Linderae Radix Ameliorates Cognitive Dysfunction by Inhibiting Neuroinflammation and Synaptic Damage in Alzheimer's Disease Models

被引:10
作者
Kim, Seong Hye [1 ]
Ju, In Gyoung [2 ,3 ]
Kim, Jin Hee [1 ]
Eo, Hyeyoon [1 ]
Son, So-Ri [1 ]
Jang, Dae Sik [1 ]
Oh, Myung Sook [1 ,2 ,3 ]
机构
[1] Kyung Hee Univ, Grad Sch, Dept Biomed & Pharmaceut Sci, 26, Kyungheedae-Ro, Seoul 02447, South Korea
[2] Kyung Hee Univ, Dept Oriental Pharmaceut Sci, 26, Kyungheedae-Ro, Seoul 02447, South Korea
[3] Kyung Hee Univ, Kyung Hee East West Pharmaceut Res Inst, Coll Pharm, 26, Kyungheedae-Ro, Seoul 02447, South Korea
基金
新加坡国家研究基金会;
关键词
Alzheimer's disease; Linderae Radix; Neuroinflammation; Synaptic damage; Amyloid beta; Lipopolysaccharide; ACTIVATED PROTEIN-KINASE; LINDENENYL ACETATE; STRYCHNIFOLIA; COX-2;
D O I
10.1007/s12035-023-03544-z
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuroinflammation and synaptic damage are important etiologies associated with the progression of Alzheimer's disease (AD). Linderae Radix ( LR) has antioxidant and anti-inflammatory properties. This study investigated whether LR attenuates microglia activation-mediated neuroinflammation and synaptic degeneration and improves AD pathological phenotypes induced by amyloid beta oligomers (A ss O) or lipopolysaccharide (LPS) toxicity. For in vitro studies, we treated LR to A ss Ostimulated HT22 cells or LR LPS- stimulated BV2 cells. For in vivo studies, we administered LR to mice and A ss O was injected by stereotaxic to induce cognitive impairment, neuroinflammation, and synaptic loss. We found that LR increased the cell viability reduced by A ss O. Moreover, LR inhibited pro-inflammatory mediators such as nitric oxide (NO), inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2), and downregulated p38 mitogen-activated protein kinase (MAPK) signaling in BV2 cells. Behavioral assessments demonstrated that LR administration significantly improved cognitive decline induced by A ss O-injection. Furthermore, we found that microglia activation increased, and the expression of synaptic proteins decreased in the hippocampus of the A ss O-injected group, which was alleviated in the LR-treated group. These findings suggest that LR may be a potential candidate for protection against neuroinflammation and synaptic loss, and may prevent or delay AD progression.
引用
收藏
页码:7196 / 7207
页数:12
相关论文
共 42 条
[1]  
An F, 2022, MOLECULES, V27
[2]   Functions of p38 MAP Kinases in the Central Nervous System [J].
Asih, Prita R. ;
Prikas, Emmanuel ;
Stefanoska, Kristie ;
Tan, Amanda R. P. ;
Ahel, Holly I. ;
Ittner, Arne .
FRONTIERS IN MOLECULAR NEUROSCIENCE, 2020, 13
[3]  
Bachstetter AD, 2010, AGING DIS, V1, P199
[4]   Modeling the early stages of Alzheimer's disease by administering intracerebroventricular injections of human native Aβ oligomers to rats [J].
Baerends, Eva ;
Soud, Katia ;
Folke, Jonas ;
Pedersen, Anna-Kathrine ;
Henmar, Simon ;
Konrad, Lisa ;
Lycas, Matthew D. ;
Mori, Yuki ;
Pakkenberg, Bente ;
Woldbye, David P. D. ;
Dmytriyeva, Oksana ;
Pankratova, Stanislava .
ACTA NEUROPATHOLOGICA COMMUNICATIONS, 2022, 10 (01)
[5]  
Bourgognon Julie-Myrtille, 2020, Brain Neurosci Adv, V4, p2398212820979802, DOI [10.1177/2398212820979802, 10.1177/2398212820979802]
[6]  
Casey David A, 2010, P T, V35, P208
[7]   Involvement of p38 mitogen-activated protein kinase in lipopolysaccharide-induced iNOS and COX-2 expression in J774 macrophages [J].
Chen, BC ;
Chen, YH ;
Lin, WW .
IMMUNOLOGY, 1999, 97 (01) :124-129
[8]   Amyloid beta: structure, biology and structure-based therapeutic development [J].
Chen, Guo-fang ;
Xu, Ting-hai ;
Yan, Yan ;
Zhou, Yu-ren ;
Jiang, Yi ;
Melcher, Karsten ;
Xu, H. Eric .
ACTA PHARMACOLOGICA SINICA, 2017, 38 (09) :1205-1235
[9]  
Chen JK, 2004, CHINESE MED HERBOLOG, P706
[10]  
Choi Yoon-Hee, 2014, Prev Nutr Food Sci, V19, P343, DOI 10.3746/pnf.2014.19.4.343