Visfatin improves the neurological repair of traumatic brain injury mice

doi:10.3877/cma.j.issn.2095-9141.2020.01.011

Abstract

Abstract:

Objective

To explore the neuroprotective effect and mechanism of visfatin in traumatic brain injury (TBI) mice model.

Methods

A total of 48 C57BL/6 mice with hydraulic shock brain injury model were established by means of hydraulic shock method, and then randomly divided into experimental group A, experimental group B and control group, 16 mice each. Three hours after the establishment of the model, experimental group A and experimental group B were given intraperitoneal injection of visfatin 15 and 30 μg/kg, respectively, once a day for 7 d, while the control group was given intraperitoneal injection of normal saline. Neurological severity scores (NSS) were compared before treatment, on day 3, day 14, and day 28 using 10 randomly selected mice. On the second day after the end of treatment, the whole brain of 3 mice in each group were randomly collected to compare the difference of positive cells after TUNEL staining, and then 3 mice were randomly collected from the brain tissue to compare the differences of apoptosis-related protein levels. The remaining 10 mice were compared with Morris water maze experiment from 24 to 28 d after treatment.

Results

There was no statistical difference in NSS scores of 3 groups at day 3 (P>0.05), but at day 14 and 28, the NSS scores of the visfatin-treated group were lower than those of the control group, with significant differences (P<0.05). There was no statistically significant difference in the latent escape period of water maze in the 3 groups at the 24^th and 25^th day (P>0.05), but at the 26^th, 27^th and 28^th day, the latent escape period of water maze in the visfatin-treated group was smaller than that in the control group (P<0.05). The number of TUNEL positive cells in the brain sections of rats treated with lipoprotein was smaller than that of the control group (P<0.05), and the expression levels of apoptosis-related protein cleave caspase-3 and cleaved PARP were also lower than those of the control group (P<0.05).

Conclusion

Visfatin can inhibit the apoptosis of neural cells peripheral lesion and reduce the expression of apoptosis-related proteins after TBI in mice, improve the repair of neural function.

Key words: Traumatic brain injury, Neural function repairment, Visfatin

Yi Wu, Zai Liang, Yong Liu, Chenghui Liu. Visfatin improves the neurological repair of traumatic brain injury mice[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2020, 06(01): 44-48.

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References 21

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组别	只数	治疗前	第3天	第14天	第28天
对照组	10	7.30±0.949	6.40±0.699	6.10±0.738	5.30±0.675
实验组A	10	7.00±0.943	5.90±0.876	5.30±0.823^a	4.30±0.823^a
实验组B	10	7.10±0.568	5.50±1.269	4.70±1.059^a	3.30±0.675^a
F值	?	0.670	2.134	5.709	9.768
P值	?	0.619	0.120	0.004	<0.001

组别	只数	治疗前	第3天	第14天	第28天
对照组	10	7.30±0.949	6.40±0.699	6.10±0.738	5.30±0.675
实验组A	10	7.00±0.943	5.90±0.876	5.30±0.823^a	4.30±0.823^a
实验组B	10	7.10±0.568	5.50±1.269	4.70±1.059^a	3.30±0.675^a
F值	?	0.670	2.134	5.709	9.768
P值	?	0.619	0.120	0.004	<0.001

组别	只数	第24天	第25天	第26天	第27天	第28天
对照组	10	70.80±13.60	65.50±9.14	62.20±7.64	56.30±8.41	49.10±8.85
实验组A	10	73.20±6.89	61.10±7.75	57.10±7.89	50.60±7.35	40.20±7.16^a
实验组B	10	69.80±10.13	57.50±5.99	48.80±6.65^a	44.60±6.90^a	28.40±6.54^ab
F值	?	0.273	2.682	8.322	5.959	18.771
P值	?	0.763	0.087	0.002	0.007	<0.001

组别	只数	第24天	第25天	第26天	第27天	第28天
对照组	10	70.80±13.60	65.50±9.14	62.20±7.64	56.30±8.41	49.10±8.85
实验组A	10	73.20±6.89	61.10±7.75	57.10±7.89	50.60±7.35	40.20±7.16^a
实验组B	10	69.80±10.13	57.50±5.99	48.80±6.65^a	44.60±6.90^a	28.40±6.54^ab
F值	?	0.273	2.682	8.322	5.959	18.771
P值	?	0.763	0.087	0.002	0.007	<0.001

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