Increasing Atherosclerosis in Streptozotocin-Induced Diabetes into Four Groups of Mice

  • Yunita Sari Pane Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Sumatera Utara, Medan
  • Aznan Lelo Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Sumatera Utara, Medan
  • Kiking Ritarwan Department of Neurology, Adam Malik General Hospital, Faculty of Medicine, Universitas Sumatera Utara, Medan
  • Nerdy Nerdy Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Universitas Sumatera Utara, Medan
Keywords: Atherosclerosis, Streptozotocin, Diabetes, Mice

Abstract

AIM: To study the protective effect of medicines on the formation of atherosclerosis in mice, it is needed to conduct the study in mice which is not genetically diabetic mice induced by streptozotocin (STZ) to produce hyperglycemia and atherosclerosis, compared with mice treated by yolk or its combination.

MATERIAL AND METHODS: Fifty-six mice, Double Deutch Webster strain, male, receive  10 weeks, 20 - 30 gr bodyweight were divided into 4 groups (n = 14) i.e. control (do not received any agents), STZ (45 mg/kg/BW was injected intraperitoneally for 5 days), yolk (0.2 cc orally daily for 6 weeks), and combination of STZ and yolk (STZ: 45 mg/kg/BW intraperitoneally add 0.2 cc yolk orally). All animals were executed in the 42nd day. Then, the aorta of the mice’s heart tissue was histopathology examined. Blood glucose and cholesterol levels were determined every week.

RESULTS: Hyperglycemia occurred in mice induced by STZ injection with the highest BGL (521.8 ± 48.2 mg/dl; 188.4%) in the 4th-week observation; after that BGL decrease. We found that, except the control, all treatment groups with STZ, egg yolk, and combination underwent atherosclerosis.

CONCLUSION: The present study was able to demonstrate the occurrence of atherosclerosis in mice treated by STZ accompanied with increasing blood glucose and cholesterol level.

Downloads

Download data is not yet available.

Metrics

Metrics Loading ...

Plum Analytics Artifact Widget Block

References

American Diabetes Association. Diagnosis and classification of diabetes. Diabetes Care. 2013; 36(Supplement 1): S67-S74. https://doi.org/10.2337/dc13-S067 PMid:23264425 PMCid:PMC3537273

Kishida K, Funahashi T, and Shimomura I. Molecular mechanisms of diabetes and atherosclerosis: role of adiponectin. Endocrine, Metabolic & Immune Disorders - Drug Targets. 2012; 12(2):118-131. https://doi.org/10.2174/187153012800493468

Kunjathoor VV, Wilson DL, LeBoeuf RC. Increased atherosclerosis in -induced diabetic mice. The Journal of Clinical Investigation. 1996; 97(7): 1767–1773. https://doi.org/10.1172/JCI118604 PMid:8601643 PMCid:PMC507242

WHO. Global status report on noncommunicable disease, 2014.

Depkes, 1986. http://litbang.depkes.go.id/riskesnas

Depkes, 2001. http://litbang.depkes.go.id/riskesnas

Depkes, 2007. Hasil Riset Kesehatan Dasar (RISKESDAS) Nasional. Jakarta: Departemen Kesehatan RI. Bajry, H. http://id.scribd.com/doc/84447591/BAB-I-III-edit-cha

Wu KK, Huan Y. Diabetic atherosclerosis mouse models. Atherosclerosis. 2007; 191(2):241-249. https://doi.org/10.1016/j.atherosclerosis.2006.08.030 PMid:16979174

Kostogrys RB, Franczyk-Żarów M, Maślak E, Gajda M, Mateuszuk L, Jackson CL, and Chłopicki S. Low carbohydrate, high protein diet promotes atherosclerosis in apolipoprotein E/low-density lipoprotein receptor double knockout mice (apoE/LDLR(-/-)). Atherosclerosis. 2012; 223(2):327-331. https://doi.org/10.1016/j.atherosclerosis.2012.05.024 PMid:22771189

Mathé D. Dyslipidemia and diabetes: animal models. Diabet Metab. 1995; 21(2):106-111. PMid:7621969

Omoruyi FO, Grindley PB, Asemota HN, and Monrision EYStA. Increased plasma and liver lipids in streptozotocin-induced diabetic rats: effects of yam (Dioscorea cayenensis) or desheen (Colocassia esculenta) extract supplements. Diabetologia Croatica. 2001; 30(3):87-92

Spence JD, Jenkins DJA, and Davignon. J Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease. The Canadian Journal of Cardiology. 2010; 26(9): e336–e339. https://doi.org/10.1016/S0828-282X(10)70456-6

