Neuroprotective Effects of beta-Myrcene Following Global Cerebral Ischemia/Reperfusion-Mediated Oxidative and Neuronal Damage in a C57BL/J6 Mouse

ÇİFTÇİ O., ÖZTANIR M. N., Cetin A.

NEUROCHEMICAL RESEARCH, cilt.39, sa.9, ss.1717-1723, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 39 Sayı: 9
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1007/s11064-014-1365-4
  • Dergi Adı: NEUROCHEMICAL RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1717-1723
  • Anahtar Kelimeler: Global cerebral I/R, Oxidative stress, Neuronal damage, beta-Myrcene, C57BL/J6, ISCHEMIA-REPERFUSION INJURY, RATS, STROKE, MODEL
  • İnönü Üniversitesi Adresli: Evet

Özet

The aim of this study was to investigate the effects of beta-myrcene (MYR) on oxidative and histological damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. Mice (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) MYR, and (4) MYR + I/R. The SH group was used as a control and received 0.1 % carboxymethyl cellulose (CMC) as a vehicle following a medial incision without carotid occlusion. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and treated with the vehicle intraperitoneally (i.p.) for 10 days. In the MYR group, mice were given 200 mg/kg MYR dissolved in 0.1 % CMC for 10 days following a medial incision without carotid occlusion. In the MYR + I/R group, the I/R procedure was performed exactly as in the I/R group, and they were then treated with the same dose of MYR for 10 days. Cerebral I/R induced oxidative stress via an increase in thiobarbituric acid reactive substances (TBARS) formation and a decrease in the antioxidant defense systems, including glutathione (GSH), catalase, glutathione peroxidase (GPx) and superoxide dismutase (SOD). However, MYR treatment protected against the oxidative effects of I/R by inducing significant increases in GSH, GPx, and SOD and a significant decrease in the formation of TBARS. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by MYR treatment. This study has demonstrated that MYR effectively attenuates oxidative and histological damage in the brain caused by global I/R. The beneficial effects of MYR probably contribute to its strong antioxidant and radical scavenging properties. In conclusion, MYR may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, may be a viable and safe alternative treatment for ischemic stroke in humans.