Abstract
Aims: To explore the effects of ligustrazine on proteinuria, urinary TxB<sub>2</sub> (metabolism of thromboxane A<sub>2</sub>, TxA<sub>2</sub>) and 6-keto-PGF<sub>1α </sub>(metabolism of prostacyclines I<sub>2</sub>, PG I<sub>2</sub>), glomerular inducible nitric oxide(NO) synthase (iNOS) mRNA, urinary NO<sup>–</sup><sub>3</sub>/NO<sup>–</sup><sub>2</sub> (decomposing products of NO) and pathological changes in rats with passive Heymann nephritis (PHN). Methods: A rat PHN model was induced by intravenous injection of rabbit anti-rat renal tubular antigen (Tub-Ag) antiserum, and ligustrazine was given intraperitoneally into PHN rats every 2 days for 1–5 weeks. Then, proteinuria, urinary TxB<sub>2</sub> and 6-keto-PGF<sub>1α</sub>, glomerular iNOS mRNA, and urinary NO<sup>–</sup><sub>3</sub>/NO<sup>–</sup><sub>2</sub> were measured by sulfosalicylic acid, radioimmunoassay (RIA), Northern blot and nitric acid reductase methods, respectively. Moreover, the damage to the renal tissue of the rats was observed under light and electron microscopy and immunofluorescence (IF). Results: The urinary TxB<sub>2</sub> in PHN rats was significantly higher than that in control rats, but the PHN rats treated with ligustrazine had significantly less proteinuria, urinary TxB<sub>2</sub> and tissue lesions, and more urinary 6-keto-PGF<sub>1α</sub>, glomerular iNOS mRNA and urinary NO<sup>–</sup><sub>2</sub>/NO<sup>–</sup><sub>3</sub> than the PHN rats without the administration of ligustrazine. Conclusion: These data indicate that ligustrazine has inhibitory roles on the glomerular injury of PHN rats, which may associate with modulating the balance of TxA<sub>2</sub>-PGI<sub>2</sub> and elevating synthesis of NO to a certain extent.
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