Voutilainen S, Nurmi A, Mursu J, Tuomainen TP, Ruusunen A, and Virtanen JK. Regular consumption of eggs does not affect carotid plaque area or risk of acute myocardial infarction in Finnish men. Atherosclerosis. 2013; 227(1):186-188. https://doi.org/10.1016/j.atherosclerosis.2012.11.031 PMid:23254277

Jung CH, Ahn J, Jeon TI, Kim TW, Ha TY. Syzygium aromaticum ethanol extract reduces high-fat diet-induced obesity in mice through downregulation of adipogenic and lipogenic gene expression. Experimental and Therapeutic Medicine. 2012; 4(3):409-414. https://doi.org/10.3892/etm.2012.609 PMid:23181109 PMCid:PMC3503535

Hishikawa K, Nakaki T, and Fujita T. Oral Flavonoid Supplementation Attenuates Aterosklerosis Development in Apolipoprotein E-Deficient Mice. American Heart Association. Arteriosclerosis, Thrombosis, and Vascular Biology. 2005; 25: 442-446. https://doi.org/10.1161/01.ATV.0000148404.24271.fc PMid:15499038

Natarajan K, Singh S, Burke TR Jr, Grunberger D, Aggarwal BB. Caffeic acid phenethyl ester is a potent and specific inhibitor of activation of nuclear transcription factor NF-kappa B. Proceedings of the National Academy of Sciences of the United States of America. 1996; 93(17):9090-9095. https://doi.org/10.1073/pnas.93.17.9090 PMid:8799159 PMCid:PMC38600

Márquez N, Sancho R, Macho A, Calzado MA, Fiebich BL, and Mu-oz E. Caffeic acid phenethyl ester inhibits T-cell activation by targeting both nuclear factor of activated T-cells and NF-kappaB transcription factors. Journal of Pharmacology and Experimental Therapeutics. 2004; 308(3):993-1001. https://doi.org/10.1124/jpet.103.060673 PMid:14617683

Takaya T, Kawashima S, Shinohara M, Yamashita T, Toh R, Sasaki N, Inoue N, Hirata K, and Yokoyama M. Angiotensin II type 1 receptor blocker telmisartan suppresses superoxide production and reduces atherosclerotic lesion formation in apolipoprotein E-deficient mice. Atherosclerosis. 2006; 186(2):402-410. https://doi.org/10.1016/j.atherosclerosis.2005.08.009 PMid:16157344

Dasu MR, Rios Velasco AC, and Jialal I. Candesartan inhibits Toll-like receptor expression and activity both In vitro and in vivo. Atherosclerosis. 2009; 202:76–83. https://doi.org/10.1016/j.atherosclerosis.2008.04.010 PMid:18495130 PMCid:PMC2676176

Mason RP. Optimal therapeutic strategy for treating patients with hypertension and atherosclerosis: focus on olmesartan medoxomil. Vascular Health and Risk Management. 2011; 7:405-416. https://doi.org/10.2147/VHRM.S20737 PMid:21796255 PMCid:PMC3141913

Kitabchi AE, Ayyagari V, Guerra SM. The efficacy of low-dose versus conventional therapy of insulin for treatment of diabetec ketoacidosis. Ann Intern Med. 1976; 84:663–638. https://doi.org/10.7326/0003-4819-84-6-633

Mythili MD, Vyas R, Akila G, Gunasekaran S. Effect of streptozotocin on the ultrastructure of rat pancreatic islets. Microscopy Research and Technique. 2004; 63, 274-281. https://doi.org/10.1002/jemt.20039 PMid:15170757

Arora S, Ojha SK, Divya V. Characterisation of Streptozotocin Induced Diabetes Mellitus in Swiss Albino Mice. Global Journal of Pharmacology. 2009; 3(2):81-84.

Mansor LS, Gonzalez ER, Cole MA, Tyler DJ, Beeson JH, Clarke K, et al. Cardiac metabolism in a new rat model of type 2 diabetes using high fat diet with low dose streptozotocin. Cardiovascular Diabetology. 2013; 12:136. https://doi.org/10.1186/1475-2840-12-136 PMid:24063408 PMCid:PMC3849358

Chono S, Tauchi Y, Deguchi Y, Morimoto K. Efficient drug delivery to atherosclerotic lesions and the antiatherosclerotic effect by dexamethasone incorporated into liposomes in atherogenic mice. Journal of Drug Targeting. 2005; 13(4):267-276. https://doi.org/10.1080/10611860500159030 PMid:16051539

Published
2018-02-14
How to Cite
1.
Pane YS, Lelo A, Ritarwan K, Nerdy N. Increasing Atherosclerosis in Streptozotocin-Induced Diabetes into Four Groups of Mice. Open Access Maced J Med Sci [Internet]. 2018Feb.14 [cited 2020Nov.25];6(2):287-92. Available from: https://www.id-press.eu/mjms/article/view/oamjms.2018.093
Section
A - Basic Science