Repository logo
Communities & Collections
All of MSAR
  • English
  • العربية
  • বাংলা
  • Català
  • Čeština
  • Deutsch
  • Ελληνικά
  • Español
  • Suomi
  • Français
  • Gàidhlig
  • हिंदी
  • Magyar
  • Italiano
  • Қазақ
  • Latviešu
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Srpski (lat)
  • Српски
  • Svenska
  • Türkçe
  • Yкраї́нська
  • Tiếng Việt
Log In
New user? Click here to register. Have you forgotten your password?
  1. Home
  2. Browse by Author

Browsing by Author "Hammam, Olfat A"

Filter results by typing the first few letters
Now showing 1 - 1 of 1
  • Results Per Page
  • Sort Options
  • Loading...
    Thumbnail Image
    Item
    Hydroxysafflor yellow A protects against thioacetamide-induced liver fibrosis in rats via suppressing proinflammatory/fibrogenic mediators and promoting hepatic stellate cell senescence and apoptosis
    (Wolters Kluwer Medknow Publications, 2023-08) Seif el-Din, Sayed H; Hammam, Olfat A; Ezzat, Shahira M; Saleh, Samira; Safar, Marwa M; El- Maadawy, Walaa H; El-Lakkany, Naglaa M
    To evaluate the effect of hydroxysafflor yellow A (HSYA) on thioacetamide-induced liver fibrosis. Methods: Thioacetamide was administered to rats intraperitoneally in doses of 200 mg/kg twice a week for 12 weeks. Thioacetamide- intoxicated rats were given silymarin (50 mg/kg) or HSYA (5 mg/ kg) orally every day for 8 weeks. Liver enzymes, fibrosis markers, histological changes as well as immunohistochemistry of TNF-α, IL-6, p21, α-SMA, and caspase-3 were examined. The effect of HSYA on HSC-T6 activation/proliferation and apoptosis was also determined in vitro. Results: HSYA decreased liver enzymes, TNF-α, IL-6, and p21 expressions, hepatic PDGF-B, TIMP-1, TGF-β1, and hydroxyproline levels, as well as fibrosis score (S2 vs. S4) compared to the thioacetamide group. HSYA also downregulated α-SMA while increasing caspase-3 expression. Surprisingly, at 500 µg/mL, HSYA had only a slightly suppressive effect on HSC proliferation, with a 9.5% reduction. However, it significantly reduced TGF-β1, inhibited α-SMA expression, induced caspase-3 expression, and promoted cell senescence. Conclusions: HSYA may be a potential therapeutic agent for delaying and reversing the progression of liver fibrosis. More research on HSYA at higher doses and for a longer period is warranted.

October University for Modern Sciences and Arts Established by Dr. Nawal El Degwi in 1996 copyright © 2019-2024

DSpace software copyright © 2002-2025 LYRASIS

  • Privacy policy
  • End User Agreement
  • Send Feedback