The Neuroprotective Mechanism of Spinal Cord Stimulation in Spinal Cord Ischemia/Reperfusion Injury

Li, Huixian; Dong, Xian‐Zhe; Yang, Yanwei; Jin, Mu; Cheng, Weiping

doi:10.1111/ner.13113

Cited by 6 publications

(4 citation statements)

References 28 publications

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“…The pathophysiological process after SCII is very complex, mainly including free radical damage, calcium channel opening, lipid peroxidation, and apoptosis, which often causes very serious damage to nerve cells and becomes an obstacle to later recovery [ 1 , 2 ]. The incidence of acute and delayed paraplegia due to SCII ranges from 3% to 18%, placing a huge emotional and financial burden on the patient's family and society [ 3 , 4 ]. Despite current improvements in surgical techniques and perioperative management, SCII is still impossible to fully predict and prevent.…”

Section: Introductionmentioning

confidence: 99%

lncRNA HOTAIR Inhibition by Regulating HMGB1/ROS/NF-κB Signal Pathway Promotes the Recovery of Spinal Cord Function

Wang

Long

Yang

et al. 2022

Computational and Mathematical Methods in Medicine

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Spinal cord ischemia-reperfusion injury (SCII) is one of the most serious complications of clinical aortic aneurysm and vascular malformation surgery. Long noncoding RNA (lncRNA) is involved in the progression of SCII, whereas long noncoding RNA HOX transcript antisense RNA (lncRNA HOTAIR) is unclear in SCII. This study is aimed at confirming the role and related mechanism of HOTAIR in SCII. Later on, a model of SCII was established by clamping the aortic arch for 14 minutes. RNA expression of HOTAIR was detected via qRT-PCR at 12 h, 24 h, 36 h, and 48 h after SCII. The Tarlov scoring system and TUNEL assay were used to evaluate neurological function and neuronal apoptosis. Oxidative stress factor levels were assessed according to the instructions of the kit. Inflammatory cytokines were assessed by ELISA. Western blot was used to detect levels of p65, p-p65, I-κBα, and p-I-κBα. We found HOTAIR was raised in SCII rats. si-HOTAIR was able to reverse SCII-induced oxidative stress in SCII rats. The HMGB1 expression was upregulated in SCII tissues and negatively correlated with HOTAIR. HMGB1 was able to partially reverse si-HOTAIR inhibition of oxidative stress, inflammatory injury, and neuronal cell apoptosis in SCII. In addition, the ROS/NF-κB signaling pathway is involved in HOTAIR/HMGB1 regulation of SCII. In a word, HOTAIR inhibition is able to inhibit oxidative stress, inflammatory injury, and neuronal apoptosis in SCII through downregulation of the high mobility group protein B1(HMGB1), which is achieved by inhibiting the ROS/NF-κB signaling pathway. The HOTAIR/HMGB1/ROS/NF-κB molecular pathway may be a new mechanism for the treatment of SCII.

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Section: Introductionmentioning

confidence: 99%

lncRNA HOTAIR Inhibition by Regulating HMGB1/ROS/NF-κB Signal Pathway Promotes the Recovery of Spinal Cord Function

Wang

Long

Yang

et al. 2022

Computational and Mathematical Methods in Medicine

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“…A recent study aimed to detect Akt/p-Akt, the signal transducer and activator of transcription 3 (STAT3)/p-STAT3, and glycogen synthase kinase (GSK-3) β/p-GSK-3 βin the tissue of white rabbits with spinal cord ischemia-reperfusion (I/R) injury using SCS. The results showed that SCS had a neuroprotective effect on rabbits with spinal cord I/R injuries; its mechanism was indicated as being related to Akt activation but not related to the independent regulation of STAT3 and GSK-3 β phosphorylation [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Investigation of the effects of high cervical spinal cord electrical stimulation on improving neurological dysfunction and its potential mechanism in rats with traumatic brain injury

