Tripatara, Pinpat, Patel, Nimesh S.A., Brancaleone, Vincenzo, Renshaw, Derek, Rocha, Joao, Sepodes, Bruno, Mota-Filipe, Helder, Perretti, Mauro and Thiemermann, Christoph (2009) Characterisation of cystathionine gamma-lyase/hydrogen sulphide pathway in ischaemia/reperfusion injury of the mouse kidney: an in vivo study. European Journal of Pharmacology, 606 (1-3). pp. 205-209. ISSN 0014-2999Full text not available from this repository.
The generation of endogenous hydrogen sulphide may either limit or contribute to the degree of tissue injury caused by ischaemia/reperfusion injury. Here, we have attempted to characterise the endogenous hydrogen sulphide synthesis pathway and the effects of sodium hydrosulphide, a hydrogen sulphide donor, in a mouse model of renal ischaemia/reperfusion injury. Anaesthetised male C57/b mice weighing 20–25 g were divided into two groups; (i) ‘Ischaemia/Reperfusion Injury’, in which mice were subjected to bilateral renal ischaemia performed by clamping the renal pedicles for 30 min followed by reperfusion for 24 h, (ii) ‘Sham’, in which mice were subjected to the same surgical procedures as above, except for renal ischaemia/reperfusion. Western blot analysis of the kidney taken at the end of the experiment demonstrated that cystathionine gamma-lyase, the enzyme responsible for generating hydrogen sulphide in the cardiovascular system, is expressed in the normal kidney and is significantly increased after ischaemia/reperfusion injury. Ischaemia/reperfusion injury significantly increased the rate of hydrogen sulphide production in kidney homogenates and increased the plasma concentration of hydrogen sulphide. In addition, we have shown that administration of the hydrogen sulphide donor sodium hydrosulphide (100 µmol/kg) 30 min prior to ischaemia and 6 h into reperfusion significantly attenuated ischaemia/reperfusion injury-induced renal dysfunction indicated by serum creatinine and urea. These findings suggest that hydrogen sulphide protects the kidney against ischaemia/reperfusion injury and that the increase in expression of the enzyme cystathionine gamma-lyase during ischaemia/reperfusion injury may be one of many endogenous mechanisms to limit renal ischaemia/reperfusion injury.
|Subjects:||University of Westminster > Science and Technology > Life Sciences, School of (No longer in use)|
|Depositing User:||Miss Nina Watts|
|Date Deposited:||12 Jan 2010 16:17|
|Last Modified:||11 Jun 2013 11:18|
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