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Research Article | Open Access

Transplantation of umbilical cord blood mononuclear cells attenuates the expression of IL-1β via the TLR4/NF-κB pathway in hypoxic-ischemic neonatal rats

Meng-Bei Zhang1Chao-Chao Song2Guang-Zu Li1Lan-Fen Chen1Rui Ma1Xiao-He Yu3Ping Gong1Xiao-Li Wang1( )
Department of Medical Imaging, Weifang Medical University, Weifang 261053, Shandong, China
Department of Digestive System, People’s Hospital of Fangzi District, Weifang 261200, Shandong, China
Department of Pediatrics, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China
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Abstract

Objective:

This study aims to observe the effects of transplantation of umbilical cord blood mononuclear cells (UCBMCs) on the expression of interleukin (IL)-1β and explore the mechanism via the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway in hypoxic-ischemic neonatal rats.

Methods:

Seven-day-old Sprague-Dawley neonatal rats were randomly divided into Sham, hypoxic-ischemic brain damage (HIBD), and UCBMC groups. The HIBD model was prepared by Rice-Vannucci method, and UCBMC were transplanted 24 h after HIBD in the UCBMC group. At 7 days after transplantation, changes in neurons and the TLR4 protein were examined by neuronal nuclei (NeuN)/TLR4 immunofluorescence staining. The expression of pNF-κB and IL-1β proteins was detected by immunohistochemical staining and enzyme linked immunosorbent assay (ELISA).

Results:

The percentage of NeuN+DAPI+ cells in the injured cortex in the UCBMC group was significantly higher than that in the HIBD group and lower than that in the Sham group (P < 0.05). The number of NeuN+TLR4+DAPI+cells in the UCBMC group was significantly lower than that in the HIBD group (P < 0.05) but higher than that in the Sham group (P < 0.05). More pNF-κB+ cells were observed in the HIBD group than in Sham and UCBMC groups (P < 0.05), and more pNF-κB+ cells were observed in the UCBMC group than in the Sham group (P < 0.05). ELISA results showed that the IL-1β expression in the injured cerebral cortex in the UCMBC group was significantly lower than that in the HIBD group but remained higher than that in the Sham group (P < 0.05).

Conclusions:

UCBMC transplantation could inhibit the IL-1β protein expression in the injured cortex, thereby alleviating HIBD in neonatal rats. The underlying mechanism might be associated with the down- regulation of TLR4 and pNF-κB proteins.

References

[1]
SK Yum, CJ Moon, YA Youn, et al. Changes in lactate dehydrogenase are associated with central gray matter lesions in newborns with hypoxic- ischemic encephalopathy. J Matern Fetal Neonatal Med. 2017, 30(10): 1177-1181.
[2]
MK Mwaniki, M Atieno, JE Lawn, et al. Long-term neurodevelopmental outcomes after intrauterine and neonatal insults: a systematic review. Lancet. 2012, 379(9814): 445-452.
[3]
LR Shiow, G Favrais, L Schirmer, et al. Reactive astrocyte COX2-PGE2 production inhibits oligodendrocyte maturation in neonatal white matter injury. Glia. 2017, 65(12): 2024-2037.
[4]
C Grasselli, D Ferrari, C Zalfa, et al. Toll-like receptor 4 modulation influences human neural stem cell proliferation and differentiation. Cell Death Dis. 2018, 9(3): 280.
[5]
EV Jones, DS Bouvier. Astrocyte-secreted matricellular proteins in CNS remodelling during development and disease. Neural Plast. 2014, 2014: 321209.
[6]
YZ Ye, T Jin, X Zhang, et al. Meisoindigo protects against focal cerebral ischemia-reperfusion injury by inhibiting NLRP3 inflammasome activation and regulating microglia/macrophage polarization via TLR4/NF-κB signaling pathway. Front Cell Neurosci. 2019, 13: 553.
[7]
YS Zhao, HY Wang, W Chen, et al. Melatonin attenuates white matter damage after focal brain ischemia in rats by regulating the TLR4/NF-κB pathway. Brain Res Bull. 2019, 150: 168-178.
[8]
MCB Paton, BJ Allison, MC Fahey, et al. Umbilical cord blood versus mesenchymal stem cells for inflammation-induced preterm brain injury in fetal sheep. Pediatr Res. 2019, 86(2): 165-173.
[9]
XL Wang, YS Zhao, X Wang. Umbilical cord blood cells regulate the differentiation of endogenous neural stem cells in hypoxic ischemic neonatal rats via the hedgehog signaling pathway. Brain Res. 2014, 1560: 18-26.
[10]
JE 3rd Rice, RC Vannucci, JB Brierley. The influence of immaturity on hypoxic-ischemic brain damage in the rat. Ann Neurol. 1981, 9(2): 131-141.
[11]
X Wang, XL Yang, WL Kong, et al. TRPV1 translocated to astrocytic membrane to promote migration and inflammatory infiltration thus promotes epilepsy after hypoxic ischemia in immature brain. J Neuroinflammation. 2019, 16(1): 214.
[12]
LJ Jiang, ZX Xu, MF Wu, et al. Resatorvid protects against hypoxic-ischemic brain damage in neonatal rats. Neural Regen Res. 2020, 15(7): 1316-1325.
[13]
W Zhang, JK Song, W Li, et al. Salvianolic acid D alleviates cerebral ischemia-reperfusion injury by suppressing the cytoplasmic translocation and release of HMGB1-triggered NF-κB activation to inhibit inflammatory response. Mediators Inflamm. 2020, 2020: 9049614.
Journal of Neurorestoratology
Pages 122-130
Cite this article:
Zhang M-B, Song C-C, Li G-Z, et al. Transplantation of umbilical cord blood mononuclear cells attenuates the expression of IL-1β via the TLR4/NF-κB pathway in hypoxic-ischemic neonatal rats. Journal of Neurorestoratology, 2020, 8(2): 122-130. https://doi.org/10.26599/JNR.2020.9040015

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Received: 21 May 2020
Revised: 11 June 2020
Accepted: 15 June 2020
Published: 04 August 2020
© The authors 2020

This article is published with open access at http://jnr.tsinghuajournals.com

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