Journals / The Anatolian Journal of Cardiology / 2016 / Cilt: 16 - Sayı: 5

Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS

Pages
310–315
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

NOS plays a role in this damage, and pentoxifylline aided in improving nNOS and iNOS expression in this damage.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate.
📊
Key Findings & Data:In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifylline on this pathology.Methods: In this experimental study, 50 Wistar albino male rats were used.
💡
Conclusion & Impact:NOS plays a role in this damage, and pentoxifylline aided in improving nNOS and iNOS expression in this damage.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate. In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifylline on this pathology.Methods: In this experimental study, 50 Wistar albino male rats were used. The rats were divided into 5 groups: group C, control; group D, only diabetes; group D+PI and D+PII, diabetes + pentoxifylline; group P, only pentoxifylline. Group D+PI rats received 50 mg/kg/day pentoxifylline over two months. However, group D+PII rats received saline in the first month and 50 mg/kg/day of pentoxifylline over the following month. At the end of two months, NOS expressions in heart tissue were assessed through immunohistochemistry analysis. The data were compared by one-way ANOVA.Results: At the end of the experiments, there was increased cytoplasmic vacuolization, myofibrillar loss, cytoplasmic eosinophilia, and degeneration of cardiomyocytes; nNOS and iNOS expressions in group D decreased compared with that in group C. In group D+PI and group D+PII, nNOS and iNOS expressions improved compared with group D.Conclusion: As a result, we found that diabetes, a known chronic disease, causes serious damage in heart tissue. NOS plays a role in this damage, and pentoxifylline aided in improving nNOS and iNOS expression in this damage.

🔖

Cite This Article

KARABULUT, D., ULUSOY, H. B., KAYMAK, E., SÖNMEZ, M. F. (2016). Therapeutic effects of pentoxifylline on diabetic heart tissue via NOS. The Anatolian Journal of Cardiology, Cilt: 16 - Sayı: 5, 310–315. https://ajindex.com/articles/365522

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Roessner C, Paasch U, Kratzsch J, Glander HJ, Grunewald S. Sperm apoptosis signalling in diabetic men. Reprod Biomed Online 2012; 25: 292-9
  2. Nagareddy PR, McNeill JH, MacLeod KM. Chronic inhibition of inducible nitric oxide synthase ameliorates cardiovascular abnormalities in streptozotocin diabetic rats. Eur J Pharmacol 2009; 611: 53-9
  3. Ansley DM, Wang B. Oxidative stress and myocardial injury in the diabetic heart. J Pathol 2013; 229: 232-41
  4. Soliman H, Craig GP, Nagareddy P, Yuen VG, Lin G, Kumar U, et al. Role of inducible nitric oxide synthase in induction of RhoA expression in hearts from diabetic rats. Cardiovasc Res 2008; 79: 322-30
  5. Van Linthout S, Riad A, Dhayat N, Spillmann F, Du J, Dhayat S, et al. Anti-inflammatory effects of atorvastatin improve left ventricular function in experimental diabetic cardiomyopathy. Diabetologia 2007; 50: 1977-86
  6. Li J, Peng L, Du H, Wang Y, Lu B, Xu Y, et al. The protective effect of beraprost sodium on diabetic cardiomyopathy through the Inhibition of the p38 MAPK signaling pathway in high-fat-induced SD Rats. Int J Endocrinol 2014; 2014: 901437
  7. Sönmez MF, Narin F, Akkuş D, Özdamar S. Effect of melatonin and vitamin C on expression of endothelial NOS in heart of chronic alcoholic rats. Toxicol Ind Health 2009; 25: 385-93
  8. Liu VW, Huang PL. Cardiovascular roles of nitric oxide: a review of insights from nitric oxide synthase gene disrupted mice. Cardiovasc Res 2008; 77: 19-29
  9. Sönmez MF, Narin F, Balcıoğlu E. Melatonin and vitamin C attenuates alcohol-induced oxidative stress in aorta. Basic Clin Pharmacol Toxicol 2009; 105: 410-5
  10. Sönmez MF, Narin F, Akkuş D, Türkmen AB. Melatonin and vitamin C ameliorate alcohol-induced oxidative stress and eNOS expression in rat kidney. Ren Fail 2012; 34: 480-6
  11. Umar S, van der Laarse A. Nitric oxide and nitric oxide synthase isoforms in the normal, hypertrophic, and failing heart. Mol Cell Biochem 2010; 333: 191-201
  12. Wang W, Zolty E, Falk S, Basava V, Reznikov L, Schrier R. Pentoxifylline protects against endotoxin-induced acute renal failure in mice. Am J Physiol Renal Physiol 2006; 291: F1090-5
  13. Motawi TK, Darwish HA, Abd El Tawab AM. The relative efficacy of aminoguanidine and pentoxifylline in modulating endotoxininduced cardiac stress. Cell Biochem Funct 2011; 29: 694-702
  14. Stosic-Grujicic S, Maksimovic D, Badovinac V, Samardzic T, Trajkovic V, Lukic M, et al. Antidiabetogenic effect of pentoxifylline is associated with syst