scholarly journals Anti-inflammatory and antioxidative effects of genistein in a model of spinal cord injury in rats

2021 ◽  
Vol 15 (5) ◽  
pp. 233-243
Author(s):  
Ercan Bal ◽  
Şahin Hanalioğlu ◽  
Aydın Sinan Apaydın ◽  
Ceylan Bal ◽  
Almila Şenat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Score ◽  
Control Group ◽  
Spinal Cord Tissue ◽  
Total Thiol ◽  
Secondary Damage ◽  
Cord Injury ◽  
Anti Inflammatory

Abstract Background Neurological damage from spinal cord injury (SCI) is a result of primary mechanical injury and secondary damage from oxidative stress and neuroinflammation. Although genistein has been shown to have potent antioxidant and anti-inflammatory effects in studies of brain injury, its effect on secondary damage in SCI has remained unknown. Objective To determine effects of genistein in a model of SCI in rats. Methods We divided 21 rats evenly into 3 groups, a control group, in which only a laminectomy was performed; a trauma group in which SCI was induced; and a genistein group in which genistein was administered subcutaneously after SCI. The rats were assessed using a Basso–Beattie and Bresnahan functional score at the 12th hour and on the 1st, 3rd, 5th, and 7th days. Biochemical analyses were conducted at the same time points to determine the serum levels of catalase, ischemia-modified albumin (IMA), disulfide (SS), total thiol (TT), native thiol (NT), disulfide/total thiol (SS/TT), and native thiol/total thiol (NT/TT). Total oxidant and antioxidant capacity, and oxidative stress index were determined in spinal cord tissue obtained on the 7th day together with immunohistochemistry for cyclooxygenase-2 levels. Result Catalase activity on the 7th day was significantly (P = 0.001) higher in the genistein-treated rats than in other groups, and IMA levels became stable earlier (3rd day) in the genistein group. SS values were significantly (P = 0.004) lower in the genistein group. NT/TT ratio were significantly (P = 0.049) higher in the genistein-treated rats on the 7th day. Conclusion Genistein has antioxidant, anti-inflammatory, and protective effects in a model of SCI in rats and warrants further study.

Neuroprotective effects of Nigella sativa on experimental spinal cord injury in rats

2006 ◽  
Vol 25 (3) ◽  
pp. 127-133 ◽  
Author(s):  
M Kanter ◽  
O Coskun ◽  
M Kalayc ◽  
S Buyukbas ◽  
F Cagavi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nigella Sativa ◽  
Protein Carbonyl ◽  
Control Group ◽  
Spinal Cord Tissue ◽  
Neuroprotective Effects ◽  
Tissue Samples ◽  
Experimental Spinal Cord Injury ◽  
Cord Injury

The aim of this study was to investigate the possible beneficial effects of Nigella sativa (NS) in comparison to methylprednisolone on experimental spinal cord injury (SCI) in rats. SCI was performed by placing an aneurysm clip extradurally at the level of T11-12. Rats were neurologically tested over 24 h after trauma and spinal cord tissue samples were harvested for both biochemical and histopathological evaluation. The neurological scores of rats were not found to be different in SCI groups. SCI significantly increased the spinal cord tissue malondialdehyde (MDA) and protein carbonyl (PC) levels, however SCI decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) enzyme activities compared to the control. Methylprednisolone and NS treatment decreased tissue MDA and PC levels and prevented inhibition of SOD, GSH-Px and CAT enzymes in the tissues. The most significant results were obtained when NS was given. In SCI and placebo groups, the neurons of spinal cord tissue became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in methylprednisolone and NS-treated groups were well protected, however, not as well as the neurons of the control group. The number of neurons in the spinal cord tissue of the SCI and placebo groups was significantly less than the control, laminectomy, methylprednisolone and NS-treated groups. In conclusion, NS treatment might be beneficial in spinal cord tissue damage, and therefore shows potential for clinical implications.

scholarly journals Preparation of Drug Sustained-Release Scaffold with De-Epithelized Human Amniotic Epithelial Cells and Thiolated Chitosan Nanocarriers and Its Repair Effect on Spinal Cord Injury

2022 ◽  
Vol 2022 ◽  
pp. 1-8
Author(s):  
Lijuan Zhu ◽  
Shaohua Tian ◽  
Zhiyong Li ◽  
Dandan Fan ◽  
Hongwei Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stem Cell ◽  
Survival Rate ◽  
Inflammatory Factors ◽  
Spinal Cord Tissue ◽  
Thiolated Chitosan ◽  
Cord Injury ◽  
Human Amniotic Epithelial Cells

