Journals / European Journal of Rheumatology / 2015 / Cilt: 2 - Sayı: 3

Genistein maddesinin bleomisine baslı deneysel sklerodermadaki dermal fibrozis üzerindeki koruyucu etkisi

Genistein protects dermal fibrosis in bleomycin-induced experimental scleroderma

Pages
99–102
Publication Date
2022-10-18
DOI
—
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AI Summary & Key Takeaways

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

However, its therapeutic potentials on human scleroderma require evaluation in future studies

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Genistein, a phytoestrogen, has anti-oxidant, anti-inflammatory, and anti-angiogenic properties.
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Key Findings & Data:Material and Methods: This study involved four groups of Balb/c mice (n=10 per group).
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Conclusion & Impact:However, its therapeutic potentials on human scleroderma require evaluation in future studies
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Genistein, a phytoestrogen, has anti-oxidant, anti-inflammatory, and anti-angiogenic properties. The aim of the present study is to evaluate the protective effect of genistein in bleomycin (BLM)-induced dermal fibrosis. Material and Methods: This study involved four groups of Balb/c mice (n=10 per group). Mice in three groups were administered BLM [100 μg/day in 100 μL phosphate-buffered saline (PBS)] subcutaneously for 4 weeks; the remaining (control) group received only 100 μL/ day of PBS subcutaneously. PBS or BLM was injected into the shaved upper back. Two of the BLM-treated groups also received genistein (1 or 3 mg/kg/day, subcutaneously, to the dorsal front of neck). At the end of the fourth week, all mice were sacrificed and blood and tissue samples were obtained. Results: The BLM applications increased the dermal thicknesses, tissue hydroxyproline contents, α-smooth muscle actin-positive cell counts, and led to histopathologically prominent dermal fibrosis. The genistein treatments decreased the tissue hydroxyproline contents and dermal thicknesses, in the BLM-injected mice. Conclusion: Genistein has antifibrotic potential in BLM-induced dermal fibrosis model. However, its therapeutic potentials on human scleroderma require evaluation in future studies

Özet

Amaç: Fitoöstrojen bir madde olan genistein, antioksidan, antiinflamatuar ve antianjiyojenik özelliklere sahiptir. Mevcut çalışmacın amacı, genisteinin bleomisine (BLM) bağlı dermal fibrozis üzerindeki koruyucu etkisini incelemektir. Gereç ve Yöntemler: Bu çalışma Balb/c türü dört grup deney faresi ile yapıldı (her grup için n=10). Üç grup fareye 4 hafta boyunca cilt altından BLM [100 μL fosfat tamponlu çözelti (PBS) içerisinde 100 μg/gün] uygulandı. Diğer bir gruba (kontrol grubu) ise cilt altından sadece 100 μL/gün dozunda PBS verildi. PBS veya BLM tıraş edilmiş olan üst sırt kısmına enjekte edildi. BLM ile tedavi edilen grupların ikisine de genistein verildi (boynun dorsal frontal bölgesine, deri altından 1 veya 3 mg/kg/gün). Dördüncü haftanın sonunda tüm fareler öldü ve kan ve doku örnekleri alındı. Bulgular: BLM uygulamaları dermal kalınlığı, doku hidroksiprolin içeriklerini ve alfa-düz kas aktin-pozitif hücre sayısını artırarak, histopatolojik olarak belirgin dermal fibrozise yol açmıştır. Diğer yandan, genistein tedavisi BLM enjekte edilen farelerde doku hidroksiprolin içeriklerini ve dermal kalınlığı azaltmıştır. Sonuç: Genistein, BLMye bağlı dermal fibrozis modelinde antifibrotik potansiyele sahiptir. Ancak, insan skleroderması üzerindeki terapötik potansiyellerinin yapılacak yeni çalışmalarda değerlendirilmesi gerekmektedir.

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Cite This Article

KOCA, S. S., IŞIK, A., GÖZEL, N., DAĞLI, A. F., YOLBAŞ, S. (2022). Genistein maddesinin bleomisine baslı deneysel sklerodermadaki dermal fibrozis üzerindeki koruyucu etkisi. European Journal of Rheumatology, Cilt: 2 - Sayı: 3, 99–102. https://ajindex.com/articles/511806

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References (14)

  1. Denton CP, Black CM. Scleroderma--clinical and pathological advances. Best Pract Res Clin Rheumatol 2004
  2. [CrossRef] 2. Gu YS, Kong J, Cheema GS, Keen CL, Wick G, Gershwin ME. The immunobiology of systemic sclerosis. Semin Arthritis Rheum 2008
  3. [CrossRef] 3. Bhattacharyya S, Wei J, Varga J. Understanding fibrosis in systemic sclerosis: shifting paradigms, emerging opportunities. Nat Rev Rheumatol 2011
  4. [CrossRef] 4. LeRoy EC. Systemic sclerosis. A vascular perspective. Rheum Dis Clin North Am 1996
  5. [CrossRef] 5. Chung L, Fiorentino D. Digital ulcers in patients with systemic sclerosis. Autoimmun Rev 2006
  6. [CrossRef] 6. Distler O, Del Rosso A, Giacomelli R, Cipriani P, Conforti ML, Guiducci S, et al. Angiogenic and angiostatic factors in systemic sclerosis: increased levels of vascular endothelial growth factor are a feature of the earliest disease stages and are associated with the absence of fingertip ulcers. Arthritis Res 2002
  7. R11. [CrossRef] 7. Distler O, Distler JH, Scheid A, Acker T, Hirth A, Rethage J, et al. Uncontrolled expression of vascular endothelial growth factor and its receptors leads to insufficient skin angiogenesis in patients with systemic sclerosis. Circ Res 2004
  8. [CrossRef] 8. Ishisaki A, Tsunobuchi H, Nakajima K, Imamura T. Possible involvement of protein kinase C activation in differentiation of human umbilical vein endothelium-derived cell into smooth muscle-like cell. Biol Cell 2004
  9. [CrossRef] 9. Chaudhuri V, Zhou L, Karasek M. Inflammatory cytokines induce the transformation of human dermal microvascular endothelial cells into myofibroblasts: a potential role in skin fibrogenesis. J Cutan Pathol 2007
  10. [CrossRef] 10. Sen U, Moshal KS, Tyagi N, Kartha GK, Tyagi SC. Homocysteine-induced myofibroblast differentiation in mouse aortic endothelial cells. J Cell Physiol 2006
  11. [CrossRef] 11. Verdrengh M, Jonsson IM, Holmdahl R, Tarkowski A. Genistein as an anti-inflammatory agent. Inflamm Res 2003
  12. [CrossRef] 12. Akiyama T, Ishida J, Nakagawa S, Ogawara H, Watanabe S, Itoh N, et al. Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem 1987
  13. Guo Y, Wang S, Hoot DR, Clinton SK. Suppression of VEGF-mediated autocrine and paracrine interactions between prostate cancer cells and vascular endothelial cells by soy isoflavones. J Nutr Biochem 2007
  14. [CrossRef] 14. Kim