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川芎内酯通过调节血管性痴呆大鼠的 SIRT1/IRE1/XBP1s/CHOP 通路改善认知障碍。

Ligustilide Improves Cognitive Impairment via Regulating the SIRT1/IRE1/XBP1s/CHOP Pathway in Vascular Dementia Rats.

机构信息

Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510120, China.

Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China.

出版信息

Oxid Med Cell Longev. 2022 Aug 16;2022:6664990. doi: 10.1155/2022/6664990. eCollection 2022.

DOI:10.1155/2022/6664990
PMID:36017237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9398841/
Abstract

Vascular dementia (VaD), the second cause of dementia, is caused by chronic cerebral hypoperfusion, producing progressive damage to cerebral cortex, hippocampus, and white matter. Ligustilide (LIG), one of the main active ingredients of , exerts the neuroprotective effect on neurodegenerative diseases. However, the mechanism remains unclear. An model of bilateral common carotid artery occlusion and model of oxygen glucose deprivation (OGD) were employed in this study. LIG (20 or 40 mg/kg/day) was intragastrically administered to the VaD rats for four weeks. The results of the Morris water maze test demonstrated that LIG effectively ameliorated learning and memory deficiency in VaD rats. LIG obviously relieved neuronal oxidative stress damage by increasing the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) and decreasing the level of malondialdehyde (MDA) in VaD rats. Nissl staining showed that LIG increased the number of the Nissl body in VaD rats. After LIG administration, the apoptotic-related protein, Bax, was decreased and Bcl-2 was increased in the hippocampus of VaD rats. Moreover, the expressions of sirtuin 1 (SIRT1) and protein disulfide isomerase (PDI) were decreased, binding immunoglobulin protein (BIP) and phospho-inositol-requiring enzyme-1 (P-IRE1), X-box binding protein 1 (XBP1s), and C/EBP-homologous protein (CHOP) were increased in VaD rats. After LIG treatment, these changes were reversed. The immunofluorescence results further showed that LIG upregulated the expression of SIRT1 and downregulated the expression of P-IRE1 in VaD rats. In addition, experiment showed that EX-527 (SIRT1 inhibitor) partly abolished the inhibitory effect of LIG on the IRE1/XBP1s/CHOP pathway. In conclusion, these studies indicated that LIG could improve cognitive impairment by regulating the SIRT1/IRE1/XBP1s/CHOP pathway in VaD rats.

摘要

血管性痴呆（VaD）是痴呆症的第二大病因，由慢性脑灌注不足引起，导致大脑皮层、海马体和白质逐渐受损。川芎嗪（LIG）是当归的主要活性成分之一，对神经退行性疾病具有神经保护作用。然而，其作用机制尚不清楚。本研究采用双侧颈总动脉结扎模型和氧葡萄糖剥夺（OGD）模型。将 LIG（20 或 40mg/kg/天）灌胃给药 VaD 大鼠四周。Morris 水迷宫测试结果表明，LIG 可有效改善 VaD 大鼠的学习记忆障碍。LIG 通过增加过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-PX）的活性，降低丙二醛（MDA）水平，明显减轻 VaD 大鼠神经元氧化应激损伤。尼氏染色显示，LIG 增加了 VaD 大鼠的尼氏体数量。LIG 给药后，海马凋亡相关蛋白 Bax 减少，Bcl-2 增加。此外，SIRT1 和蛋白二硫键异构酶（PDI）的表达减少，结合免疫球蛋白蛋白（BIP）和磷酸肌醇需要酶 1（P-IRE1）、X 盒结合蛋白 1（XBP1s）和 C/EBP 同源蛋白（CHOP）在 VaD 大鼠中增加。LIG 治疗后，这些变化得到逆转。免疫荧光结果进一步显示，LIG 上调了 VaD 大鼠 SIRT1 的表达，下调了 P-IRE1 的表达。此外，EX-527（SIRT1 抑制剂）实验部分消除了 LIG 对 IRE1/XBP1s/CHOP 通路的抑制作用。综上所述，这些研究表明，LIG 可通过调节 VaD 大鼠的 SIRT1/IRE1/XBP1s/CHOP 通路改善认知障碍。

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