Experimental research of expression and intervention of NOGO-A in brain tissue of rats after traumatic brain injury

doi:10.3877/cma.j.issn.2095-9141.2022.01.002

Abstract

Abstract:

Objective

To study the changes of the content of the NOGO-A and the ultrastructure in rat brain tissue after traumatic brain injury (TBI), and their relationship with RHOA/ROCK transduction pathway.

Methods

Forty-five healthy SD rats were randomly divided into control group, moderate trauma group and intervention group, with 15 rats in each group. The TBI rat model was established by hammer and free falling rod in moderate trauma group and intervention group. The rats in the intervention group were given fasudil hydrochloride injection intravenously immediately after trauma. The rats in each group were sacrificed 24 h after TBI. The ultrastructural changes of brain tissue cells in the injured area of each group were observed by electron microscope, the content of NOGO-A protein in brain tissue of each group was observed by immunohistochemical technique, and the gray value of NOGO-A protein was measured.

Results

Twenty-four hours after TBI, pathological injury occurred in the brain tissue injury area of rats in the moderate trauma group and the intervention group, and the intervention group was less severe than in the moderate trauma group. There was significant difference in the expression of NOGO-A protein in the brain tissue of the three groups (F=176.085, P<0.05). The moderate trauma group had the highest NOGO-A protein content, followed by the intervention group and the lowest in the control group.

Conclusion

Twenty-four hours after TBI, the injure of cell nucleus、mitochondria and cells edema appeared in the damage area of brains of rats, the distribution and the content of the NOGO-A in the damage area of rats increased. Blocking of the RHO/ROCK signaling pathway can improve the damage of the ultrastructure of the brain cell in the damage area and reduce the content and distribution of NOGO-A.

Key words: RHOA/ROCK signaling pathway, Traumatic brain injury, Ultrastructure of nerve cells, NOGO-A

Gang Cui, Huan Wang, Maowu Fu, Ying Wang, Hubin Duan. Experimental research of expression and intervention of NOGO-A in brain tissue of rats after traumatic brain injury[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2022, 08(01): 6-10.

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Figures/Tables 4

References 15

[1]	Tarapore PE, Vassar MJ, Cooper S, et al. Establishing a TBI program of care: benchmarking outcomes after institutional adoption of evidence-based guidelines[J]. J Neurotrauma, 2016, 33(22): 2026-2033.
[2]	Majdan M, Rusnák M, Bražinová A, et al. Severity, causes and outcomes of traumatic brain injuries occurring at different locations: implications for prevention and public health[J]. Cent Eur J Public Health, 2015, 23(2): 142-148.
[3]	Maas AIR, Menon DK, Adelson PD, et al. Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research[J]. Lancet Neurol, 2017, 16(12): 987-1048.
[4]	Zelinkova V, Brazinova A, Taylor MS, et al. Location of traumatic brain injury-related deaths: epidemiological analysis of 11 European countries[J]. Brain Inj, 2019, 33(7): 830-835.
[5]	Zusman BE, Kochanek PM, Jha RM. Cerebral edema in traumatic brain injury: a historical framework for current therapy[J]. Curr Treat Options Neurol, 2020, 22(3): 9.
[6]	Amano M, Nakayama M, Kaibuchi K. Rho-kinase/ROCK: a key regulator of the cytoskeleton and cell polarity[J]. Cytoskeleton (Hoboken), 2010, 67(9): 545-554.
[7]	Shi J, Wei L. Rho kinase in the regulation of cell death and survival[J]. Arch Immunol Ther Exp (Warsz), 2007, 55(2): 61-75.
[8]	Chen MS, Huber AB, van der Haar ME, et al. Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1[J]. Nature, 2000, 403(6768): 434-439.
[9]	Fournier AE, GrandPre T, Strittmatter SM. Identification of a receptor mediating Nogo-66 inhibition of axonal regeneration[J]. Nature, 2001, 18, 409(6818): 341-346.
[10]	Grandpre T, Li S, Strittmatter SM. Nogo-66 receptor antagonist peptide promotes axonal regeneration[J]. Nature, 2002, 417(6888): 547-551.
[11]	Wang X, Chun SJ, Treloar H, et al. Localization of Nogo-A and Nogo-66 receptor proteins at sites of axon-myelin and synaptic contact[J]. J Neurosci, 2002, 22(13): 5505-5515.
[12]	Skaper SD, Moore SE, Walsh FS. Cell signalling cascades regulating neuronal growth-promoting and inhibitory cues[J]. Prog Neurobiol, 2001, 65(6): 593-608.
[13]	Neumann S, Bradke F, Tessier-Lavigne M, et al. Regeneration of sensory axons within the injured spinal cord induced by intraganglionic cAMP elevation[J]. Neuron, 2002, 34(6): 885-893.
[14]	Cai D, Deng K, Mellado W, et al. Arginase I and polyamines act downstream from cyclic AMP in overcoming inhibition of axonal growth MAG and myelin in vitro[J]. Neuron, 2002, 35(4): 711-719.
[15]	Ryan TJ, Grant SG. The origin and evolution of synapses[J]. Nat Rev Neurosci, 2009, 10(10): 701-712.

组别	只数	NOGO-A蛋白表达量
对照组	15	100.10±8.25
干预组	15	127.44±9.48^a
中度创伤组	15	157.92±7.47^ab
F值		176.085
P值		<0.001

组别	只数	NOGO-A蛋白表达量
对照组	15	100.10±8.25
干预组	15	127.44±9.48^a
中度创伤组	15	157.92±7.47^ab
F值		176.085
P值		<0.001

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