Protective effect of Boldine against neuroinflammation in spinal cord injury in rats

2021 ◽  
pp. 1-7
Author(s):  
Jigao Feng ◽  
Junchi Liu ◽  
Xu Liu ◽  
Zhaoyou Qiu ◽  
Caicai Zhang
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Protective Effect ◽  
Locomotor Function ◽  
Medical Need ◽  
Tnf Α ◽  
Flow Cytometry Experiment ◽  
Cord Injury ◽  
Biomarkers Of Oxidative Stress

Abstract The successful clinical management of spinal cord injury (SCI) is still a unmet medical need. Despite advances in novel therapeutics, the multifactorial etiology of SCI still poses significant challenge to the mankind. Thus, in the present study, we intend to scrutinize the protective effect of Boldine (BOL), an alkaloid obtained from the boldo tree against experimental spinal cord injury. The effect of BOL was investigated on locomotor function of rats with various biomarkers of oxidative stress (MDA, SOD and GSH), inflammation (TNF-α, IL-1β and IL-6), and apoptosis. Results suggest that BOL showed improvement in locomotor function (on BBB scale) of rats with does-dependent reduction in oxidative stress and inflammation. It also reduces neuronal apoptosis in flow cytometry experiment. The study successfully demonstrated the possible clinical utility of BOL against SCI.

scholarly journals miRNA-221 Regulates Spinal Cord Injury-Induced Inflammatory Response through Targeting TNF-α Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Feng Sun ◽  
Haiwei Zhang ◽  
Tianwen Huang ◽  
Jianhui Shi ◽  
Tianli Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Luciferase Reporter ◽  
Spinal Cord Tissue ◽  
Tnf Α ◽  
Cord Injury ◽  
And Oxidative Stress

Objectives. To investigate the roles of miR-221 in spinal cord injury (SCI) as well as the underlying mechanism. Methods. A mouse model of SCI was generated and used to examine dynamic changes in grip strength of the mouse upper and lower limbs. The expression of miR-221 and tumor necrosis factor-α (TNF-α) was detected by RT-qPCR and Western blot. Levels of inflammation and oxidative stress in microglia cells of the injured mice overexpressing miR-221 were then measured by ELISA. Bioinformatics analysis and dual-luciferase reporter assay were conducted to identify the miR-221 target. Results. We successfully constructed SCI mouse model. The results of qRT-PCR showed that miR-221 was gradually upregulated in the spinal cord tissue of mice in the SCI group with the prolonged injury time. At the same time, the mRNA and protein of TNF-α gradually decreased. We further confirmed through cell experiments that the inflammatory factors TNF-α and IL-6, as well as iNOS and eROS, were upregulated in spinal cord microglia cells of SCI mice, and upregulation of miR-122 can inhibit their expression. Finally, the luciferase reporter experiment confirmed that miR-122 targeted TNF-α. Conclusions. We present evidence that miR-221 promotes functional recovery of the injured spinal cord through targeting TNF-α, while alleviating inflammatory response and oxidative stress.

scholarly journals Systemic Inflammation and the Breakdown of Intestinal Homeostasis Are Key Events in Chronic Spinal Cord Injury Patients

2021 ◽  
Vol 22 (2) ◽  
pp. 744
Author(s):  
David Diaz ◽  
Elisa Lopez-Dolado ◽  
Sergio Haro ◽  
Jorge Monserrat ◽  
Carlos Martinez-Alonso ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Bacterial Translocation ◽  
Binding Protein ◽  
Gut Barrier ◽  
Chronic Spinal Cord Injury ◽  
Fatty Acid Binding ◽  
Tnf Α ◽  
Cord Injury ◽  
Subset Distribution

Our aim was to investigate the subset distribution and function of circulating monocytes, proinflammatory cytokine levels, gut barrier damage, and bacterial translocation in chronic spinal cord injury (SCI) patients. Thus, 56 SCI patients and 28 healthy donors were studied. The levels of circulating CD14+highCD16−, CD14+highCD16+, and CD14+lowCD16+ monocytes, membrane TLR2, TLR4, and TLR9, phagocytic activity, ROS generation, and intracytoplasmic TNF-α, IL-1, IL-6, and IL-10 after lipopolysaccharide (LPS) stimulation were analyzed by polychromatic flow cytometry. Serum TNF-α, IL-1, IL-6 and IL-10 levels were measured by Luminex and LPS-binding protein (LBP), intestinal fatty acid-binding protein (I-FABP) and zonulin by ELISA. SCI patients had normal monocyte counts and subset distribution. CD14+highCD16− and CD14+highCD16+ monocytes exhibited decreased TLR4, normal TLR2 and increased TLR9 expression. CD14+highCD16− monocytes had increased LPS-induced TNF-α but normal IL-1, IL-6, and IL-10 production. Monocytes exhibited defective phagocytosis but normal ROS production. Patients had enhanced serum TNF-α and IL-6 levels, normal IL-1 and IL-10 levels, and increased circulating LBP, I-FABP, and zonulin levels. Chronic SCI patients displayed impaired circulating monocyte function. These patients exhibited a systemic proinflammatory state characterized by enhanced serum TNF-α and IL-6 levels. These patients also had increased bacterial translocation and gut barrier damage.

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