Dimethyl itaconate attenuates CFA-induced inflammatory pain via NLRP3/ IL-1β signaling pathway

Abstract Background Itaconate plays potent anti-inflammatory effects and has gradually been discovered as a promising drug candidate for treating inflammatory diseases. However, its roles and underlying mechanism on pain remain unknown. Methods In the current work, we investigated the effects and mechanisms of dimethyl itaconate (DI, a derivative of itaconate) in a mouse model of complete Freund's adjuvant (CFA)-induced inflammatory pain. Male/Female C57 BL/6 mice were randomly divided into five groups: a vehicle group, an CFA group ,an CFA+PBS group and an CFA + DI(10mg /d and 20 mg/d) group.DI was performed for 11 consecutive days after CFA models were established.Paw withdrawal frequencies and paw withdrawal latencies were used to Behavioral Tests. The activation of macrophages and microglia, the level of proinflammatory cytokine production, the number of M1/M2 macrophages were evaluated .The possible involvement of the NLRP3/ IL-1β signaling pathway was also investigated. Results DI significantly reduced mechanical allodynia and thermal hyperalgesia, decreased peripheral inflammatory cell infiltration and the expression of pro-inflammatory factors IL-1β and TNF-α, and upregulated anti-inflammatory factor IL-10. Interestingly, DI promoted macrophages at the inflammatory site polarization from M1 into M2 type. Additionally, DI inhibited activation of macrophages in dorsal root ganglion (DRG) and microglia in the spinal cord, exhibiting reduced expressions of pro-inflammatory cytokines. Mechanismly, DI exerts the analgesic action primarily via inhibiting the activation of NLRP3 inflammasome complex and the release of IL-1β in derived and resident macrophages in the hind paw, DRG and spinal cord. Conclusion DI could alleviate the pain-like behavior of CFA mice by inhibiting the infiltration of plantar inflammatory cells and macrophages activation in DRG and microglia in the spinal cord. The analgesic behavior of itaconate was related to the inhibition of NLRP3 inflammasome. This study suggested possible evidence for prospective itaconate utilization in the management of inflammatory pain for the first time.

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Ulinastatin Activated The ERK5/Mer Signaling Pathway To Promote Macrophage Efferocytosis And Ameliorate Lung Inflammation

10.21203/rs.3.rs-1091035/v1 ◽

2021 ◽

Author(s):

Jinju Li ◽

Rongge Shao ◽

Qiuwen Xie ◽

XueKe Du

Keyword(s):

Lung Injury ◽

Signaling Pathway ◽

Lung Inflammation ◽

Raw264.7 Cells ◽

Inflammatory Factors ◽

Inflammatory Factor ◽

Dependent Manner ◽

Anti Inflammatory

Abstract Purpose:Ulinastatin (UTI) is an endogenous protease inhibitor with potent anti-inflammatory, antioxidant and organ protective effects. The inhibitor has been reported to ameliorate inflammatory lung injury but precise mechanisms remain unclear. Methods: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). The number of neutrophils and the phagocytosis of apoptotic neutrophils were observed by Diff- Quick method. Lung injury was observed by HE staining .BALF cells were counted by hemocytometer and concentrations of protein plus inflammatory factors were measured with a BCA test kit. During in vitro experiments, RAW264.7 cells were pretreated with UTI (1000 and 5000U/ mL), stained with CellTrackerTM Green B0DIPYTM and HL60 cells added with UV-induced apoptosis and PKH26 Red staining. The expression of ERK5\Mer related proteins was detected by western blot and immunofluorescence.Results: An in vivo model of lung injury has been constructed by intratracheal infusion of lipopolysaccharide (LPS). UTI treatment enhanced the phagocytotic effect of mouse alveolar macrophages on neutrophils, alleviated lung lesions, decreased the pro-inflammatory factor and total protein content of BALF and increased levels of anti-inflammatory factors. in vitro experiments ，UTI enhanced the phagocytosis of apoptotic bodies by RAW264.7 cells in a dose-dependent manner. Increased expression levels of ERK5 and Mer by UTI were shown by Western blotting and immunofluorescence.Conclusions: UTI mediated the activation of the ERK5/Mer signaling pathway, enhanced phagocytosis of neutrophils by macrophages and improved lung inflammation. The current study indicates potential new clinical approaches for accelerating the recovery from lung inflammation.

