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首页> 外文会议>International Symposium on Amyloidosis >TRANSMISSION OF MOUSE AApoAII AMYLOIDOSIS BY THE AMYLOID FIBRILS; INHIBITORY EFFECTS ON TRANSMISSION BY THE DENATURATION/ DEGRADATION OF AMYLOID FIBRILS
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TRANSMISSION OF MOUSE AApoAII AMYLOIDOSIS BY THE AMYLOID FIBRILS; INHIBITORY EFFECTS ON TRANSMISSION BY THE DENATURATION/ DEGRADATION OF AMYLOID FIBRILS

机译：用淀粉样蛋白原纤维传递小鼠Aapoaii淀粉样蛋白化;通过淀粉样蛋白原纤维的变性/降解传播的抑制作用

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Data is accumulating to suggest that a certain amyloidosis including AA and mouse AApoAII amyloidosis are transmissible (1 - 3). It is postulated that invasion of preexisted amyloid seed into the hosts plays a critical role in the transmission. In order to search for a measure to eliminate or attenuate amyloid-seeding (and transmission) activity, we evaluated inhibitory effects of several treatments and medical reagents on amyloid fibril in the mouse AApoAII transmission model system. AApoAII fibril was isolated as a water suspension from the liver of an R1.P1-Apoa2~c mouse, and denatured or degradated by the following treatments or reagents; autoclaving, freeze-thaw, guanidine hydrochloride (Gdn-HCI), alkaline solution, formic acid, antibiotics {tetracycline, rifampicin, etc) or polyphenols (resveratrol, piceatannol, etc). The degree of denaturation was evaluated by thioflavine T fluorescence assay of aliquot. Two-month-old female R1 P1.P1-Apoa2~c mice were administered intravenously with native or denatured fibril. After two months, the mice were sacrificed and the organs were collected. The degree of AApoAII amyloid deposition was evaluated in sections of these organs by Congo red staining and polarizing microscopy. 6M Gdn-HCI and formic acid completely inhibited amyloid induction. Generally amyloid deposition was decreased in mice administered with denatured fibrils as compared with that in mice administered native fibril. Tetracycline suppressed the amyloid deposition well. Polyphenols, which is known to effectively denature prion and Abeta fibrils, failed to denature AApoAII fibrils. This data should shed a new light on the development of a measure to prevent amyloid transmission.
机译：数据积累，表明包括AA和小鼠Aapoaii淀粉样淀粉样蛋白病的某种淀粉样症（1 - 3）。假设侵入预先存在的淀粉样品种子进入宿主的侵袭在传输中起着关键作用。为了寻找消除或衰减淀粉样液（和透射）活性的措施，我们评估了几种治疗和医用试剂对小鼠Aapoaii传输模型系统中淀粉样蛋白原纤维的抑制作用。将Aapoaii纤维分离为来自R1.P1-APOA2〜C小鼠的肝脏的水悬浮液，并通过以下处理或试剂变性或降解;高压灭菌，冻融，盐酸胍（GDN-HCI），碱性溶液，甲酸，抗生素{四环素，利福平等）或多酚（白藜芦醇，Piceatannol等）。通过等分试样的硫伐T荧光测定评估变性程度。静脉内施用2个月历史的雌性R1 P1.P1-APOA2〜C小鼠与天然或变性原纤维施用。两年后，处死小鼠并收集器官。通过刚果红染色和偏振显微镜在这些器官的部分中评价Aapoaii淀粉样蛋白沉积的程度。 6M GDN-HCl和甲酸完全抑制淀粉样蛋白诱导。与施用天然原纤维的小鼠相比，在用变性原纤维施用的小鼠中，通常淀粉样蛋白沉积降低。四环素抑制淀粉样蛋白沉积孔。众所周知的多酚有效地变性朊病毒和Abeta原纤维，未能变性Aapoaii原纤维。这种数据应该在开发措施上进行新的光线以防止淀粉样蛋白传输。

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