The neuroprotective effect of mesenchymal stem cells in colistin-induced neurotoxicity

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Öz Gergin Ö., Gergin I. Ş., Pehlivan S. S., Cengiz Mat Ö., Turan I. T., Bayram A., ...Daha Fazla

TOXICOLOGY MECHANISMS AND METHODS, cilt.33, sa.2, ss.95-103, 2023 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 2
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1080/15376516.2022.2090303
  • Dergi Adı: TOXICOLOGY MECHANISMS AND METHODS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Environment Index, Food Science & Technology Abstracts, MEDLINE, Veterinary Science Database
  • Sayfa Sayıları: ss.95-103
  • Anahtar Kelimeler: Colistin, immunohistochemistry, mesenchymal stem cells, neurotoxicity, oxidative stress, MITOCHONDRIAL DYSFUNCTION, INDUCED APOPTOSIS, OXIDATIVE STRESS, BRAIN, ASTROCYTES, MARROW, METHANESULFONATE, NEPHROTOXICITY, SUPPRESSION, EXPRESSION
  • Erciyes Üniversitesi Adresli: Evet

Özet

Colistin is an effective antibiotic against multidrug-resistant gram-negative bacterial infections; however, neurotoxic effects are fundamental dose-limiting factors for this treatment. Stem cell therapy is a promising method for treating neuronal diseases. Multipotent mesenchymal stromal cells (MSC) represent a promising source for regenerative medicine. Identification of neuroprotective agents that can be co-administered with colistin has the potential to allow the clinical application of this essential drug. This study was conducted to assess the potential protective effects of MSC, against colistin-induced neurotoxicity, and the possible mechanisms underlying any effect. Forty adult female albino rats were randomly classified into four equal groups; the control group, the MSC-treated group (A single dose of 1 x 106/mL MSCs through the tail vein), the colistin-treated group (36 mg/kg/d colistin was given for 7 d) and the colistin and MSC treated group (36 mg/kg/d colistin was administered for 7 d, and 1 x 106/mL MSCs). Colistin administration significantly increased GFAP, NGF, Beclin-1, IL-6, and TNF-alpha immunreactivity intensity. MSC administration in colistin-treated rats partially restored each of these markers. Histopathological changes in brain tissues were also alleviated by MSC co-treatment. Our study reveals a critical role of inflammation, autophagy, and apoptosis in colistin-induced neurotoxicity and showed that they were markedly ameliorated by MSC co-administration. Therefore, MSC could represent a promising agent for prevention of colistin-induced neurotoxicity.