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Tempol, a Superoxide Dismutase Mimetic Agent, Inhibits Superoxide Anion-Induced Inflammatory Pain in Mice

BioMed Research International ◽

10.1155/2017/9584819 ◽

2017 ◽

Vol 2017 ◽

pp. 1-15 ◽

Cited By ~ 14

Author(s):

Catia C. F. Bernardy ◽

Ana C. Zarpelon ◽

Felipe A. Pinho-Ribeiro ◽

Cássia Calixto-Campos ◽

Thacyana T. Carvalho ◽

...

Keyword(s):

Spinal Cord ◽

Superoxide Dismutase ◽

Mrna Expression ◽

Inflammatory Pain ◽

Superoxide Anion ◽

Thermal Hyperalgesia ◽

Mechanical Hyperalgesia ◽

Antioxidant Defenses ◽

Paw Edema ◽

Anti Inflammatory

The present study evaluated the anti-inflammatory and analgesic effects of the superoxide dismutase mimetic agent tempol in superoxide anion-induced pain and inflammation. Mice were treated intraperitoneally with tempol (10–100 mg/kg) 40 min before the intraplantar injection of a superoxide anion donor, potassium superoxide (KO2, 30 μg). Mechanical hyperalgesia and thermal hyperalgesia, paw edema, and mRNA expression of peripheral and spinal cord mediators involved in inflammatory pain, TNFα, IL-1β, IL-10, COX-2, preproET-1, gp91phox, Nrf2, GFAP, and Iba-1, were evaluated. Peripheral and spinal cord reductions of antioxidant defenses and superoxide anion were also assessed. Tempol reduced KO2-induced mechanical hyperalgesia and thermal hyperalgesia and paw edema. The increased mRNA expression of the evaluated mediators and oxidative stress in the paw skin and spinal cord and increased mRNA expression of glial markers in the spinal cord induced by KO2 were successfully inhibited by tempol. KO2-induced reduction in Nrf2 mRNA expression in paw skin and spinal cord was also reverted by tempol. Corroborating the effect of tempol in the KO2 model, tempol also inhibited carrageenan and CFA inflammatory hyperalgesia. The present study demonstrates that tempol inhibits superoxide anion-induced molecular and behavioral alterations, indicating that tempol deserves further preclinical studies as a promising analgesic and anti-inflammatory molecule for the treatment of inflammatory pain.

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Neuregulin1-ErbB4 Signaling in Spinal Cord Participates in Electroacupuncture Analgesia in Inflammatory Pain

Frontiers in Neuroscience ◽

10.3389/fnins.2021.636348 ◽

2021 ◽

Vol 15 ◽

Author(s):

Chaofan Wan ◽

Yunlong Xu ◽

Baoyan Cen ◽

Yucen Xia ◽

Lin Yao ◽

...

Keyword(s):

Spinal Cord ◽

Inflammatory Pain ◽

Life Quality ◽

Thermal Hyperalgesia ◽

Conditional Knockout ◽

Inflammatory Factors ◽

Complementary And Alternative Therapy ◽

Genetic Ablation ◽

Chronic Inflammatory Pain

Chronic inflammatory pain is a severe clinical symptom that aggravates the life quality of patients and places a huge economic burden on individuals and society. As one complementary and alternative therapy, electroacupuncture (EA) is widely used in clinical practice to treat chronic inflammatory pain based on its safety and efficacy. Previous studies have revealed the potential role of adenosine, neuropeptides, and inflammatory factors in EA analgesia in various pain models, but the identity of some of the signaling pathways involved remain unknown. In the present study, we explored whether neuregulin1 (NRG1)-ErbB4 signaling is involved in EA analgesia in inflammatory pain. Repeated EA treatment at the acupoints Zusanli (ST36) and Sanyinjiao (SP6) for 3 consecutive days remarkably attenuated mechanical allodynia and thermal hyperalgesia in complete Freund’s adjuvant (CFA)-treated mice, with an increased expression of NRG1 in spinal cord (SC). We found that ErbB4 kinase participated in both the EA and NRG1 mediated analgesic effects on inflammatory pain by pharmacological inhibition or genetic ablation ErbB4 in vivo. Intriguingly, the mice with conditional knockout of ErbB4 from PV+ interneurons in SC showed abnormal basal mechanical threshold. Meanwhile, NRG1 treatment could not relieve tactile allodynia in PV-Erbb4–/– mice or AAV-PV-Erbb4–/– mice after CFA injection. These experimental results suggest that regulating NRG1-ErbB4 signaling in SC could reduce pain hypersensitivity and contribute to EA analgesia in inflammatory pain.

