeda, N. (2010). Cardiac disturbances in diabetes mellitus. Pathophysiology, 17: 83-88.
Turner, R.C., Millns, H., Neil, H.A., Stratton, I.M., Manley, S.E., Matthews, D.R., et al. (1998). Risk factors for coronary artery disease in non-insulin dependent diabetes mellitus United Kingdom Prospective Diabetes Study (UKPDS: 23). British Medical Journal, 317: 693-694.
Vasiliadis, I., Kolovou, G., Mavrogeni, S., Nair, D.R. and Mikhailidis, D.P. (2014). Sudden cardiac death and diabetes mellitus. Journal of Diabetes and Its Complications 28: 573-579.
Zhang, L., Cannell, M.B., Phillips, A.R.J., Cooper, G.J.S. and Ward, M.L. (2008). Altered Calcium Homeostasis Does Not Explain the Contractile Deficit of Diabetic Cardiomyopathy. Diabetes, 57(8): 2158-2166.
