Journals / Clinical and Experimental Health Sciences / 2017 / Cilt: 7 - Sayı: 2

Riboflavin Treatment Reduces Apoptosis and Oxidative DNA Damage in a Rat Spinal Cord Injury Model

Omurilik Hasarı Oluşturulan Sıçan Modelinde Riboflavin Tedavisi Apoptozu ve Oksidan DNA Hasarını Azaltır

Pages
55–63
Publication Date
2022-10-11
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)

Moreover, our study demonstrated that riboflavin not only exerts antioxidant and antiapoptotic effects on the spinal cord but also has a significant impact on preventing kidney damage secondary to SCI.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Spinal cord injury (SCI) leads to an inflammatory response and results in oxidative stress, which has deleterious effects on several organ systems.
📊
Key Findings & Data:Methods: In order to induce SCI, the standard weight-drop method was used to induce a moderately severe injury (100 g/cm force) at the T10 vertebral level.
💡
Conclusion & Impact:Moreover, our study demonstrated that riboflavin not only exerts antioxidant and antiapoptotic effects on the spinal cord but also has a significant impact on preventing kidney damage secondary to SCI.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Omurilik hasarı · riboflavin · oksidan hasar

Abstract

Objective: Spinal cord injury (SCI) leads to an inflammatory response and results in oxidative stress, which has deleterious effects on several organ systems. Riboflavin is an easily absorbed micronutrient that plays an important role in maintaining health in humans and animals. The present study was designed to investigate the putative protective effect of riboflavin against SCI-induced spinal cord and kidney damage. Methods: In order to induce SCI, the standard weight-drop method was used to induce a moderately severe injury (100 g/cm force) at the T10 vertebral level. Injured animals were given either 25 mg/kg riboflavin or carboxymethyl cellulose 15 min after injury, and this regimen was repeated twice daily for 7 days. On the 7th post-injury day, a neurological examination was performed and rats were sacrificed. Spinal cord and kidney samples were harvested and prepared for a histological examination. Tissue levels of malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) and activities of myeloperoxidase (MPO), superoxide dismutase (SOD), and caspase-3 were determined. Results: SCI caused a significant decrease in tissue GSH levels and SOD activities, which were accompanied by significant increases in MDA and 8-OHdG levels and MPO and caspase-3 activities. However, riboflavin treatment reversed these parameters and improved histological findings. Conclusion: SCI caused tissue injury through oxidative stress and neutrophil infiltration into tissues. Riboflavin inhibited tissue injury through its neuroprotective and antiapoptotic effects. Moreover, our study demonstrated that riboflavin not only exerts antioxidant and antiapoptotic effects on the spinal cord but also has a significant impact on preventing kidney damage secondary to SCI.

Özet

Amaç: Omurilik hasarı inflamatuar yanıta ve oksidatif strese yol açarak çeşitli organ sistemlerinde zararlı etkiler oluşturur. Riboflavin insan ve hayvanda sağlığın sürdürülmesinde önemli role sahip olan ve kolayca absorbe edilen mikrobesindir. Bu çalışma omurilik yaralanmasına bağlı omurilik ve böbrek dokusunda riboflavinin koruyucu etkilerini araştırmak üzere planlandı. Yöntemler: Omurilik hasarı oluşturmak için anestezi altındaki sıçanlara T10 seviyesinde 100 g/cm şiddetinde ağırlık düşürme metodu uygulandı. Hasarlı hayvanlara riboflavin 25 mg/kg dozunda ya da taşıyıcı çözelti tedavisi hasardan 15 dakika sonra verildi ve 7 gün süreyle devam edildi. Hasardan sonra 7.günde nörolojik testin arkasından hayvanlar dekapite edilerek spinal ve böbrek dokuları alındı. Dokularda histolojik tayinler yapıldı ve malondialdehit (MDA), glutatyon (GSH), 8-hidroksi-2-deoksiguanozin (8-OHdG) düzeyleri ile myeloperoksidaz (MPO), süperoksid dismutaz (SOD) ve katalaz aktiviteleri tayin edildi. Bulgular: Omurilik hasarı dokularda GSH düzeylerinde ve SOD aktivitesinde azalamaya, MDA düzeyinde ve MPO ve kaspaz aktivitelerinde artışa neden oldu. Riboflavin tedavisi bu parametreleri geri çevirdi ve histolojik bulgularda düzelme gösterdi. Sonuç: Çalışmamızda Omurilik hasarı, dokuya nötrofil göçüne ve oksidan strese yol açarken, antiapoptotik ve nöroprotektif özellikleri ile riboflavin lipid peroksidasyonunu ve nötrofillerin dokuya infiltrasyonunu inhibe etti. Ayrıca, çalışmamız riboflavinin antiapoptotik ve antioksidan etkisinin sadece omurilikte değil omurilik hasarında ikincil olarak ortaya çıkan böbrek hasarında da önemli faydaları olduğunu gösterdi.