The disability rate of spinal cord injury (SCI) is extremely high, and stem cell inhibition is one of the most effective schemes in treating the spinal cord, but the survival rate is extremely low after stem cell transplantation, so it cannot be widely used in clinic. Studies have revealed that loading stem cells with biological scaffolds can effectively improve the survival rate and effect after stem cell transplantation. Therefore, this research was devised to analyze the repair effect of thiolated chitosan nanocarriers scaffold carrying de-epithelized human amniotic epithelial cells (HAECs) on SCI. And we used thiolated chitosan as nanocarriers, aiming to provide a reliable theoretical basis for future clinical practice. Through experiments, we concluded that the Tarlov and BBB scores of rats with SCI were raised under the intervention of thiolated chitosan carrying HAECs, while the inflammatory factors in serum, oxidative stress reaction in spinal cord tissue, apoptosis rate of nerve cells, and autophagy protein expression were all suppressed. Thus, the thiolated chitosan carrying HAECs may be applied to treat SCI by suppressing autophagy protein expression, oxidative stress response, and release of inflammatory factors in spinal cord tissue, which may be a new clinical therapy for SCI in the future. Even though we cannot understand exactly the therapeutic mechanism of thiolated chitosan carrying HAECs for SCI, the real clinical application of thiolated chitosan carrying HAECs needs to be confirmed by human experiments.

Modulation of nitric oxide homeostasis in a mouse model of spinal cord injury

2006 ◽  
Vol 4 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Tiziana Genovese ◽  
Emanuela Mazzon ◽  
Sofia Mariotto ◽  
Marta Menegazzi ◽  
Salvatore Cardali ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neutrophil Infiltration ◽  
Adenosine Diphosphate ◽  
Spinal Cord Tissue ◽  
Secondary Damage ◽  
Cord Injury ◽  
Primary Damage ◽  
Oxide Synthase

Object A traumatic spinal cord injury (SCI) immediately induces primary damage, and this is followed by secondary damage characterized by a series of events among which is a progressive extension of cell death within the damaged tissue. In this study, the authors investigated the role of inducible nitric oxide synthase (iNOS) in an experimental model of SCI in mice. Methods In wild-type (iNOS+/+) mice, SCI rapidly induced an inflammatory response as shown by nitrotyrosine formation, activation of the nuclear enzyme poly(adenosine diphosphate-ribose) polymerase (PARP), neutrophil infiltration, and spinal cord tissue histopathological changes, indicating the involvement of iNOS-derived massive amounts of NO in SCI. Conclusions Genetic inhibition of iNOS, however, resulted in a significant reduction in secondary damage, and this therapeutic efficacy was associated with the prevention of an SCI-induced drop in neuronal and endothelial NOS activity.

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 Engineered Exosomes Derived From Primary M2 Macrophages With Anti-inflammatory And Neuroprotective Properties For The Treatment of Spinal Cord Injury.

2021 ◽  
Author(s):  
Chuanjie Zhang ◽  
Daoyong Li ◽  
Hengshuo Hu ◽  
Zhe Wang ◽  
Jinyu An ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nerve Cell ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
M2 Macrophages ◽  
Secondary Damage ◽  
Cord Injury ◽  
Anti Inflammatory

Abstract Background: Uncontrollable inflammation and nerve cell apoptosis are the most destructive pathological response after spinal cord injury (SCI). So, inflammation suppression combined with neuroprotection is one of the most promising strategies to treat SCI. Engineered exosomes with anti-inflammatory and neuroprotective properties are promising candidates for the implementation of this strategies for the treatment of SCI. Results: By combining nerve growth factor (NGF) and curcumin (Cur), we prepared stable engineered exosomes of approximately 120 nm from primary M2 macrophages with anti-inflammatory and neuroprotective properties (Cur@EXs-cl-NGF). Notably, NGF was coupled with EXs by matrix metalloproteinase 9 (MMP9)-cleavable linker to accurately release at the injured site. Through targeted experiments, we found that these exosomes could actively and effectively accumulate at the injured site of SCI mice, which greatly improved the bioavailability of the drugs. Subsequently, Cur@EXs-cl-NGF reached the injured site and could effectively inhibit the uncontrollable inflammatory response to protect the spinal cord from secondary damage; in addition, Cur@EXs-cl-NGF could release NGF into the microenvironment in time to exert a neuroprotective effect against nerve cell damage. Conclusions: A series of in vivo and in vitro experiments showed that the engineered exosomes significantly improved the microenvironment after injury and promoted the recovery of motor function after SCI. We provide a new method for inflammation suppression combined with neuroprotective strategies to treat 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.

