Inhibition of intra-peritoneal carbonyl stress by carbonyl adsorbing beads or carbonyl stress inhibitor

腹膜（PM）功能衰竭的分子机制仍不明确。慢性尿毒症本身改变PM并增加有效腹膜表面积（EPSA）。腹膜透析（PD）期间PM恶化的结果，至少部分是由于存在于热灭菌的PD液中的活性羰基化合物（RCOs）的积累。我们提出了两种假设的方法来减少腹膜内羰基应激。最近发现的pyridoxamine， ARB及其类似物是一类新的晚期糖基化终产物（AGEs）抑制剂，通过其氨基捕获RCO前体。另一种减少腹膜内羰基应激的方法是RCO吸附珠。吡哆沙明给予尿毒症大鼠PD，显著改善功能和结构改变。这种改善伴随着AGE积累和血管生成细胞因子表达的减少。与葡萄糖PD液混合，吡唑啉酮-聚乙烯亚胺与纤维素珠（PPCB）显著降低RCOs (?？二羰基和醛)，并抑制戊苷（一种AGE）的产生，其水平与过滤消毒的PD液相似。其有效性比以前开发的珠子高出一个数量级以上。

The molecular mechanisms underlying the peritoneal membrane (PM) failure remain elusive. Chronic uremia by itself modifies the PM and increases the effective peritoneal surface area (EPSA). PM deterioration during peritoneal Dialysis (PD) results, at least in part, from the accumulation of reactive carbonyl compounds (RCOs) present in heat-sterilized PD fluid. We have proposed two hypothetical approaches to reduce intra-peritoneal carbonyl stress. The more recently identified pyridoxamine, ARB and its analog a new class of advanced glycation end products (AGEs) inhibitors, traps RCO precursors by its amino group. Another approach to reduce intra-peritoneal carbonyl stress is the RCO adsorbing beads. Pyridoxamine, given in uremic rats with PD, significantly improved functional and structural alterations. This improvement was accompanied by reduction of AGE accumulation and of angiogenic cytokines expressions. Mixed with glucose PD fluid, pyrazolinones-polyethyleneimine, with cellulose beads (PPCB) markedly lowers RCOs (??dicarbonyls and aldehydes) and inhibits the generation of pentosidine, an AGE, to levels similar to those of filter-sterilized PD fluid. Its effectiveness is more than one order of magnitude above those of previously developed beads.