Orally Administered Cinnamon Extract Attenuates Cognitive and Neuronal Deficits Following Traumatic Brain Injury

被引:13
作者
Qubty, Doaa [1 ]
Rubovitch, Vardit [1 ]
Benromano, Tali [1 ]
Ovadia, Michael [2 ]
Pick, Chaim G. [1 ,3 ,4 ,5 ,6 ]
机构
[1] Tel Aviv Univ, Sackler Sch Med, Dept Anat & Anthropol, Tel Aviv, Israel
[2] Tel Aviv Univ, Dept Zool, Tel Aviv, Israel
[3] Tel Aviv Univ, Dr Miriam & Sheldon G Adelson Chair, Tel Aviv, Israel
[4] Tel Aviv Univ, Ctr Biol Addict Dis, Tel Aviv, Israel
[5] Tel Aviv Univ, Sagol Sch Neurosci, Tel Aviv, Israel
[6] Tel Aviv Univ, Sylvan Adams Sports Inst, Tel Aviv, Israel
关键词
Traumatic brain injury (TBI); Cognitive impairments; Cinnamon extract (CE); Neurodegenerative disease; Neuronal survival; Spatial memory; Visual memory; ALZHEIMERS-DISEASE; ESSENTIAL OIL; HEAD-INJURY; PATHOPHYSIOLOGY; CONSEQUENCES; INHIBITION; RISK;
D O I
10.1007/s12031-020-01688-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The present paper shows how cinnamon extract (CE) consumption mitigates neuronal loss and memory impairment following traumatic brain injury (TBI), one of the world's most common neurodegenerative diseases. TBI patients suffer short- and long-term behavioral, cognitive, and emotional impairments, including difficulties in concentration, memory loss, and depression. Research shows that CE application can mitigate cognitive and behavioral impairments in animal models for Alzheimer's and Parkinson's disease, whose pathophysiology is similar to that of TBI. This study builds on prior research by showing similar results in TBI mice models. After drinking CE for a week, mice were injured using our 70-g weight drop TBI device. For 2 weeks thereafter, the mice continued drinking CE alongside standard lab nutrition. Subsequently, the mice underwent behavioral tests to assess their memory, motor activity, and anxiety. The mice brains were harvested for immunohistochemistry staining to evaluate overall neuronal survival. Our results show that CE consumption almost completely mitigates memory impairment and decreases neuronal loss after TBI. Mice that did not consume CE demonstrated impaired memory. Our results also show that CE consumption attenuated neuronal loss in the temporal cortex and the dentate gyrus. Mice that did not consume CE suffered a significant neuronal loss. There were no significant differences in anxiety levels and motor activity between all groups. These findings show a new therapeutic approach to improve cognitive function and decrease memory loss after TBI.
引用
收藏
页码:178 / 186
页数:9
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