CXCL1/CXCR2在坏死性小肠结肠炎新生大鼠肠脑组织中的表达及意义

doi:10.3969/j.issn.1006-6233.2022.07.05

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Abstract Objective: To investigate the expression of chemokine CXCL1 and its receptor CXCR2 in the intestinal tissues and brain tissues of neonatal Sprague-Dawley rats with necrotizing enterocolitis (NEC),and to explore the pathogenesis of NEC-related preterm brain injury,providing a theoretical basis for the prevention and treatment of preterm brain injury. Methods: Forty-three SPF one-day-old rats(1 died) purchased from Experimental Animal Center of North Sichuan Medical University were selected and randomly divided into the experimental group (21 rats) and the control group (21rats).NEC model of immature rats was established,that is,the experimental group was gavaged 3% Dextran Sulfate Sodium Salt (DSS) 4 times a day for 3 days.The control group was gavaged with saline in the same way.The neonatal mice (6 rats at each time point) were sacrificed by head decapitation at 3h,24h and 72h after intragastric administration.The whole brain and intestine tissues were removed and the contents of CXCL1 and CXCR2 proteins in the intestine and brain tissues were measured by Western Blot at 3h,24h and 72h after gavage,respectively.The western blot bands were analysed in grey scale using GelPro software.Three animals from each group were stained with hematoxylin-eosin at 72 h after gavage for pathological sections of brain and intestinal tissues.Pathological tissue was examined for pathological description and analysis. Results: Compared with the control group,the intestinal tissue of rats in the experimental group was swollen,gas accumulation in the intestinal lumen was obvious,and the intestinal wall was thinner.The intestinal villi were damaged,exfoliated and necrotic,the intestinal glandular body was disorganized and missing,the submucosa and muscle layer was edema and separated,the base was thinned,and inflammatory cells were infiltrated.Brain tissue cell hierarchy is not clear,periventricular white matter porous,loose,decreased glial cells.WB results showed that,compared with the control group,the intestinal CXCL1 protein content in the experimental group increased at 3h and 72h after intragastric administration,with statistical significance (F=9.476,P<0.05).There was no significant difference in the intestinal CXCR2 protein content between the control group and the experimental group at each time point after intragastric administration (F=2.012,P>0.05).Compared with the control group,the brain CXCL1 protein content in the experimental group increased at 72h after intragastric administration,and the difference was statistically significant (F=35.767,P<0.05).Compared with the control group,the expression of CXCR2 protein in the brain tissues of the experimental group increased at 3h、24h and 72h after intragastric administration,with statistical significance (F=50.083,P<0.05). Conclusion: CXCL1/CXCR2 plays an important role in NEC-associated brain injury in preterm infants.And CXCL1/CXCR2 may be involved in the pathogenesis of gut-brain axis in transmitting intestinal inflammation to developing brain injury.

Key words： Neonatal rat Premature CXCL1 CXCR2 Necrotizing enterocolitis

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	HE Ling
	HOU Li
	ZHAO Jing

Cite this article:

HE Ling,HOU Li,ZHAO Jing. Expression and Significance of CXCL1/CXCR2 in Intestinal and Brain Tissues of Neonatal Rats with Necrotizing Enterocolitis[J]. HeBei Med, 2022, 28(7): 1076-1080.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2022.07.05 OR http://www.hbyxzzs.cn/EN/Y2022/V28/I7/1076

[1] Alshaikh BN,Reyes Loredo A,Knauff M,et al.The role of dietary fats in the development and prevention of necrotizing enterocolitis[J].Nutrients,2021,14(1):145.
[2] 王超,崔铭玲,王三南等.早产极低出生体重儿肠道菌群变化与坏死性小肠结肠炎的相关性[J].中华儿科杂志,2022,60(2):101-107.
[3] Humberg A,Spiegler J,Fortmann MI,et al.Surgical necrotizing enterocolitis but not spontaneous intestinal perforation is associated with adverse neurological outcome at school age[J].Sci Rep,2020,10(1):2373.
[4] Matei A,Montalva L,Goodbaum A,et al.Neurodevelopmental impairment in necrotising enterocolitis survivors:systematic review and meta-analysis[J].Arch Dis Child Fetal Neonatal Ed,2020,105(4):432-439.
[5] Serdar M,Kempe K,Herrmann R,et al.Involvement of CXCL1/CXCR2 during microglia activation following inflammation-sensitized hypoxic-ischemic brain injury in neonatal rats[J].Front Neurol,2020,11:540878.
[6] Ginzel M,Feng X,Kuebler JF,et al.Dextran sodium sulfate (DSS) induces necrotizing enterocolitis-like lesions in neonatal mice[J].PLoS One,2017,12(8):e0182732.
[7] Alsaied A,Islam N,Thalib L.Global incidence of necrotizing enterocolitis:a systematic review and Meta-analysis[J].BMC Pediatr,2020,20,344.
[8] Biouss G,Antounians L,Li B,et al.Experimental necrotizing enterocolitis induces neuroinflammation in the neonatal brain[J].Neuroinflammation,2019,16(1):97.
[9] Urbantat,RM,Jelgersma,C,Brandenburg,S,et al Tumor-associated microglia/macrophages as a predictor for survival in glioblastoma and temozolomide-induced changes in CXCR2 signaling with new resistance overcoming strategy by combination therapy[J].International journal of molecular sciences,2021,22(20),11180.
[10] Editorial Office.Erratum to fibroblast activation protein α-positive pancreatic stellate cells promote the migration and invasion of pancreatic cancer by CXCL1-mediated Akt phosphorylation[J].Ann Transl Med,2021,9(19):1511.
[11] Wu F,Chen X,Zhai L,et al.CXCR2 antagonist attenuates neutrophil transmigration into brain in a murine model of LPS induced neuroinflammation[J].Biochem Biophys Res Commun,2020,529(3):839-845.