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Changes of iNOS gene expression in kidney following ischemia and reperfusion of limbs and their significance in rats / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1986.
Artículo en Chino | WPRIM | ID: wpr-522139
ABSTRACT

AIM:

To detect the changes of inducible nitric oxide synthase (iNOS) expression in kidney following ischemia-reperfusion(I-R)of hindlimbs and to elucidate their significance.

METHODS:

I-R was established using the occlusion of the femoral arteries for 4 h and re-opening for 2-24 h in rats. The expression of iNOS mRNA,and iNOS protein and the nitrotyrosine (NT),a marker of peroxynitrite (ONOO -),in renal tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique,respectively. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents in renal tissue were spectraphotometrically measured. The observation of pathologic changes of renal tissue was made following the inhibition of iNOS by aminoguanidine (AG).

RESULTS:

Compared with control group,the relative expression level of iNOS mRNA significantly increased in I-R group. There were more iNOS and more NT positive product in the epithelial cells of renal proximal convoluted tubules and thick segments of Henle′ loops in I-R group than control group. The contents of MDA markedly increased,while the activity of SOD significantly decreased in I-R group,compared to those in the control groups. The pathologic changes of kidney became milder in I-R group following the inhibition of iNOS by AG.

CONCLUSION:

The expression of iNOS mRNA and protein in renal tissue were significantly upregulated,excess induction of NO contributed to the kidney injury during the I-R of hindlimbs.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 1986 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 1986 Tipo del documento: Artículo