Protective Effects of Chrysin Against Oxidative Stress and Inflammation Induced by Lead Acetate in Rat Kidneys: a Biochemical and Histopathological Approach

Küçükler S., Benzer F., Yıldırım S., Gür C., Kandemir F. M., Bengu A. S., ...Daha Fazla

BIOLOGICAL TRACE ELEMENT RESEARCH, cilt.199, sa.4, ss.1501-1514, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 199 Sayı: 4
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1007/s12011-020-02268-8
  • Dergi Adı: BIOLOGICAL TRACE ELEMENT RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Food Science & Technology Abstracts, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Sayfa Sayıları: ss.1501-1514
  • Anahtar Kelimeler: Apoptosis, Chrysin, Inflammation, Lead acetate, Nephrotoxicity, Oxidative stress, INDUCED NEPHROTOXICITY, GLUTATHIONE-PEROXIDASE, DNA-DAMAGE, ANTIOXIDANT, APOPTOSIS, TOXICITY, LIVER, PERMEABILITY, SUPPRESSION, AQUAPORINS
  • Atatürk Üniversitesi Adresli: Evet

Özet

In this study, the protective effects of chrysin (CR) on lead acetate (PbAc)-induced renal toxicity in Sprague-Dawley rats were investigated with biochemical, histopathological, and immunohistochemical methods. In the study, rats were given orally at 30 mg/kg/body weight (BW) PbAc after CR of 25 and 50 mg/kg/BW was administered to them orally (a total of 7 administrations for 7 days). The results showed that CR reduced urea and creatinine levels by alleviating PbAc-induced kidney damage. It was determined that CR decreases PbAc-induced lipid peroxidation due to its antioxidant properties and increases catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and glutathione (GSH) levels. It was also detected that CR protects DNA from the toxic effects of PbAc and reduces 8-hydroxy-2 '-deoxyguanosine (8-OHdG) levels. Biochemical and immunohistochemical findings demonstrated that CR had anti-inflammatory and antiapoptotic effects and reduced nuclear factor kappa-B (NF-kappa B), interleukin-33 (IL-33), prostaglandin-E2 (PGE-2), tumor necrosis factor-alpha (TNF-alpha), p53 levels, and the activities of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which were increased with PbAc administration. Moreover, CR was found to increase the levels of aquaporin-1 (AQP-1) and nephrine in PbAc-induced kidney tissue. CR decreased the contents of lead (Pb), zinc (Zn), iron (Fe), sodium (Na), and copper (Cu) and increased those of potassium (K) calcium (Ca) in renal tissue. These results indicated that CR considerably alleviates kidney toxicity caused by PbAc.