These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Dual effects of hydrogen sulphide on focal cerebral ischaemic injury via modulation of oxidative stress-induced apoptosis.
    Author: Li GF, Luo HK, Li LF, Zhang QZ, Xie LJ, Jiang H, Li LP, Hao N, Wang WW, Zhang JX.
    Journal: Clin Exp Pharmacol Physiol; 2012 Sep; 39(9):765-71. PubMed ID: 22928638.
    Abstract:
    1. Hydrogen sulphide (H₂S), one of three signalling gasotransmitters, plays an important role in oxidative stress and apoptosis. However, the effects of H₂S on oxidative stress-induced apoptosis in focal cerebral ischaemic injury in rats have not been clarified. 2. In the present study, sodium hydrosulphide (NaHS) was used as the H₂S donor. Eighty-four Sprague-Dawley rats were randomly divided into six groups: sham, sham + low-dose (2.8 mg/kg) NaHS, sham + high-dose (11.2 mg/kg) NaHS, infarct, infarct + low-dose NaHS and infarct + high-dose NaHS. The focal cerebral ischaemic model was created by cranially inserting a nylon thread with a rounded tip into an internal carotid artery. Rats were killed 21 h after administration of NaHS. 3. In the infarct + low-dose NaHS compared with infarct group, infarct volume was significantly decreased and injury to the mitochondria in nerve cells was mitigated. Furthermore, significant increases were seen in mitochondrial superoxide dismutase and glutathione peroxidase activity and neuronal bcl-2 protein levels, whereas mitochondrial malondialdehyde content and neuronal bax and caspase 3 protein levels were significantly decreased, in the infarct + low-dose NaHS compared with infarct group. The effects seen in the infarct group were significantly aggravated in the infarct + high-dose NaHS group. 4. The findings of the present study provide novel evidence for the dual effects of H₂S on focal cerebral ischaemic injury via modulation of oxidative stress-induced apoptosis.
    [Abstract] [Full Text] [Related] [New Search]