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[1α,25-二羟维生素D3对实验性大鼠肾毒性血清肾炎的影响]

[Effect of 1 alpha, 25(OH)2D3 on experimental rat nephrotoxic serum nephritis].

作者信息

Hattori M

机构信息

Department of Pediatric Nephrology, Tokyo Women's Medical College.

出版信息

Nihon Jinzo Gakkai Shi. 1990 Feb;32(2):147-59.

PMID:2352358
Abstract

We studied immunoregulatory effects of 1 alpha, 25(OH)2D3 in vivo using experimental rat nephrotoxic serum nephritis (NTSN). Experimental rats were divided into 3 groups according to the doses of 1 alpha (OH)D3, i.e. the control group (untreated group), the D30.02 group (0.02 microgram/Kg/day), and D30.5 group (0.5 microgram/Kg/day). The present study demonstrated that rats with NTSN receiving 0.5 microgram/Kg/day of 1 alpha (OH)D3 showed much lower urinary protein excretion as well as lesser histopathological changes in both heterologous and autologous phase as compared with rats without such treatments. On the other hand, the results in the D30.02 group varied. And also, the following were demonstrated in the D30.5 group as compared with the control group: 1) CH50 levels were maintained almost normally, 2) the staining of rat C3 was clearly lesser, 3) the number of intraglomerular OX41 and W3/13 labelled cells was significantly lower, 4) the response of cultured spleen lymphocytes stimulated with ConA and LPS was clearly inhibited, 5) the helper T cell/suppressor T cell ratio was lower, and 6) the staining of rat IgG was lesser. Therefore, it was speculated that the inhibitory effects of 1 alpha, 25(OH)2D3 on complement activation might play important roles. And also, we postulated that the following mechanisms were involved: 1) the inhibition of antibody generation due to the blocking of T lymphocyte proliferation and functions and; 2) the inhibition of intraglomerular macrophage infiltration caused by blocking of T lymphocyte functions. In conclusion, our study indicated that 1 alpha, 25(OH)2D3 had a new facet of immunoregulatory function in experimental rat NTSN.

摘要

我们使用实验性大鼠肾毒性血清肾炎(NTSN)在体内研究了1α,25(OH)₂D₃的免疫调节作用。根据1α(OH)D₃的剂量将实验大鼠分为3组,即对照组(未治疗组)、D30.02组(0.02微克/千克/天)和D30.5组(0.5微克/千克/天)。本研究表明,与未接受此类治疗的大鼠相比,接受0.5微克/千克/天1α(OH)D₃的NTSN大鼠在异源期和同源期的尿蛋白排泄均显著降低,组织病理学变化也较小。另一方面,D30.02组的结果有所不同。此外,与对照组相比,D30.5组还表现出以下情况:1)CH50水平几乎维持正常;2)大鼠C3的染色明显减轻;3)肾小球内OX41和W3/13标记细胞的数量显著减少;4)用ConA和LPS刺激的培养脾淋巴细胞的反应明显受到抑制;5)辅助性T细胞/抑制性T细胞比值降低;6)大鼠IgG的染色减轻。因此,推测1α,25(OH)₂D₃对补体激活的抑制作用可能起重要作用。我们还推测涉及以下机制:1)由于T淋巴细胞增殖和功能受阻而抑制抗体产生;2)通过阻断T淋巴细胞功能抑制肾小球内巨噬细胞浸润。总之,我们的研究表明1α,25(OH)₂D₃在实验性大鼠NTSN中具有免疫调节功能的新方面。

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