Protective effects of syringic acid on neurobehavioral deficits and hippocampal tissue damages induced by sub-chronic deltamethrin exposure.


Ogut E., ŞEKERCİ R., Akcay G., YILDIRIM F. B., DERİN N., Aslan M., ...Daha Fazla

Neurotoxicology and teratology, cilt.76, ss.106839, 2019 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 76
  • Basım Tarihi: 2019
  • Doi Numarası: 10.1016/j.ntt.2019.106839
  • Dergi Adı: Neurotoxicology and teratology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.106839
  • Anahtar Kelimeler: Sub-chronic deltamethrin exposure, Hippocampus, Syringic acid, Syringic acid administration, Syringic acid treatment, OXIDATIVE STRESS, PYRETHROID INSECTICIDES, MORUS-NIGRA, ANTIOXIDANT, RAT, INJURY, CHANNELS, PARAMETERS, TOXICITY, BEHAVIOR
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Recent developments in the field of insecticide exposure have led to a renewed interest in alternative antioxidant therapy. The present study was to investigate the neuroprotective role of syringic acid (SA, 25 mg/kg/day) on the neurotoxicity and oxidative damage induced by deltamethrin (DTM, 1.28 mg/kg/day during two months) in CA1/3 pyramidal neurons. Animals were divided into 4 groups (n = 16/group) (250-270 g) for control, DTM, SA and DTM + SA. DTM and SA were administered by oral gavage daily. Rats that were given sub-chronic DTM had revealed a significant increase in caspase-3 levels, impaired recognition memory, reduced antioxidant activity and enhanced free radicals in the hippocampus. The results showed that SA ameliorated neurobehavioral alterations, reduced reactive oxygen/nitrogen species, pyknosis in the CA1/3 and increased antioxidant enzyme activity. In conclusion, SA (25 mg/kg/day) had potential neuroprotective and therapeutic impacts against sub-chronic DTM exposure via its antioxidant and antiapoptotic efficacy. Therefore, it can be used as a neuroprotective natural plant-derived agent against DTM-induced neurotoxicity.