Protective effect of Allium scorodoprasum L. ethanolic extract in cyclophosphamide-induced hepatotoxicity model in rats


Gungor H., Ekici M., Karatas Ö., Dik B.

The Journal of pharmacy and pharmacology, cilt.75, sa.5, ss.625-634, 2023 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 75 Sayı: 5
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1093/jpp/rgad002
  • Dergi Adı: The Journal of pharmacy and pharmacology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, Chemical Abstracts Core, EMBASE, International Pharmaceutical Abstracts, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.625-634
  • Anahtar Kelimeler: Allium scorodoprasum extract, cyclophosphamide, inflammation, liver toxicity, oxidative stress
  • Sivas Cumhuriyet Üniversitesi Adresli: Evet

Özet

OBJECTIVES: Cyclophosphamide is a chemotherapeutic agent and immunosuppressant drug; however, it damages the liver. This study investigates the protective effect of ethanolic extract of Allium scorodoprasum (ASE) on cyclophosphamide-induced liver injury. METHODS: Twenty-eight Wistar albino rats were randomly divided into four groups (n = 7 per group): healthy rats, cyclophosphamide (200 mg/kg), cyclophosphamide (200 mg/kg) + ASE (100 mg/kg) and cyclophosphamide (200 mg/kg) + ASE (200 mg/kg). ASE was administered for 14 days, and the rats were euthanized 24 h after cyclophosphamide administration. KEY FINDINGS: Cyclophosphamide treatment leads to an increase in serum levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, total cholesterol, triglycerides, low-density lipoprotein and very low-density lipoprotein, as well as an increase in the liver levels of malondialdehyde, tumour necrosis factor, interleukin (IL)-1β and IL-6, while high-density lipoprotein levels decrease. Treatment with cyclophosphamide caused liver necrosis and postnecrotic cell infiltration; however, pathological changes were prevented by ASE. 8-Hydroxy-2'-deoxyguanosine, anti-4-hydroxynenal antibody and anti-dityrosine levels increased in rats treated with cyclophosphamide and decreased in the groups treated with ASE. These changes were dose dependent in the ASE-treated groups. CONCLUSIONS: Treatment with cyclophosphamide caused liver damage due to oxidative stress and inflammation. ASE regulated the damage at high doses because it has potent antioxidant and anti-inflammatory ingredients. In future studies, it may be beneficial to administer ASE in higher doses or for longer periods of time.