Research on Differentiation of Bone Marrow Stromal Cells (BMSCs) Prompted by MicroRNA-124 and Effect on Inflammatory Reaction of Spinal Cord Injury Nerve Cells

2022 ◽  
Vol 12 (3) ◽  
pp. 588-596
Author(s):  
Ming Xu ◽  
Guo Yong Tan ◽  
Xian Ming Tao
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Mechanical Damage ◽  
Nerve Cells ◽  
Sod Activity ◽  
Cord Injury ◽  
Proliferation And Differentiation ◽  
Microrna 124 ◽  
Apoptotic Activity ◽  
And Oxidative Stress

The major feature of spinal cord injury (SCI) was the damage of nervous tissue in spinal cord. The damaged spinal cord was difficult to be repaired and regenerated. MicroRNA-124 could play a role in the repairing and recovering the injured tissue. The BMSCs could participate in repairing the damage. However, the regulatory effect of MicroRNA-124 on BMSCs and the inflammatory response of SCI was still not illustrated. These spinal cord nerve cells were assigned into group of mechanical damage, BMSCs and BMSCs with miR-124 overexpression followed by analysis of proliferation of nerve cells by MTT assay, apoptotic activity, expression of miR-124, GFAP and BDNF by Real time PCR, levels of TNF-α and IL-6 by ELISA as well as MDH and SOD activity. miR-124 mimics transfection significantly promoted BMSCs proliferation and increased ALK activity and the expression of GFAP and BDNF. In conclusion, the proliferation and differentiation of BMSCs could be regulated by miR-124. The inflammation and oxidative stress could be restrained so as to prompt the proliferation and repair of SCI cells and restrain apoptosis, indicating that it might be beneficial to recover the SCI.

scholarly journals Systemic Administration of Fibroblast Growth Factor 21 Improves the Recovery of Spinal Cord Injury (SCI) in Rats and Attenuates SCI-Induced Autophagy

2021 ◽  
Vol 11 ◽  
Author(s):  
Sipin Zhu ◽  
Yibo Ying ◽  
Lin Ye ◽  
Weiyang Ying ◽  
Jiahui Ye ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Functional Recovery ◽  
Nerve Cells ◽  
Systemic Administration ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Cord Injury

Protecting the death of nerve cells is an essential tactic for spinal cord injury (SCI) repair. Recent studies show that nerve growth factors can reduce the death of nerve cells and promote the healing of nerve injury. To investigate the conducive effect of fibroblast growth factor 21 (FGF21) on SCI repair. FGF21 proteins were systemically delivered into rat model of SCI via tail vein injection. We found that administration of FGF21 significantly promoted the functional recovery of SCI as assessed by BBB scale and inclined plane test, and attenuated cell death in the injured area by histopathological examination with Nissl staining. This was accompanied with increased expression of NeuN, GAP43 and NF200, and deceased expression of GFAP. Interestingly, FGF21 was found to attenuate the elevated expression level of the autophagy marker LC3-II (microtubules associated protein 1 light chain 3-II) induced by SCI in a dose-dependent manner. These data show that FGF21 promotes the functional recovery of SCI via restraining injury-induced cell autophagy, suggesting that systemic administration of FGF21 could have a therapeutic potential for SCI repair.

scholarly journals MicroRNA-219 Inhibits Proliferation and Induces Differentiation of Oligodendrocyte Precursor Cells after Contusion Spinal Cord Injury in Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Fang Li ◽  
Mou-Wang Zhou ◽  
Nan Liu ◽  
Yan-Yan Yang ◽  
Hua-Yi Xing ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Precursor Cells ◽  
Blue Staining ◽  
Oligodendrocyte Precursor Cells ◽  
Monocarboxylate Transporter 1 ◽  
Cord Injury ◽  
Proliferation And Differentiation ◽  
Oligodendrocyte Precursor

