دوره 29، شماره 132 - ( 10-1399 )                   جلد 29 شماره 132 صفحات 27-21 | برگشت به فهرست نسخه ها


XML English Abstract Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Mahdavifard S, Nakhjavani M. Effect of Pyridoxal Phosphate on Atherosclerosis and Nephropathy Progression in Atherosclerotic Rats. J Adv Med Biomed Res 2021; 29 (132) :21-27
URL: http://journal.zums.ac.ir/article-1-6080-fa.html
Effect of Pyridoxal Phosphate on Atherosclerosis and Nephropathy Progression in Atherosclerotic Rats. Journal of Advances in Medical and Biomedical Research. 1399; 29 (132) :21-27

URL: http://journal.zums.ac.ir/article-1-6080-fa.html


چکیده:   (146735 مشاهده)

 Background & Objective:  Diabetes vascular complications are the leading cause of death in the world. Therefore, we investigated the effect of pyridoxal phosphate (PLP) on the formation of atheromatous plaque and renal function in atherosclerotic rats.
 Materials & Methods:  Forty male Wistar rats were randomly divided into four groups of normal, atherosclerotic, and two similar groups under PLP treatment. Atherosclerosis was induced in rats by an atherogenic diet and all groups were treated with 0.18% of PLP in drinking water daily for three months. Hematoxylin and eosin stain was applied to assess the histopathological changes in the aorta of subjects. Insulin resistance index, the activity of the glyoxalase (GLO) system, lipid profile, low-density lipoprotein (LDL) oxidation markers, advanced oxidation protein products, and inflammatory markers, such as high-sensitivity C-reactive protein (hs-CRP) and TGF-β1 were examined in all rats. In addition, serum creatinine levels and urinary protein excretion of all animals were measured.
 Results:  Atheromatous lesions were not observed in the aorta of PLP-treated atherosclerotic rats. Furthermore, PLP seemed to improve insulin function, lipid profile, kidney function parameters, GLO system activity, and inflammation. We found that PLP treatment decreased the formation of LDL oxidation products both in vitro and in vivo (P<0.001).
 Conclusion:  According to our findings, PLP imposed a beneficial effect on vascular complications in atherosclerotic rats, which could be attributed to its antioxidant and anti-inflammatory properties. Moreover, PLP has positive impacts on insulin function, dyslipidemia, and GLO system activity.

متن کامل [PDF 470 kb]   (154114 دریافت)    
نوع مطالعه: مقاله پژوهشی | موضوع مقاله: Medical Biology
دریافت: 1399/4/3 | پذیرش: 1399/5/22 | انتشار: 1399/8/21

