Valproic acid induced oxidative brain injury in rats: Protective effect of edaravone

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Hacıhasanoğlu Çakmak N., Yanardağ R.

ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI, cilt.73, sa.2, ss.185-193, 2026 (SCI-Expanded, Scopus, TRDizin)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 73 Sayı: 2
  • Basım Tarihi: 2026
  • Doi Numarası: 10.33988/auvfd.1738110
  • Dergi Adı: ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI
  • Derginin Tarandığı İndeksler: Scopus, Science Citation Index Expanded (SCI-EXPANDED), EMBASE, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.185-193
  • İstanbul Medipol Üniversitesi Adresli: Evet

Özet

Valproic acid (2-propyl valeric acid, VPA) is the drug of choice for the treatment of migraine, bipolar disorder, and

epileptic disorders in both children and adults. Although VPA has beneficial effects, long-term administration is

reported to damage many tissues and organs. VPA administration increases free-radical production. Edaravone (3-

methyl-1-phenyl-2-pyrazolin-5-one, EDA) is a potent antioxidant that protects against oxidative stress. The aim of our

study was to investigate the protective effects of EDA against brain damage in VPA-treated rats. Male Sprague Dawley

rats were used in our study. The rats were randomly divided into four groups: control, EDA, VPA, and VPA+EDA. EDA

and VPA were administered intraperitoneally at doses of 30 mg/kg and 0.5 g/kg, respectively daily for 7 days. On day

8, all animals were sacrificed under anesthesia, and brain tissues were removed. VPA caused decreases in the levels

of reduced glutathione (GSH, P<0.05), glutathione peroxidase (GPx, P<0.001), glutathione reductase (GR, P<0.001),

and paraoxonase (PON, P<0.0001). On the other hand, VPA increased values of lipid peroxidation (LPO, P<0.05),

catalase (CAT, P<0.05), superoxide dismutase (SOD, P<0.0001), glutathione-S-transferase (GST, P<0.01), xanthine

oxidase (XO, P<0.01), adenosine deaminase (ADA, P<0.001), protein carbonyl (PC, P<0.0001), myeloperoxidase (MPO,

P<0.0001), sialic acid (SA, P<0.0001), and acetylcholinesterase (AChE, P<0.0001) compared with the control group.

EDA reversed all values. These results suggest that EDA administration potentially reduces VPA-induced brain injury.