Ramipril blunts glycerol-induced acute renal failure in rats through its anti-apoptosis, anti- inflammatory, anti-oxidant, and renin-inhibiting properties

Acute Kidney Injury (AKI) is a sudden episode of kidney
failure or kidney damage that happens within a few hours
or a few days and causes a buildup of waste products in
the blood making it hard for the kidney to keep the right
balance of fluid in the body. It affects other organs such
as the heart, brain and lungs [1]. Renal tubular damage
is a pathological characteristic of AKI. Currently, animal
models of glycerol-induced AKI are widely used [2]. Glycerol
injection into the muscle causes the release of myoglobin
and other muscle contents into the circulation,
ultimately resulting in AKI. Studies have demonstrated
that the pathogenesis of glycerol-induced AKI involves
myoglobin toxicity [3, 4], reactive oxygen species (ROS)
[5], inflammation [6], apoptosis [7] and redox-active iron
[5].
In this study ramipril and pioglitazone (reference drug)
were evaluated for their potential therapy in glycerol-induced
AKI in rats. Twenty animals divided into four
groups of five animals per group were used. Group I
served as control while group II received glycerol on day
8 only. Groups III and IV were administered with pioglitazone
and ramipril for 7 days respectively and on day 8
received glycerol. On day 9 blood samples were collected
for serum biochemical analysis of markers of oxidative
stress, enzymatic and non-enzymatic antioxidants, creatinine
and blood urea nitrogen. Animals were sacrificed
thereafter; and kidney tissues were harvested for histopathology
and immunohistochemistry. Expression of
caspase 3, renin receptor, NK-KB, and KIM-1 were carried
out.

Author(s): Adeolu Alex Adedapo

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