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Gut Microbiota Disorders Promote Inflammation and Aggravate Spinal Cord Injury Through the TLR4/MyD88 Signaling Pathway

Frontiers in Nutrition ◽

10.3389/fnut.2021.702659 ◽

2021 ◽

Vol 8 ◽

Author(s):

Zijie Rong ◽

Yuliang Huang ◽

Honghua Cai ◽

Min Chen ◽

Hao Wang ◽

...

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Gut Microbiota ◽

Signaling Pathway ◽

Nerve Cells ◽

Inflammatory Factors ◽

Arginase 1 ◽

Cord Injury ◽

Anti Inflammatory ◽

Myd88 Signaling

Background: In spinal cord injury (SCI), systemic inflammation and the death of nerve cells in the spinal cord are life threatening. The connection between gut microbiota and signaling pathways has been a hot research topic in recent years. The Toll-like receptor 4/Myeloid differentiation factor 88 (TLR4/MyD88) signaling pathway is closely related to the inflammatory response. This study explored whether the gut microbiota imbalance could affect the TLR4/MyD88 signaling pathway to regulate SCI to provide a new basis for SCI research and treatment.Methods: An SCI model was constructed to study the influence on the injury of gut microbiota. 16S amplicon sequencing was used to identify the diversity and abundance of gut microbes. Fecal microbiota transplantation was performed in mice with SCI. ELISA was used to detect the serum levels of pro-inflammatory and anti-inflammatory factors in mice. Hematoxylin and eosin staining was used to observe SCI in mice. Immunofluorescence was used to detect the rates of loss glial fibrillary acidic protein (GFAP), neuronal nuclear protein (NeuN), and ionized calcium-binding adapter molecule 1 (IBA1) in the spinal cord as indicators of apoptosis. The expression of the TLR4/MyD88 signaling pathway was detected by qRT-PCR and western blotting.Results: Significant differences were observed in the gut microbiota of SCI mice and normal mice. The gut microbiota of SCI mice was imbalanced. The levels of pro-inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 in SCI mice were increased, as was the level of the toxic induced nitric oxide synthase. The levels of anti-inflammatory factors IL-4, transforming growth factor-β, and IL-10 were decreased, as was the level of arginase-1. The apoptosis rates of GFAP, NeuN, and IBA1 were increased. The TLR4/MyD88 signaling pathway was activated. In the SCI group, inflammation increased after fecal transplantation, apoptosis of GFAP, NeuN, and IBA1 increased, and SCI was more serious.Conclusion: The TLR4/MyD88 signaling pathway promotes the death of nerve cells by inducing inflammation. Gut microbiota dysregulation can lead to aggravated SCI by activating the TLR4/MyD88 signaling pathway.

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Short-chain fatty acids contribute to neuropathic pain via regulating microglia activation and polarization

Molecular Pain ◽

10.1177/1744806921996520 ◽

2021 ◽

Vol 17 ◽

pp. 174480692199652

Author(s):

Feng Zhou ◽

Xian Wang ◽

Baoyu Han ◽

Xiaohui Tang ◽

Ru Liu ◽

...

Keyword(s):

