PROTECTION FROM BB RAT DIABETES BY THE PLATELET-ACTIVATING-FACTOR INHIBITOR BN50730

被引：5

作者：

JOBE, LW ^{[1
]}

UBUNGEN, R ^{[1
]}

GOODNER, CJ ^{[1
]}

BASKIN, DG ^{[1
]}

BRAQUET, P ^{[1
]}

LERNMARK, A ^{[1
]}

机构：

[1] UNIV WASHINGTON,DEPT MED,RH WILLIAMS LAB,SEATTLE,WA 98195

来源：

AUTOIMMUNITY | 1993年 / 16卷 / 04期

关键词：

PAF; BIOBREEDING (BB) RATS; IDDM (INSULIN-DEPENDENT DIABETES MELLITUS); INSULITIS;

D O I：

10.3109/08916939309014644

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The platelet-activating factor inhibitor BN50730, a hetrazepine, was injected intraperitoneally daily from 30 days of age into diabetes-prone BB rats. While 96% (22/23) Tween 80 injected control rats developed diabetes, 0.05 mg/kg BN50730 decreased the frequency to 72% (17/24; n.s.) and 0.5 mg/kg to 56% (14/25; p < 0.01). Mean onset age in controls was 81 +/- 9 days (mean +/-SD), but BN50730 delayed onset to 87 +/- 15 days in the low and 93 +/- 12. days (p < 0.01) in high dose rats. The relative degree of insulitis was reduced in both low (p < 0.01) and high (p < 0.05) dose treated groups. Serum insulin in young prediabetic controls decreased from 84 +/- 34 mu U/ml to 38 +/- 20 in the 22 rats developing diabetes (p < 0.001). Serum insulin in BN50730-protected compared to unprotected rats was 114 +/- 49 and 32 +/- 22 (p < 0.001) in the low, and 91+/-46 and 21 +/- 15 (p < 0.001) mu U/ml in the high dose group, respectively. Increased serum insulin correlated with preserved islet beta cells and decreased insulitis. Treatment did not affect thyroiditis. Thus, platelet-activating factor may be involved in insulitis pathogenesis and platelet-activating factor inhibitors may decrease autoimmune beta cell destruction.

引用

页码：259 / 266

页数：8

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