Protective effects of Ginkgo biloba extract against mercury(II)-induced cardiovascular oxidative damage in rats


Tunali-Akbay T. , Sener G. , Salvarli H., Sehirli O., Yarat A.

Phytotherapy Research, cilt.21, sa.1, ss.26-31, 2007 (SCI Expanded İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 21 Konu: 1
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1002/ptr.2007
  • Dergi Adı: Phytotherapy Research
  • Sayfa Sayıları: ss.26-31

Özet

This study was designed to determine the possible protective effect of Ginkgo biloba extract (EGb) against Hg II-induced oxidative damage and also thromboplastic activity in the aorta and heart tissues. Wistar albino rats of either sex (200-250 g) were divided into four groups. Rats were injected intraperitoneally with (1) control (C) group: 0.9% NaCl; (2) EGb group: Ginkgo biloba extract (Abdi Ibrahim Pharmaceutical Company, Istanbul, Turkey) at a dose of 50 mg/kg/day; (3) Hg group: a single dose of 5 mg/kg mercuric chloride (HgCl2); and (4) Hg + EGb group: First day EGb at a dose of 50 mg/kg/day, i.p., 1 hour after HgCl2 (5 mg/kg) injection; following four days EGb at a dose 50 mg/kg/day, i.p. After decapitation of the rats, trunk blood was obtained and serum tumor necrosis factor-alpha (TNF-alpha), lactate dehydrogenase (LDH) activity, and malondialdehyde (MDA) and glutathione (GSH) levels were analysed. In the aorta and heart tissues total protein, NIDA, GSH levels and thromboplastic activity were determined. The results revealed that HgCl, induced oxidative tissue damage, as evidenced by increases in MDA levels and decreased GSH levels both in serum and tissue samples. Thromboplastic activity was increased significantly following Hg administration, which verifies the cardiotoxic effects of HgCl,. Serum LDH and TNF-a were elevated in the Hg group compared with the control group. Since EGb treatment reversed these responses, it seems likely that Ginkgo biloba extract can protect the cardiovascular tissues against HgCl2-induced oxidative damage. Copyright 0 (c) 2006 John Wiley & Sons, Ltd.