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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
[Sodium hydrosulfide for prevention of kidney damage in rats after amputation]
Ying Zhang1, Ning Liu, Qingai Ren
1First Surgery Department of South Building, General Hospital of PLA, Beijing 100853, China.
Objective:
To explore the mechanism of kidney injury in rats following amputation and the protective effects of sodium hydrosulfide (NaHS) on kidney structure and function.
Methods:
Male Wistar rats were randomly divided into normal control, 6 h after operation, NaHS intervention, and propargyl glycine (PPG) intervention groups (n=7). Plasma level of H2S, kidney injury molecule-1 (KIM-1), myeloperoxidase enzyme (MPO), malondialdehyde (MDA), nitric oxide (NO), urea nitrogen, creatinine, and renal tissue MPO, MDA, and KIM-1 levels, and activity of CSE were measured and the renal histological and mitochondrial structural changes were observed using optical and electron microscopy. In another experiment with SD rats, the rats were randomized also into these 4 groups (n=8) for measurement of renal mitochondrial respiratory control ratio, membrane potential and ATP activity.
Results:
Traumatic changes in rat kidney cells and mitochondrial structure occurred in the rats 6 h after amputation with significantly increased plasma and renal KIM-1 (P<0.01) but significantly decreased H2S/CSE levels (P<0.01). Plasma H2S/kidney CSE level was significantly increased following NaHS intervention (P<0.01), which reduce the damage of the kidney tissue and significantly lower plasma and renal KIM-1, NO, BUN, Cr, MPO, and MDA (P<0.01). Rat kidney mitochondrial respiratory control ratio, membrane potential and ATP activity all decreased significantly after amputation (P<0.01) increased significantly after the application of NaHS; such improvements did not occur following PPG treatment.
Conclusions:
Amputation can lead to damage to the structure and function of the rat kidneys, and NaHS can significantly improve mitochondrial function and further reduce renal structural and functional impairments, suggesting that H2S, as an endogenous mediator, may act on the mitochondria through several pathways to regulate energy metabolism and participate in the pathophysiological processes of tissue damage and repair.