MicroRNA-219 (miR-219) regulates the proliferation and differentiation of oligodendrocyte precursor cells (OPCs) during central nervous system (CNS) development. OPCs only differentiate into oligodendrocytes (OLs) in the healthy CNS, but can generate astrocytes (As) after injury. We hypothesized that miR-219 may modulate OPC proliferation and differentiation in a cervical C5 contusion spinal cord injury (SCI) model. After injury, we observed a decrease in the miR-219 level and quantity of OLs and an increase in the number of OPCs and As. Silencing of miR-219 by its antagomir in vivo produced similar results, but of greater magnitude. Overexpression of miR-219 by its agomir in vivo increased the number of OLs and suppressed generation of OPCs and As. Luxol fast blue staining confirmed that SCI caused demyelination and that the extent of demyelination was attenuated by miR-219 overexpression, but aggravated by miR-219 reduction. Monocarboxylate transporter 1 (MCT-1) may be implicated in the regulation of OPC proliferation and differentiation mediated by miR-219 following contusion SCI. Collectively, our data suggest that miR-219 may mediate SCI-induced OPC proliferation and differentiation, and MCT-1 may participate in this process as a target of miR-219.

Effect of Electroacupuncture on Spinal Cord Injury in Mice: Inhibition Of Inflammatory Response and Oxidative Stress via ApoE and Nrf2

2020 ◽  
Author(s):  
Ni Dai ◽  
Chenglin Tang ◽  
Hongdi Zhao ◽  
Pan Dai ◽  
Siqin Huang
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Neuroprotective Effect ◽  
Related Factor ◽  
Cord Injury ◽  
Anti Inflammatory ◽  
And Oxidative Stress

Abstract Background: Spinal cord injury (SCI) is a catastrophic central nervous system disease. Inflammatory response and oxidative stress are two critical factors in the pathophysiological process of SCI and closely involved with Apolipoprotein E(ApoE) and Nuclear factor erythroid 2-related factor (Nrf2). Electroacupuncture (EA) has perfectly neuroprotective effect on SCI. However, the underlying mechanism by which EA mediates the inflammatory response and oxidative stress is not completely elucidated. In the present study, we investigated the signaling pathways that EA regulates inflammatory response and oxidative stress through elevation of ApoE and Nrf2 after SCI.Methods: C57BL/6 Wide Type (WT) mice and ApoE -/- mice were subjected to SCI model by a serrefine clamping. Neurological function was detected by BMS scores, ultrastructure of demyelinationed axons was observed by transmission electron microscopy. ApoE, pro- and anti- inflammatory cytokines, oxidative stress-relevant proteins were determined by histochemistry technology. Two-way ANOVA was applied to BMS scores. One-way ANOVA and Bonferroni's multiple comparison test were used to analyse differences among groups.Results: BMS scores were increased gradually and demyelinated axons were improved by EA gradually with the expression of ApoE. EA can inhibit inflammatory response by activation of ApoE, which decreased pro-inflammatory cytokines(TNF-α, IL-6, and IL-1β) expression and increased anti-inflammatory cytokines(IL-10 and TGF-β1).Meanwhile, EA can also inhibit oxidative stress by elevation of Nrf2,which induced HO-1 and NQO1 expression in WT and ApoE -/- mice.Conclusions: EA is a reliable treatment for promoting functional recovery of SCI. Thesynergisticrole of ApoE and Nrf2 in EA regulating inflammatory response and oxidative stress is decisiveto recovery after SCI.

scholarly journals Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats

Spinal Cord ◽  
2006 ◽  
Vol 44 (11) ◽  
pp. 662-667 ◽  
Author(s):  
Q Ao ◽  
X-H Sun ◽  
A-J Wang ◽  
P-F Fu ◽  
K Gong ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Ginkgo Biloba ◽  
Nerve Cells ◽  
Protective Effects ◽  
Egb 761 ◽  
Cord Injury
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