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钙通道阻滞改善内嗅皮质淀粉样病变诱导的海马内质网应激。

Calcium Channel Blockade Ameliorates Endoplasmic Reticulum Stress in the Hippocampus Induced by Amyloidopathy in the Entorhinal Cortex.

作者信息

Ghanbari-Maman Azam, Ghasemian-Roudsari Forouzan, Aliakbari Shayan, Gholami Pourbadie Hamid, Khodagholi Fariba, Shaerzadeh Fatemeh, Daftari Mahtab

机构信息

Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.

Department of Biology, Faculty of Sciences, University of Zanjan, Zanjan, Iran.

出版信息

Iran J Pharm Res. 2019 Summer;18(3):1466-1476. doi: 10.22037/ijpr.2019.111532.13216.

Abstract

Entorhinal cortex (EC) is one of the first cerebral regions affected in Alzheimer's disease (AD). The pathology propagates to neighboring cerebral regions through a prion-like mechanism. In AD, intracellular calcium dyshomeostasis is associated with endoplasmic reticulum (ER) stress. This study was designed to examine hippocampal ER stress following EC amyloidopathy. Aβ1-42 was bilaterally microinjected into the EC under stereotaxic surgery. Rats were daily treated with 30 μg of isradipine, nimodipine, or placebo over one week. Passive avoidance and novel object recognition (NOR) tasks were performed using shuttle box and NOR test, respectively. GRP78/BiP and CHOP levels were measured in the hippocampal dentate gyrus (DG) by western blot technique. The glutathione (GSH) level and PDI activity were also assessed in the hippocampus by colorimetric spectrophotometer. Aβ treated group developed passive avoidance and novel recognition memory deficit compared to the control group. However, treatment with calcium channel blockers reversed the impairment. BiP and CHOP level increased in the hippocampus following amyloidopathy in the EC. PDI activity and GSH level in the hippocampus decreased in the Aβ treated group, but calcium channel blockers restored them toward the control level. In conclusion, memory impairment due to EC amyloidopathy is associated with ER stress related bio-molecular changes in the hippocampus, and treatment with L-type calcium channel blockers may prevent the changes and ultimately improve cognitive performance.

摘要

内嗅皮质(EC)是阿尔茨海默病(AD)中最早受影响的脑区之一。病理学变化通过一种朊病毒样机制传播到邻近脑区。在AD中,细胞内钙稳态失调与内质网(ER)应激相关。本研究旨在检测EC淀粉样病变后海马体中的ER应激。在立体定向手术下,将Aβ1-42双侧微量注射到EC中。大鼠在一周内每天接受30μg伊拉地平、尼莫地平或安慰剂治疗。分别使用穿梭箱和新物体识别(NOR)试验进行被动回避和新物体识别(NOR)任务。通过蛋白质印迹技术测量海马齿状回(DG)中的GRP78/BiP和CHOP水平。还通过比色分光光度计评估海马体中的谷胱甘肽(GSH)水平和PDI活性。与对照组相比,Aβ治疗组出现被动回避和新识别记忆缺陷。然而,钙通道阻滞剂治疗可逆转这种损伤。EC淀粉样病变后海马体中的BiP和CHOP水平升高。Aβ治疗组海马体中的PDI活性和GSH水平降低,但钙通道阻滞剂将它们恢复到对照水平。总之,EC淀粉样病变导致的记忆损伤与海马体中与ER应激相关的生物分子变化有关,L型钙通道阻滞剂治疗可能预防这些变化并最终改善认知表现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6779/6934951/871e8a5accc5/ijpr-18-1466-g001.jpg

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