🔖

Cite This Article

ÇEVİK, Ö., ERŞAHİN, M., ŞENER, G., ERCAN, F., SAKARCAN, S., EMİNOĞLU, M. E., AK, E. (2022). Riboflavin Treatment Reduces Apoptosis and Oxidative DNA Damage in a Rat Spinal Cord Injury Model. Clinical and Experimental Health Sciences, Cilt: 7 - Sayı: 2, 55–63. https://ajindex.com/articles/474430

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Cristante AF, Barros Filho TE, Marcon RM, Letaif OB, Rocha ID. Therapeutic approaches for spinal cord injury. Clinics (Sao Paulo) 2012
  2. [CrossRef] 2. Boulenguez P, Vinay L. Strategies to restore motor functions after spinal cord injury. Curr Opin Neurobiol 2009
  3. [CrossRef] 3. Hulsebosch CE. Recent advances in pathophysiology and treatment of spinal cord injury. Adv Physiol Educ 2002
  4. [CrossRef] 4. Azbill RD, Mu X, Bruce-Keller AJ, Mattson MP, Springer JE. Impaired mitochondrial function, oxidative stress and altered antioxidant enzyme activities following traumatic spinal cord injury. Brain Res 1997
  5. [CrossRef] 5. Park E, Velumian AA, Fehlings MG. The role of excitotoxicity in secondary mechanisms of spinal cord injury: a review with an emphasis on the implications for white matter degeneration. J Neurotrauma 2004
  6. [CrossRef] 6. Hall ED. Antioxidant therapies for acute spinal cord injury. Neurotherapeutics 2011
  7. [CrossRef] 7. Bastani NE, Kostovski E, Sakhi AK, Karlsen A, Carlsen MH, Hjeltnes N, et al. Reduced antioxidant defense and increased oxidative stress in spinal cord injured patients. Arch Phys Med Rehabil 2012
  8. [CrossRef] 8. Powers HJ. Riboflavin (vitamin B-2) and health. Am J Clin Nutr 2003
  9. Depeint F, Bruce WR, Shangari N, Mehta R, O'Brien PJ. Mitochondrial function and toxicity: role of the B vitamin family on mitochondrial energy metabolism. Chem Biol Interact 2006
  10. [CrossRef ] 10. Bodiga VL, Bodiga S, Surampudi S, Boindala S, Putcha U, Nagalla B, et al. Effect of vitamin supplementation on cisplatin-induced intestinal epithelial cell apoptosis in Wistar/NIN rats. Nutrition 2012
  11. [CrossRef] 11. Al-Harbi NO, Imam F, Nadeem A, Al-Harbi MM, Korashy HM, SayedAhmed MM, et al. Riboflavin attenuates lipopolysaccharide-induced lung injury in rats. Toxicol Mech Methods 2015
  12. [CrossRef] 12. Yu Z, Morimoto K, Yu J, Bao W, Okita Y, Okada K. Endogenous superoxide dismutase activation by oral administration of riboflavin reduces abdominal aortic aneurysm formation in rats. J Vasc Surg 2016
  13. [CrossRef] 13. Bertollo CM, Oliveira AC, Rocha LT, Costa KA, Nascimento EB Jr, Coelho MM. Characterization of the antinociceptive and anti-inflammatory activities of riboflavin in different experimental models. Eur J Pharmacol 2006
  14. [CrossRef] 14. Granados-Soto V, Terán-Rosales F, Rocha-González HI, Reyes-