الفهرس 
Introduction and Aim of WorkOnly 14 pages are availabe for public view
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Abstract
Acute renal failure (ARF), also known as acute kidney injury, is a
rapid loss of renal functions due to damage to the kidneys, resulting in
retention of the nitrogenous compounds (urea and creatinine) and nonnitrogenous
waste products that are normally excreted in urine.
In clinical practice, ischemia-reperfusion (I/R) injury is the most
common cause for acute renal failure. The pathogenic events in
ischemia/reperfusion injury include acute tubular necrosis, apoptosis,
glomerular injury and inflammation.
Stem cell therapy holds a great promise for the repair of injured
tissues and organs, including the kidney. Stem cells are undifferentiated
cells that undergo both self-renewal and differentiation into one or more
cell types & are found in adult and embryonic tissues and have potential
uses in therapies designed to repair and regenerate organs. There has been
considerable focus on the ability of stem cells to differentiate into nonhaematopoietic
cells of various tissue lineages, including cells of the
kidney. This growing evidence has led to a reconsideration of the source
of cells contributing to renal repair following injury.
There are reports that antioxidants such as N N’-diphenyl-1, 4-
phenylenediamine (DPPD) inhibit acute renal injury induced by
Ischemia-Reperfusion. It prevents the increases in content of lipid
peroxides and nephrotoxicity induced by Ischemia-Reperfusion, where
antioxidants are able to make trapping for free radicals.
The materials of this study comprised 60 rats that were divided into 6
groups (10 rats each group) as follow;
group 1 (Sham group), where 10 rats were subjected to right
nephrectomy without exposure to left renal pedicle ischemia.
group 2 (Positive control group), where 10 rats were subjected to
right nephrectomy and left renal ischemia where renal pedicles
were clamped with atraumatic vascular clamps for1 hr. Then the
vascular clamps were released to allow the reperfusion of the
ischemic kidney.
group 3 (Treated 1 group), where 10 rats were subjected to right
nephrectomy and left renal ischemia where renal pedicles were
clamped with atraumatic vascular clamps for1 hr. Then the
vascular clamp were released to allow the reperfusion of the
ischemic kidney. This group was received DPPD (0.5 g / kg, i.p.)
24 hr before the induction of ARF.
group 4 (Treated 2 group), where 10 rats were subjected to right
nephrectomy and left renal ischemia where renal pedicles were
clamped with atraumatic vascular clamps for1 hr. Then the
vascular clamps were released to allow the reperfusion of the
ischemic kidney. This group was received DPPD (0.5 g / kg, i.p.)
24 hr after the induction of ARF.
group 5 (Treated 3 group), where 10 rats were subjected to right
nephrectomy and left renal ischemia where renal pedicles were
clamped with atraumatic vascular clamps for 1hr. Then the
vascular clamps were released to allow the reperfusion of the
ischemic kidney. This group was received DPPD (0.5 g / kg, i.p.)
48 hr after the induction of ARF.
group 6 (Treated 4 group), where 10 rats were subjected to right
nephrectomy and left renal ischemia where renal pedicles were
clamped with atraumatic vascular clamps for1 hr. Then the
vascular clamps were released to allow the reperfusion of the
ischemic kidney. This group was received MSCs, which were
processed and cultured for 14 days, in a dose of (106) by IV
infusion at the rat tail vein 24 hr after the induction of ARF.
Blood samples were collected from the retro-orbital vein 4 days after
operation. Sera were separated. The rats of all groups were sacrificed (by
CO2narcosis) after 4 days of induction of the acute renal failure to obtain
renal tissue specimens
The results of this study are analyzed and the following conclusions
can be drawn:
1) I/R caused impairment of renal functions manifested by significant
elevation in serum creatinine, BUN, magnesium, urinary protein and
NAG and significant decline of creatinine clearance.
2) I/R enhanced oxidative stress in kidney tissues manifested by
significant elevation in MDA content and significant decline in
superoxide dismutase and glutathione reduced in kidney tissues.
3) Also, I/R deteriorated renal morphology in the form of
glomerulosclerosis, tubular atrophy and necrosis and interstitial
haemorrhage and fibrosis.
4) Treatment with antioxidant (DPPD) 24 hr before induction of I/R
induced acute renal injury caused marvelous improvement in kidney
function, renal injury and renal morphology.
5) Treatment with antioxidant (DPPD) 24 hr and 48 hr after induction of
I/R induced acute renal injury caused significant improvement in
kidney function, renal injury and renal morphology.
6) Early intervention with DPPD is more protective against the harmful
effects of I/R.
7) Also, treatment with MSC in case of I/R induced acute renal injury
caused significant marvelous improvement in renal function,
interstitial injury and renal morphology.
8) MSCs and DPPD were found to significantly inhibit inflammation,
oxidative stress and tubulointerstitial injury in I/R induced
nephrotoxicity rat model and early intervention with DPPD is found to
be more protective than late intervention.