الآثار النسيجية والكيميائية الحيوية لعقار إنالابريل وبيريدكسامين على كلى إناث الفئران المصابة بمرض السكري المستحث بالستربتوزوتوسين . The histopathological and biochemical effects of enalapril and pyridoxamine on the kidney of streptozotocin diabetic female rats.
• 2013
Publication Information
Authors
د. عبير مصطفي المحلاوي1 –د. علا احمد الجوهري2 أ.م.د. خالد عبد القوي إبراهيم3- د.أوديت وهبة4 أقسام الأنسجة وبيولوجيا الخلية1 وعلم وظائف الاعضاء2 وطب الأطفال3, كلية طب بنها- جامعة بنها , قسم الباثولوجيا الاكلينيكية4 , كلية طب القاهرة, جامعة القاهرة.
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International
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Abstract
Objective
The aim of this study was to evaluate the histopathological and biochemical effects of
enalapril (an angiotensin-converting enzyme inhibitor) and pyridoxamine (an advanced
glycation end product inhibitor) on the kidneys of streptozotocin diabetic female rats.
Materials and methods
Eighty adult female rats weighing 150–200 g were used for the study and divided into
four groups: group I (control nondiabetic group), group II (diabetic untreated group),
group III (diabetic group treated with enalapril), and group IV (diabetic group treated
with pyridoxamine), with each group comprising 20 rats (n = 20). Diabetes was
induced by a single intraperitoneal injection of streptozotocin (55 mg/kg). Enalapril was
administered (50 mg/l) in the drinking water and pyridoxamine was administered (1 g/l)
in the drinking water for 28 weeks. Biochemical estimation of fasting blood glucose,
serum creatinine, and plasma tumor necrosis factor-a (TNF-a) was performed. The
kidneys of the rats were collected for examination of clinical biochemistry, which
included measurement of levels of tissue malondialdehyde (MDA), enzymatic
antioxidants such as superoxide dismutase (SOD) and catalase (CAT), and
nonenzymatic antioxidants such as reduced glutathione (GSH), and were studied
histopathologically by light microscopy and immunohistochemistry.
Results
Fasting blood glucose was significantly increased, whereas the levels of serum
creatinine and plasma TNF-a were highly significantly increased in the diabetic
untreated group but the levels of serum creatinine and plasma TNF-a were significantly
reduced in the diabetic group treated with enalapril and pyridoxamine. The level of
MDA was significantly increased, whereas the levels of SOD, CAT, and GSH were
significantly decreased in the kidneys of the diabetic untreated group; however, the
level of MDA was decreased, whereas levels of SOD, CAT, and GSH were increased
in the diabetic group treated with enalapril and pyridoxamine. Kidney histopathology of
streptozotocin in diabetic rats showed pathological changes. However, treatment with
enalapril and pyridoxamine attenuated the histopathological changes and corrected
the biochemical parameters mentioned above.
Conclusion
Diabetic nephropathy is one of the most frequent and serious complications of
diabetes mellitus. Enalapril and pyridoxamine have renoprotective effects, which have
been shown to inhibit structural and functional aspects of diabetic nephropathy and
attenuate oxidative stress involved in the streptozotocin diabetic kidn
The aim of this study was to evaluate the histopathological and biochemical effects of
enalapril (an angiotensin-converting enzyme inhibitor) and pyridoxamine (an advanced
glycation end product inhibitor) on the kidneys of streptozotocin diabetic female rats.
Materials and methods
Eighty adult female rats weighing 150–200 g were used for the study and divided into
four groups: group I (control nondiabetic group), group II (diabetic untreated group),
group III (diabetic group treated with enalapril), and group IV (diabetic group treated
with pyridoxamine), with each group comprising 20 rats (n = 20). Diabetes was
induced by a single intraperitoneal injection of streptozotocin (55 mg/kg). Enalapril was
administered (50 mg/l) in the drinking water and pyridoxamine was administered (1 g/l)
in the drinking water for 28 weeks. Biochemical estimation of fasting blood glucose,
serum creatinine, and plasma tumor necrosis factor-a (TNF-a) was performed. The
kidneys of the rats were collected for examination of clinical biochemistry, which
included measurement of levels of tissue malondialdehyde (MDA), enzymatic
antioxidants such as superoxide dismutase (SOD) and catalase (CAT), and
nonenzymatic antioxidants such as reduced glutathione (GSH), and were studied
histopathologically by light microscopy and immunohistochemistry.
Results
Fasting blood glucose was significantly increased, whereas the levels of serum
creatinine and plasma TNF-a were highly significantly increased in the diabetic
untreated group but the levels of serum creatinine and plasma TNF-a were significantly
reduced in the diabetic group treated with enalapril and pyridoxamine. The level of
MDA was significantly increased, whereas the levels of SOD, CAT, and GSH were
significantly decreased in the kidneys of the diabetic untreated group; however, the
level of MDA was decreased, whereas levels of SOD, CAT, and GSH were increased
in the diabetic group treated with enalapril and pyridoxamine. Kidney histopathology of
streptozotocin in diabetic rats showed pathological changes. However, treatment with
enalapril and pyridoxamine attenuated the histopathological changes and corrected
the biochemical parameters mentioned above.
Conclusion
Diabetic nephropathy is one of the most frequent and serious complications of
diabetes mellitus. Enalapril and pyridoxamine have renoprotective effects, which have
been shown to inhibit structural and functional aspects of diabetic nephropathy and
attenuate oxidative stress involved in the streptozotocin diabetic kidn
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