Lnx1 expression in cortical neurons of rats with traumatic brain injury and mechanisms involved in secondary brain injury
- VernacularTitle:创伤性脑损伤大鼠皮质神经元中Lnx1表达及参与继发性脑损伤的机制
- Author:
Yanxia MA
1
,
2
;
Yanwei YANG
;
Yuhang MA
;
Di LI
;
Xiaoyan WANG
;
Mingming ZOU
;
Shanwen WEI
Author Information
- Keywords: traumatic brain injury; secondary brain injury; neuron; SD rat; Lnx1; PBK; BCR; ctgf
- From: Chinese Journal of Tissue Engineering Research 2025;29(1):24-30
- CountryChina
- Language:Chinese
- Abstract: BACKGROUND:Apoptosis plays an important role in secondary brain injury.Therefore,to explore the pathophysiological mechanism of promoting nerve cell survival after traumatic brain injury provides a new direction and theoretical basis for the prevention and treatment of traumatic brain injury. OBJECTIVE:To explore the expression changes of Lnx1 molecule in mammalian cortical neurons after brain injury and the possible mechanism involved in secondary brain injury. METHODS:Eighty adult SD rats were divided into 20 male and 20 female mice in sham operation group and 20 male and 20 female mice in traumatic brain injury group.The traumatic brain injury rat model was established by heavy falling method.At 6,12,24,48,and 72 hours after brain injury,the expression of related molecules in damaged cortical neurons was analyzed by RT-qPCR,western blot assay,and immunofluorescence staining. RESULTS AND CONCLUSION:(1)The brain tissue of traumatic brain injury group was bleeding and obvious tissue injury could be observed.Water content of brain tissue increased after traumatic brain injury.(2)Compared with the sham operation group,the expression of Lnx1 in cortical neurons after traumatic brain injury increased significantly at 24 hours after injury.(3)After traumatic brain injury,the expression of PBK and BCR protein decreased,and the pro-survival factor ctgf increased.(4)These findings suggest that after traumatic brain injury,the expression of Lnx1 is up-regulated in neurons,which may be due to the decrease of the expression of its target molecules PBK and BCR,and further promote the expression of living factor ctgf,which has a protective effect on the damaged neurons.
