脑卒中后认知障碍（PSCI）是脑卒中患者常见的并发症，严重影响患者的生活质量和社会功能。近年来，随着认知储备理论的发展和早期干预理念的普及，PSCI的早期干预模式逐渐成为研究热点。文章综述了PSCI早期干预模式的研究现状与进展，包括干预的理论基础、具体措施及未来发展方向，以期为临床实践和科研提供参考。
Post-stroke cognitive impairment（PSCI）is a common complication among stroke patients．It seriously affects the patients’ quality of life and social functions．In recent years，with the development of the cognitive reserve theory and the popularization of the concept of early intervention，the early intervention model for PSCI has gradually become a research hotspot．This article reviews the current research status and progress of the early intervention model for PSCI，including the theoretical basis of the intervention，specific measures，and future development directions，aiming to provide references for clinical practice and scientific research．
瘦素(leptin)是由控制各种生理过程的脂肪组织合成和分泌的一类激素,通过作用于靶细胞膜上的瘦素受体并经信号传导在各器官和系统中发挥一系列生物学效应。肾脏是高血压常见的靶器官之一。相关研究表明,瘦素在高血压肾损害中发挥作用,其机制可能与氧化应激及其炎症反应有关。本文以瘦素对高血压肾损害及其相关机制作一综述,并探讨瘦素对高血压肾损害发病机制研究进展。
Leptin which is a kind of synthesis and secretion of hormone that participates in various physiological processes is the role of the leptin receptor on the target cell membrane and the signal transduction through a series of biological effects in different organs and systems. Kidney is one of the common target organs of hypertension, and related research shows that leptin plays a role in hypertensive kidney damage, whose mechanism may be related to oxidative stress and its inflammatory reaction. The paper reviewed leptin on renal damage in hypertension and its related mechanisms, to explore the leptin on renal pathogenesis of hypertension research progress.
瘦素是维持人体能量代谢平衡的蛋白质,在人体中主要由白色脂肪组织分泌,通过与瘦素受体结合发挥作用。近年来有许多与瘦素相关的研究证明高血压患者及代谢综合征患者的血清瘦素水平较健康人群明显升高。两种疾病均可出现心室肥厚,蛋白尿,动脉粥样硬化等表现,说明二者存在共同的靶器官。瘦素代谢异常可出现瘦素抵抗并通过影响肾素-血管紧张素-醛固酮系统(renin angiotensin aldosterone system, RAAS)及炎症细胞因子来损伤靶器官。本文旨在总结瘦素在高血压及代谢综合征中的作用机制,并探讨瘦素对高血压合并代谢综合征靶器官损伤作用的研究进展。
Leptin is a protein that maintains the balance of energy metabolism in human body. It is mainly secreted by white adipose tissue in human body. In recent years, many studies have shown that the serum leptin level in patients with hypertension complicated with metabolic syndrome is significantly higher than that of healthy people. Both of the diseases can lead to left ventricular hypertrophy, proteinuria, atherosclerosis and other manifestations. The abnormal metabolism of leptin may contribute to leptin resistance which damages target organs by affecting the angiotensin aldosterone system and inflammatory cytokines. The aim of this article is to summarize the mechanism of leptin in hypertension and metabolic syndrome, and to explore its effect on the target organ damage in patients with hypertension complicated with metabolic syndrome.
