Protective effects of morin against acrylamide-induced hepatotoxicity and nephrotoxicity: A multi-biomarker approach


Creative Commons License

Kandemir F. M., Yıldırım S., Küçükler S., Caglayan C., Darendelioğlu E., Dortbudak M. B.

Food and Chemical Toxicology, cilt.138, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 138
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1016/j.fct.2020.111190
  • Dergi Adı: Food and Chemical Toxicology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, Chemical Abstracts Core, Chimica, EMBASE, Environment Index, Food Science & Technology Abstracts, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Anahtar Kelimeler: Acrylamide, Apoptosis, Hepatotoxicity, Morin, Nephrotoxicity, Oxidative stress, INDUCED OXIDATIVE STRESS, AQUAPORIN-2 WATER CHANNEL, INDUCED TOXICITY, NEPHRIN EXPRESSION, IN-VITRO, INFLAMMATION, APOPTOSIS, AUTOPHAGY, DAMAGE, CELLS
  • Atatürk Üniversitesi Adresli: Evet

Özet

Acrylamide (ACR) is a heat-induced carcinogen substance that is found in some foods due to cooking or other

thermal processes. The aim of present study was to assess the probable protective effects of morin against ACRinduced

hepatorenal toxicity in rats. The rats were treated with ACR (38.27 mg/kg b.w., p.o.) alone or with

morin (50 and 100 mg/kg b.w., p.o.) for 10 consecutive days. Morin treatment attenuated the ACR-induced liver

and kidney tissue injury by diminishing the serum AST, ALP, ALT, urea and creatinine levels. Morin increased

activities of SOD, CAT and GPx and levels of GSH, and suppressed lipid peroxidation in ACR induced tissues.

Histopathological changes and immunohistochemical expressions of p53, EGFR, nephrin and AQP2 in the ACRinduced

liver and kidney tissues were decreased after administration of morin. In addition, morin reversed the

changes in levels of apoptotic, autophagic and inflammatory parameters such as caspase-3, bax, bcl-2, cytochrome

c, beclin-1, LC3A, LC3B, p38α MAPK, NF-κB, IL-1β, IL-6, TNF-α and COX-2 in the ACR-induced toxicity.

Morin also affected the protein levels by regulating the PI3K/Akt/mTOR signaling pathway and thus alleviated

ACR-induced apoptosis and autophagy. Overall, these findings may shed some lights on new approaches for the

treatment of ACR-induced hepatotoxicity and nephrotoxicity.