NDGA reduces secondary damage after spinal cord injury in rats via anti-inflammatory effects

2013 ◽  
Vol 1516 ◽  
pp. 83-92 ◽  
Author(s):  
Hui Xue ◽  
Xiu-ying Zhang ◽  
Jia-mei Liu ◽  
Yu Song ◽  
Ting-ting Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Secondary Damage ◽  
Cord Injury ◽  
Anti Inflammatory

scholarly journals Metallothionein-I + II Reduces Oxidative Damage and Apoptosis after Traumatic Spinal Cord Injury in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Camilo Rios ◽  
Iván Santander ◽  
Marisela Méndez-Armenta ◽  
Concepción Nava-Ruiz ◽  
Sandra Orozco-Suárez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Sham Group ◽  
Annexin V ◽  
Neurological Deficits ◽  
Spinal Cord Tissue ◽  
Protective Effects ◽  
Cord Injury ◽  
Markers Of Oxidative Stress

After spinal cord injury (SCI), some self-destructive mechanisms start leading to irreversible neurological deficits. It is known that oxidative stress and apoptosis play a major role in increasing damage after SCI. Metallothioneins I and II (MT) are endogenous peptides with known antioxidant, neuroprotective capacities. Taking advantage of those capacities, we administered exogenous MT to rats after SCI in order to evaluate the protective effects of MT on the production of reactive oxygen species (ROS) and lipid peroxidation (LP), as markers of oxidative stress. The activities of caspases-9 and -3 and the number of annexin V and TUNEL-positive cells in the spinal cord tissue were also measured as markers of apoptosis. Rats were subjected to either sham surgery or SCI and received vehicle or two doses of MT (10 μg per rat) at 2 and 8 h after surgical procedure. The results showed a significant increase in levels of MT protein by effect of SCI and SCI plus treatment at 12 h, while at 24 h an increase of MT was observed only in the injury plus treatment group (p<0.05). ROS production was decreased by effect of MT in lesioned tissue; likewise, we observed diminished LP levels by MT effect both in the sham group and in the group with SCI. Also, the results showed an increase in the activity of caspase-9 due to SCI, without changes by effect of MT, as compared to the sham group. Caspase-3 activity was increased by SCI, and again, MT treatment reduced this effect only at 24 h after injury. Finally, the results of the number of cells positive to annexin V and TUNEL showed a reduction due to MT treatment both at 24 and 72 h after the injury. With the findings of this work, we conclude that exogenously administered MT has antioxidant and antiapoptotic effects after SCI.

The Regulation of Bone Morphogenetic Protein/Smads Signaling Pathway in Spinal Cord Injury

2020 ◽  
Vol 10 (3) ◽  
pp. 323-328
Author(s):  
Zhigang Zhou ◽  
Kai Cao ◽  
Jianping Liao ◽  
Song Zhou ◽  
Liangliang Zhou ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Treatment Group ◽  
Signaling Pathway ◽  
Rating Scale ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Spinal Cord Tissue ◽  
Cord Injury ◽  
Smad5 Mrna

The incidence of spinal cord injury (SCI) increases year by year. SCI is characterized as high disability rate and poor prognosis. BMP/Smads signaling participates in the formation of osteoblasts and renal failure. This article will explore the regulation of BMP/Smads signaling pathway in SCI. Wistar rats were divided into control group; SCI group; and BMP-2 treatment group that were treated by tail vein injection of BMP-2 antisense oligonucleotide BMP-2 phosphorothioate AODN at 30 min after modeling. Real-time PCR and Western blot were used to detect BMP-2, Smad1, and Smad5 expressions. Hematoxylin-eosin (HE) staining was applied to analyze the change of SCI in each group. Immunohistochemistry (IHC) was selected to test BMPR Ia expression. Basso, Beattie Bresnahan-cocomotor rating scale (BBB) scale and Reuter score were compared. Enzyme-linked immunosorbent assay (ELISA) was adopted to detect TNF-α and Interleukin-2 (IL-2) expressions. Compared with the control group, BMP-2, Smad1, and Smad5 mRNA and protein expressions increased, BBB score declined, Reuter score elevated, and TNF-α and IL-2 secretion enhanced in the SCI group (P < 0.05). HE staining showed spinal cord injury, and IHC exhibited increased expression of BMPR Ia. The TGF-β treatment group significantly reduced the expressions of BMP-2, Smad1, and Smad5 mRNA and protein, increased BBB score, reduced Reuter score, and weakened the secretions of TNF-α and IL-2 (P < 0.05). HE staining demonstrated decreased reduction of spinal cord tissue and declined expression of BMPR Ia. SCI activated BMP/Smads signaling pathway, up-regulated BMPR Ia expression, and promoted inflammation. Regulation of BMP/Smads signaling pathway can downregulate BMPR Ia expression and inhibit inflammation to effectively relieve SCI.

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