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獐牙菜苦苷通过改善2型糖尿病大鼠的高血糖和神经炎症、激活PI3K/AKT/GSK3β信号通路来改善认知功能障碍。

Swertiamarin ameliorates cognitive dysfunction by improving hyperglycemia and neuroinflammation in type 2 diabetic rats activation of the PI3K/AKT/GSK3β signaling pathway.

作者信息

Tan Bingyin, Liu Li, Wu Tao, Yuan Fangjie, Wang Cheng

机构信息

Department of Pharmacy, Wuhan Fourth Hospital, Wuhan 430033, China.

Department of Orthopedics, Wuhan Fourth Hospital, Wuhan 430033, China.

出版信息

Cent Eur J Immunol. 2024;49(4):425-435. doi: 10.5114/ceji.2024.145754. Epub 2024 Dec 12.

DOI:10.5114/ceji.2024.145754
PMID:39944258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11811717/
Abstract

INTRODUCTION

Diabetic encephalopathy (DE) is a central nervous complication of type 2 diabetes (T2D). Swertiamarin (SW) is a secoiridoid glycoside reported to have anti-hyperglycemic properties in T2D animal models. Nonetheless, the precise function of SW in T2D-induced DE remains unclarified.

MATERIAL AND METHODS

A T2D rat model was established by high-fat diet feeding plus streptozotocin injection, followed by SW administration. Fasting blood glucose and insulin levels were determined. The Morris water maze test was implemented to evaluate rat cognitive function. Hematoxylin-eosin staining was performed for hippocampal morphological observation. Hippocampal p-tau level was detected using immunofluorescence staining. ELISA was utilized to determine inflammatory cytokine production. Western blotting was performed to estimate PI3K/Akt/GSK3 signaling-related protein levels.

RESULTS

Swertiamarin treatment improved spatial learning and memory and reduced fasting blood glucose as well as insulin levels in T2D rats. SW ameliorated hippocampal morphological changes, reduced tau phosphorylation, and attenuated the inflammatory response in T2D rat hippocampal tissues. SW restored PI3K/Akt/GSK3 signaling in diabetic rat hippocampus.

CONCLUSIONS

Swertiamarin exerts anti-diabetic and anti-inflammatory effects possibly by activating PI3K/Akt/GSK3 signaling, thereby ameliorating cognitive impairment in T2D rats.

摘要

引言

糖尿病性脑病（DE）是2型糖尿病（T2D）的一种中枢神经系统并发症。獐牙菜苦苷（SW）是一种裂环烯醚萜苷，据报道在T2D动物模型中具有降血糖特性。然而，SW在T2D诱导的DE中的具体作用仍不清楚。

材料与方法

通过高脂饮食喂养加链脲佐菌素注射建立T2D大鼠模型，随后给予SW。测定空腹血糖和胰岛素水平。采用Morris水迷宫试验评估大鼠认知功能。进行苏木精-伊红染色以观察海马形态。使用免疫荧光染色检测海马p- tau水平。采用ELISA法测定炎症细胞因子的产生。进行蛋白质免疫印迹法以评估PI3K/Akt/GSK3信号相关蛋白水平。

结果

獐牙菜苦苷治疗改善了T2D大鼠的空间学习和记忆能力，降低了空腹血糖和胰岛素水平。SW改善了T2D大鼠海马的形态学变化，减少了tau蛋白磷酸化，并减轻了T2D大鼠海马组织中的炎症反应。SW恢复了糖尿病大鼠海马中的PI3K/Akt/GSK3信号。

结论

獐牙菜苦苷可能通过激活PI3K/Akt/GSK3信号发挥抗糖尿病和抗炎作用，从而改善T2D大鼠的认知障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/75e6a5d09e24/CEJI-49-55297-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/7211d9abbeda/CEJI-49-55297-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/5984a8a1b8ff/CEJI-49-55297-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/75e6a5d09e24/CEJI-49-55297-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/7211d9abbeda/CEJI-49-55297-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/fc659e56535b/CEJI-49-55297-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/1762c437dd6f/CEJI-49-55297-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/15810f1d5abf/CEJI-49-55297-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/5984a8a1b8ff/CEJI-49-55297-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0bc/11811717/75e6a5d09e24/CEJI-49-55297-g006.jpg

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Pyruvate dehydrogenase kinase 1 protects against neuronal injury and memory loss in mouse models of diabetes.丙酮酸脱氢酶激酶 1 可保护糖尿病小鼠模型免受神经元损伤和记忆丧失。
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Exendin-4 ameliorates tau hyperphosphorylation and cognitive impairment in type 2 diabetes through acting on Wnt/β-catenin/NeuroD1 pathway.
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Mol Med. 2023 Sep 4;29(1):118. doi: 10.1186/s10020-023-00718-2.
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