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首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Protective effect of iridoid glycosides from Paederia scandens (LOUR.) MERRILL (Rubiaceae) on uric acid nephropathy rats induced by yeast and potassium oxonate
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Protective effect of iridoid glycosides from Paederia scandens (LOUR.) MERRILL (Rubiaceae) on uric acid nephropathy rats induced by yeast and potassium oxonate

机译:scan藜(LOUR。)梅瑞尔(茜草科)的烯藤酮苷对酵母和草酸钾诱导的尿酸肾病的保护作用

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摘要

Iridoid glycosides of Paederia scandens (IGPS) are an active component isolated from Chinese herb P. scandens (LOUR.) MERRILL (Rubiaceae). Uric acid nephropathy (UAN) is caused by excessive uric acid, which results in damage of kidney tissue via urate crystals deposition in the kidneys. This study aimed to investigate the protective effects of IGPS on UAN in rats induced by yeast and potassium oxonate. Treatment groups received different doses of IGPS and allopurinol (AP) daily for 35 days respectively. The results showed that treatment with IGPS significantly prevented the increases of uric acid in serum and the elevation of systolic blood pressure (SBP), attenuated renal tissue injury, improved renal function and reserved the biological activity of NOS-1. IGPS also inhibited the biological activity of TNF-a and TGF-betal, and suppressed the mRNA expressions of TNF-a and TGF-pi in renal tissue. Taken together, the present and our previous findings suggest that IGPS exerts protective effects against kidney damage in UAN rats through its uric acid-lowering, anti-inflammatory and immunomodulatory properties. Furthermore, decreasing SBP by up regulation of NOS-1 expression and down regulation of TNF-a and TGF-pi expression are involved in the effect of IGPS on high uric acid-induced nephropathy.
机译:Pa草(Pasteria scandens,IGPS)的鸢尾糖苷是从中草药M草(M.ILLER)MERRILL(Rubiaceae)中分离的活性成分。尿酸肾病(UAN)是由过多的尿酸引起的,尿酸结晶沉积在肾脏中会导致肾脏组织受损。本研究旨在探讨IGPS对酵母菌和草酸钾诱导的UAN的保护作用。治疗组每天分别接受35天的不同剂量的IGPS和别嘌呤醇(AP)。结果表明,用IGPS处理可显着阻止血清尿酸的升高和收缩压(SBP)的升高,减轻肾组织损伤,改善肾功能,并保留NOS-1的生物学活性。 IGPS还抑制TNF-α和TGF-β1的生物学活性,并抑制肾组织中TNF-α和TGF-β的mRNA表达。两者合计,目前和我们以前的发现表明IGPS通过降低尿酸,抗炎和免疫调节特性对UAN大鼠的肾脏损害具有保护作用。此外,通过上调NOS-1表达来降低SBP以及下调TNF-a和TGF-pi表达来降低IBP参与IGPS对高尿酸诱导的肾病的作用。

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