子痫前期（PE）是常见的妊娠期并发症，缺血缺氧的胎盘滋养细胞释放多种因子到母体循环，导致其发生。晚期氧化蛋白产物（AOPP）是一种新型的蛋白类氧化应激标志物。课题组前期研究发现AOPP在PE胎盘、血浆中高表达，引起滋养细胞功能异常，且分泌的外泌体可抑制内皮细胞功能。进一步通过外泌体测序发现LncRNA AC092115.3显著低表达，结合共表达网络及数据库分析，预测其调控基因为EGR1/HSPA1B。敲低LncRNA AC可抑制内皮细胞功能，激活MAPK通路。因此，我们推测AOPP刺激下滋养细胞外泌体LncRNA AC调控EGR1/HSPA1B激活MAPK通路导致内皮细胞功能受损，引起PE全身症状发生。本研究拟采取体内外实验，阐明外泌体LncRNA AC的潜在分子机制，并通过临床试验，明确外泌体LncRNA AC是否可作为PE的生物标志物，为子痫前期早期诊断和治疗提供新策略。

Preeclampsia is a common pregnancy complication. Hypoxia-deficient placental trophoblasts release a variety of factors into the maternal circulation and lead to preeclampsia. Advanced Oxidation Protein Product (AOPP) is a novel marker of oxidative stress protein. Previous studies have shown that patients with preeclampsia have a higher level of AOPP in plasma and placental. AOPP could impair the function of trophoblasts , and exosomes secreted by trophoblasts could inhibit endothelial cell function. Furthermore, LncRNA AC092115.3 was significantly downregulated through exosomal sequencing. Combined with co-expression network and analysis from databases, it was predicted that the regulatory genes were EGR1/HSPA1B. Knockdown of LncRNA AC inhibited endothelial cell function and activated MAPK signal pathway. Therefore, we hypothesize that exo- LncRNA AC from trophoblasts which is stimulated by AOPP to regulate EGR1/HSPA1B through MAPK signal pathway on the damage of endothelial cells , causing systemic symptoms of PE. This study intends to conduct experiments in vitro and in vivo to elucidate the underlying molecular mechanism of exosomal LncRNA AC. Further clinical trials will be confirmed to determine whether exosomal LncRNA AC can be used as a biomarker for PE, to provide a new strategy for early diagnosis and treatment of preeclampsia.