فهرست منابع
1. Chilelli N, Burlina S, Lapolla A. AGEs, rather than hyperglycemia, are responsible for microvascular complications in diabetes: a "glycoxidation-centric" point of view. Nutr, Metab, Cardiovasc Dis. 2013;23(10):913-9. [DOI:10.1016/j.numecd.2013.04.004]
2. De Nicola LG, Liberti FB, Sagliocca ME, Conte A, Minutolo G. Sodium/glucose cotransporter 2 inhibitors and prevention of diabetic nephropathy: Targeting the renal tubule in diabetes. . Am J Kidney Dis. 2014;64 16-24. [DOI:10.1053/j.ajkd.2014.02.010]
3. Tangvarasittichai S. Oxidative stress and inflammation in diabetic complications. World J Diabetes. 2015;6(3):456-80. [DOI:10.4239/wjd.v6.i3.456]
4. Huang D, Refaat M, Mohammedi K, Jayyousi A, Al Suwaidi J, Abi Khalil C. Macrovascular complications in patients with diabetes and prediabetes. BioMed Res Int. 2017;2017: 7839101 [DOI:10.1155/2017/7839101]
5. Bornfeldt KE, Tabas I. Insulin resistance, hyperglycemia, and atherosclerosis. Cell Metab. 2011;14(5):575-85. [DOI:10.1016/j.cmet.2011.07.015]
6. Kawanami D MK, Utsunomiya K. Dyslipidemia in diabetic nephropathy. Replace Ther 2016;2:16. [DOI:10.1186/s41100-016-0028-0]
7. Sarkar P, Kar K, Mondal MC, Chakraborty I, Kar M. Elevated level of carbonyl compounds correlates with insulin resistance in type 2 diabetes. Ann Acad Med Singapore. 2010;39(12):909-4.
8. Okura T, Ueta E, Nakamura R, et al. High serum advanced glycation end products are associated with decreased insulin secretion in patients with type 2 diabetes: A brief report. J Diabetes Res. 2017;2017:5139750. [DOI:10.1155/2017/5139750]
9. Wortmann M, Peters AS, Hakimi M, Bockler D, Dihlmann S. Glyoxalase I (Glo1) and its metabolites in vascular disease. Biochem Soc Trans. 2014;42(2):528-33. [DOI:10.1042/BST20140003]
10. Dimitropoulos A, Rosado CJ, Thomas MC. Dicarbonyl-mediated AGEing and diabetic kidney disease. J Nephrol. 2020. [DOI:10.1007/s40620-020-00718-z]
11. Nigro C, Leone A, Raciti GA, et al. Methylglyoxal-glyoxalase 1 balance: The root of vascular damage. Int J Mol Sci. 2017;18(1):188-202. [DOI:10.3390/ijms18010188]
12. Nagai R, Shirakawa J, Fujiwara Y, et al. Detection of aGEs as markers for carbohydrate metabolism and protein denaturation. J Clin Biochem Nutr. 2014;55(1):1-6. [DOI:10.3164/jcbn.13-112]
13. Mahdavifard S NM. Effect of cysteine on transforming growth factor β1 as the main cause of renal disorder in a rat model of diabetic nephropathy. J Mazandaran Univ Med Sci. 2019;29:95-101.
14. Mahdavifard S, Nakhjavani M. Effect of glutamine on oxidative stress, inflammatory, and glycation markers, and the activity of glyoxalase system in diabetic rats with atherosclerosis. J Mazandaran Univ Med Sci. 2019;28(170):33-42.
15. Mahdavifard S, Nakhjavani M. Effect of linalool on the activity of glyoxalase-I and diverse glycation products in rats with type 2 diabetes. J Mazandaran Univ Med Sci. 2020;30(186):24-33.
16. Nix WA, Zirwes R, Bangert V, et al. Vitamin B status in patients with type 2 diabetes mellitus with and without incipient nephropathy. Diabetes Res Clin Pract. 2015;107(1):157-65. [DOI:10.1016/j.diabres.2014.09.058]
17. Duncan A, Talwar D, McMillan DC, Stefanowicz F, O'Reilly DS. Quantitative data on the magnitude of the systemic inflammatory response and its effect on micronutrient status based on plasma measurements. Am J Clin Nutr. 2012;95(1):64-71. [DOI:10.3945/ajcn.111.023812]
18. Ueland PM, McCann A, Midttun O, Ulvik A. Inflammation, vitamin B6 and related pathways. Mol Aspects Med. 2017;53:10-27. [DOI:10.1016/j.mam.2016.08.001]
19. Cole T, Kuisk I, Patsch W, Schonfeld G. Effects of high cholesterol diets on rat plasma lipoproteins and lipoprotein-cell interactions. J Lipid Res. 1984;25(6):593-603.
20. Mahdavifard S, Bathaie S, Nakhjavani M, Heidarzadeh H. L-cysteine is a potent inhibitor of protein glycation on both albumin and LDL, and prevents the diabetic complications in diabetic-atherosclerotic rat. Food Res Int. 2014;62:909-16. [DOI:10.1016/j.foodres.2014.05.008]
21. Mahdavifard S, Bathaie SZ, Nakhjavani M, Taghikhani M. The synergistic effect of antiglycating agents (MB-92) on inhibition of protein glycation, misfolding and diabetic complications in diabetic-atherosclerotic rat. Eur J Med Chem. 2016;121:892-902. [DOI:10.1016/j.ejmech.2015.11.035]
22. Ravid M, Brosh D, Ravid-Safran D, Levy Z, Rachmani R. Main risk factors for nephropathy in type 2 diabetes mellitus are plasma cholesterol levels, mean blood pressure, and hyperglycemia. Arch Intern Med. 1998;158(9):998. [DOI:10.1001/archinte.158.9.998]
23. Kiran SG, Dorisetty RK, Umrani MR, et al. Pyridoxal 5′ phosphate protects islets against streptozotocin-induced beta-cell dysfunction-in vitro and in vivo. Exp Biol Med. 2011;236(4):456-65. [DOI:10.1258/ebm.2011.010361]
24. Bilgir O, Yavuz M, Bilgir F, et al. Relationship between insulin resistance, hs-CRP, and body fat and serum osteoprotegerin/RANKL in prediabetic patients. Minerva Endocrinol. 2018;43(1):19-26.
25. Swastini DA, Wiryanthini IAD, Ariastuti NLP, Muliantara A. Atherosclerosis prediction with high sensitivity C-reactive protein (hs-CRP) and related risk factor in patient with dyslipidemia. Macedonian J Med Sci. 2019;7(22):3887-90. [DOI:10.3889/oamjms.2019.526]
26. Sinha SK, Nicholas SB, Sung JH, et al. hs-CRP is associated with incident diabetic nephropathy: findings from the Jackson heart study. Diabetes Care. 2019;42(11):2083-9. [DOI:10.2337/dc18-2563]
27. Cheng CH, Huang SC, Chiang TY, Wong Y, Huang YC. Higher plasma pyridoxal phosphate is associated with increased antioxidant enzyme activities in critically Ill surgical patients. BioMed Res Int. 2013;2013:1-7. [DOI:10.1155/2013/572081]
28. Barter PJ. Lipoprotein metabolism and CKD: Overview. Clin Exp Nephrol. 2014;18:243-6. [DOI:10.1007/s10157-013-0866-9]

بازنشر اطلاعات
Creative Commons License این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است.

کلیه حقوق این وب سایت متعلق به Journal of Advances in Medical and Biomedical Research می باشد.

طراحی و برنامه نویسی : یکتاوب افزار شرق

© 2025 CC BY-NC 4.0 | Journal of Advances in Medical and Biomedical Research

Designed & Developed by : Yektaweb