Zhao

Huang²,

Xu³

et al. 2022

NeuroReport

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To explore the effects of high cervical spinal cord electrical stimulation (cSCS) on the recovery of neurological function and its possible mechanism in rats with traumatic brain injury (TBI). 72 rats were randomly divided into: (1) a sham group; (2) a traumatic brain injury (TBI) group; (3) a TBI+cSCS group; (4) a LY294002+TBI+cSCS group. The degree of neurological dysfunction was evaluated by modified Neurological severity score (mNSS). The pathological changes of the brain tissue in the injured area were observed by HE staining, and the apoptosis of neuron cells were observed by TUNEL staining. The expressions of BDNF and VEGFmRNA were detected by polymerase chain reaction (PCR), and the expressions of p-AKT, AKT, Bcl-2, Bax and caspase-3 proteins were detected by western blot. Compared with that of the TBI and LY294002+TBI+cSCS groups, the mNSS of the TBI+cSCS group were significantly lower on day 3 and 7 ( P <0.05). Compared with that in the TBI and LY294002+TBI+cSCS groups, the apoptosis of neuron cells in the TBI+cSCS group decreased significantly ( P < 0.05). Compared with the TBI and LY294002+TBI+cSCS group, the expression of Bcl-2 protein increased and the expressions of Bax and Caspase-3 proteins decreased in the TBI+cSCS group ( P < 0.05). Compared with that in the TBI and LY294002+TBI+cSCS groups, the intensity of p-Akt/Akt in the TBI+cSCS group increased ( P < 0.05). We found that cSCS had a protective effect on neuron cells after craniocerebral injury and could improve neurological dysfunction in rats, the mechanism of which might be that cSCS made the PI3K/Akt pathway more active after TBI.

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“…There are currently a variety of treatments to prevent/treat SCIRI, including improved surgical techniques, hypothermia, and drug assistance [ 57 , 58 ]; however, there is still a lack of effective measures to prevent/treat SCIRI. Therefore, it is urgent to study the mechanism of SCIRI and then find an effective treatment for it [ 59 ]. Baicalein is a component of the roots of the herb Scutellaria baicalensis, which has anti-tumor, antibacterial, antiviral, antioxidant, and anti-inflammatory pharmacological effects [ 60 , 61 ].…”

Section: The Role Of Pyroptosis and Autophagy In Ischemia/reperfusion...mentioning

confidence: 99%

The Role of Pyroptosis and Autophagy in Ischemia Reperfusion Injury

Zhao

Yang

et al. 2022

Biomolecules

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Pyroptosis is a process of programmed cell death mediated by gasdermin (GSDM) found in recent years. In the process of pyroptosis, caspase-1 or caspase-11/4/5 is activated, which cleaves gasdermin D and separates its N-terminal pore-forming domain (PFD). The oligomers of PFD bind to the cell membrane and form macropores on the membrane, resulting in cell swelling and membrane rupture. Increasing evidence indicates that pyroptosis is involved in many diseases, including ischemia reperfusion injury. Autophagy is a highly conserved catabolic process in eukaryotic cells. It plays an important role in the survival and maintenance of cells by degrading organelles, proteins, and macromolecules in the cytoplasm and recycling degradation products. Increasing evidence shows that dysfunctional autophagy participates in many diseases. Recently, autophagy and pyroptosis have been reported to play a vital role in the process of ischemia/reperfusion injury, but the related mechanisms are not completely clear. Therefore, this article reviews the role of autophagy and pyroptosis in ischemia–reperfusion injury and analyzes the related mechanisms to provide a basis for future research.

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The Neuroprotective Mechanism of Spinal Cord Stimulation in Spinal Cord Ischemia/Reperfusion Injury

Cited by 6 publications

References 28 publications

lncRNA HOTAIR Inhibition by Regulating HMGB1/ROS/NF-κB Signal Pathway Promotes the Recovery of Spinal Cord Function

lncRNA HOTAIR Inhibition by Regulating HMGB1/ROS/NF-κB Signal Pathway Promotes the Recovery of Spinal Cord Function

Investigation of the effects of high cervical spinal cord electrical stimulation on improving neurological dysfunction and its potential mechanism in rats with traumatic brain injury

The Role of Pyroptosis and Autophagy in Ischemia Reperfusion Injury

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