环氧合酶-2介导镉诱导肾损伤的内质网应激调控机制研究
Cyclooxygenase-2 Mediates Cadmium-induced Kidney Injury via Endoplasmic Reticulum Stress
Abstract
目的：镉及其化合物对哺乳动物的肝、肾、骨骼等脏器具有毒性损害作用。环氧合酶-2(cyclooxygenase-2，COX-2)是花生四烯酸代谢形成前列腺素家族(prostaglandins，PGs)成员通路中的关键限速酶，其在调控细胞增殖、转移、凋亡和血管形成中发挥重要作用。已有报道镉经由ROS诱导大鼠肾细胞中COX-2表达升高而引起肾损伤，同时也有报道自噬在镉诱导的肾损伤中扮演重要的作用，但是COX-2和自噬在镉暴露诱导肾毒性损伤中的作用及其机制尚待阐明。本研究拟探讨COX-2的表达是否参与镉诱导的肾毒性损伤及其调控机制。 方法：(1)体内试验，采用8~10周雄性ICR小鼠，分为4组，包括... Objectives: As a toxic heavy metal, cadmium (Cd) and its compound has toxic effect on liver, kidney, bone and other organs in mammals. As one of the key rate-limiting enzyme of arachidonic acid metabolism and prostaglandins (PGs) synthesis, cyclooxygenase-2 (COX-2) has been described to play an important role in regulation of cell proliferation, transformation, apoptosis, and angiogenesis. Recent ...