Morin attenuates ifosfamide-induced neurotoxicity in rats via suppression of oxidative stress, neuroinflammation and neuronal apoptosis
NeuroToxicology, cilt.76, ss.126-137, 2020 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 76
- Basım Tarihi: 2020
- Doi Numarası: 10.1016/j.neuro.2019.11.004
- Dergi Adı: NeuroToxicology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, Agricultural & Environmental Science Database, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, EMBASE, Environment Index, MEDLINE, Veterinary Science Database
- Sayfa Sayıları: ss.126-137
- Anahtar Kelimeler: Apoptosis, Ifosfamide, Inflammation, Morin, Neurotoxicity, Oxidative stress, IN-VITRO, INDUCED NEPHROTOXICITY, GENE-EXPRESSION, BRAIN, INFLAMMATION, ACID, ACTIVATION, INJURY, ENCEPHALOPATHY, DELTAMETHRIN
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Atatürk Üniversitesi Adresli: Evet
Özet
Ifosfamide (IFA), a commonly used chemotherapeutic drug, has been frequently associated with encephalopathy and central nervous system toxicity. The present study aims to investigate whether morin could protect against acute IFA-induced neurotoxicity. Morin was administered to male rats once daily for 2 consecutive days at doses of 100 and 200 mg/kg body weight (BW) orally. IFA (500 mg/kg BW; i.p.) was administered on second day. The results showed that morin markedly inhibited the production of acetylcholinesterase (AChE), butrylcholinesterase (BChE), carbonic anhydrase (CA), glial fibrillary acidic protein (GFAP), brain-derived neurotrophic factor (BDNF) and nuclear factor erythroid 2-related factor 2 (Nrf-2) induced by IFA. Morin ameliorated IFA-induced lipid peroxidation, glutathione (GSH) depletion, and decrease antioxidant enzyme activities, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx). Histopathological changes and immunohistochemical expressions of c-Jun N-terminal kinase (JNK) and c-Fos in the IFA-induced brain tissues were decreased after administration of morin. Furthermore, morin was able to down regulate the levels of inflammatory and apoptotic markers such as nuclear factor kappa B (NF-kappa B), neuronal nitric oxide synthase (nNOS), tumor necrosis factor-alpha (TNF-alpha), p53, cysteine aspartate specific protease-3 (caspase-3) and B-cell lymphoma-2 (Bcl-2). Taken together, our results demonstrated that morin elicited a typical chemoprotective effect on IFA-induced acute neurotoxicity.