本项目在前期工作基础上，拟首先采用正常SD大鼠，使用CRISPR-cas9和过表达质粒原核显微注射技术，敲除和过表达miR-1283；采用自发性高血压大鼠，给予miR-1283antagomir和miR-1283agomir，抑制和过表达miR-1283；并利用人主动脉内皮细胞，给予miR-1283antagomir和miR-1283agomir。结合体内外实验，揭示miR-1283的功能及其在高血压病血瘀证形成中的作用。其次，利用人主动脉内皮细胞，同时抑制miR-1283以及ATF4/CHOP信号通路，弄清miR-1283对高血压病血瘀证形成的影响是否依赖于ATF4/CHOP信号通路。最后，基于方证相应原理，阐明活血化瘀代表方桃红四物汤对miR-1283及其调控的ATF4/CHOP信号通路的干预效应。为防治高血压病提供新的策略，具有重要理论意义和临床应用价值。

On the basis of previous work, we plan to use the CRISPR-Cas9 and overexpression plasmid prokaryotic microinjection technologies to knock out and high express miR-1283 in SD rats; Spontaneously hypertensive rats will be given antagomir or agomir of miR-1283 to inhibit or high express miR-1283; In vitro experiment, the human aortic endothelial cells will be intervented with antagomir or agomir of miR-1283. Combined with the experiments in vivo and vitro, we will reveal the function of miR-1283 and its role in the development of blood stasis syndrome of hypertension. Secondly,we inhibit miR-1283 and ATF4/CHOP signaling pathway simultaneously in human aortic endothelial cells to clarify whether the role of miR-1283 in the development of blood stasis syndrome of hypertension is depended on ATF4/CHOP signaling pathway. Finally, this study will illuminate the intervention effects of Taohong Siwu Decoction on miR-1283 and ATF4/CHOP signaling pathway according to the correspondence between prescription and syndrome. It will provide new measures of prevention and treatment of hypertension, thus, it has important theoretical signficance and clinical value.