Spinal Cord ◽

Neuropathic Pain ◽

Thermal Hyperalgesia ◽

Short Chain Fatty Acids ◽

Antibiotic Administration ◽

Tnf Α ◽

Microglia Polarization ◽

Inflammatory Phenotype ◽

Phenotype Markers ◽

Anti Inflammatory

Microglia activation and subsequent pro-inflammatory responses play a key role in the development of neuropathic pain. The process of microglia polarization towards pro-inflammatory phenotype often occurs during neuroinflammation. Recent studies have demonstrated an active role for the gut microbiota in promoting microglial full maturation and inflammatory capabilities via the production of Short-Chain Fatty Acids (SCFAs). However, it remains unclear whether SCFAs is involved in pro-inflammatory/anti-inflammatory phenotypes microglia polarization in the neuropathic pain. In the present study, chronic constriction injury (CCI) was used to induce neuropathic pain in mice, the mechanical withdrawal threshold, thermal hyperalgesia were accomplished. The levels of microglia markers including ionized calcium-binding adaptor molecule 1 (Iba1), cluster of differentiation 11b (CD11b), pro-inflammatory phenotype markers including CD68, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and anti-inflammatory phenotype markers including CD206, IL-4 in the hippocampus and spinal cord were determined on day 21 after CCI. The results showed that CCI produced mechanical allodynia and thermal hyperalgesia, and also increased the expressions of microglia markers (Iba1, CD11b) and pro-inflammatory phenotype markers (CD68, IL-1β, and TNF-α), but not anti-inflammatory phenotype marker (CD206, IL-4) in the hippocampus and spinal cord, accompanied by increased SCFAs in the gut. Notably, antibiotic administration reversed these abnormalities, and its effects was also bloked by SCFAs administration. In conclusion, data from our study suggest that CCI can lead to mechanical and thermal hyperalgesia, while SCFAs play a key role in the pathogenesis of neuropathic pain by regulating microglial activation and subsequent pro-inflammatory phenotype polarization. Antibiotic administration may be a new treatment for neuropathic pain by reducing the production of SCFAs and further inhibiting the process of microglia polarization.

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Potential role of a series of lysine-/leucine-rich antimicrobial peptide in inhibiting lipopolysaccharide-induced inflammation

Biochemical Journal ◽

10.1042/bcj20180483 ◽

2018 ◽

Vol 475 (22) ◽

pp. 3687-3706 ◽

Cited By ~ 3

Author(s):

Weibing Dong ◽

Xin Zhu ◽

Xuan Zhou ◽

Ying Yang ◽

Xin Yan ◽

...

Keyword(s):

Cell Membrane ◽

Signaling Pathway ◽

Inflammatory Responses ◽

Antimicrobial Activities ◽

Host Cells ◽

Inflammatory Factors ◽

Human Macrophage ◽

U937 Cells ◽

Wide Range ◽

Anti Inflammatory

Antimicrobial peptides have broad-spectrum killing activities against bacteria, enveloped viruses, fungi and several parasites via cell membrane permeation and exhibit primarily immunomodulatory and anti-infective functions in their interactions with host cells. However, the mechanism underlying their anti-inflammatory activity remains to be elucidated. L-K6, an analog of temporin-1CEb isolated from the skin secretion of Rana chensinensis, has demonstrated a wide range of antimicrobial activities against gram-negative and gram-positive bacteria. In this study, the potent anti-inflammatory mechanism of L-K6 and its analogs in lipopolysaccharide (LPS)-stimulated human macrophage U937 cells were evaluated. We found that L-K6 suppressed the expression of inflammatory factors by two downstream signaling components in the MyD88-dependent pathway, including the mitogen-activated protein kinases (MAPKs) and the NF (nuclear factor)-κB signaling pathway, but its analog L-K5, which had the same amino acid sequence as L-K6 but no Lys residue at the –COOH terminal, only inhibited the phosphorylation of I-κB and NF-κB. Importantly, L-K6 and L-K5 were actively taken up by U937 cells through an independent cell membrane disruption mechanism and were eventually localized to the perinuclear region. The L-K6 uptake process was mediated by endocytosis, but L-K5 was specifically taken up by U937 cells via TLR4 endocytosis. Our results demonstrated that L-K6 can neutralize LPS and diassociate LPS micelles to inhibit LPS from triggering the proinflammatory signaling pathway, and by partially inhibiting inflammatory responses by the intracellular target. However, L-K5 may mainly inhibit proinflammatory responses by intracellular reporters to modulate the NF-κB signaling pathway.

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Long Noncoding RNA HOXA Cluster Anti-Sense RNA 2 Inhibits Mycoplasma pneumoniae-Induced Inflammation by Regulating the Nuclear Factor-KappaB Signaling Pathway

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2810 ◽

2021 ◽

Vol 11 (11) ◽

pp. 2262-2273

Author(s):

Mei Feng ◽

Chengjie Zhuo ◽

Xuefen Zhu

Keyword(s):

Cell Viability ◽

Signaling Pathway ◽

Mycoplasma Pneumoniae ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Flow Cytometric Analysis ◽

Inflammatory Factors ◽

Epithelial Cell Line ◽

Inflammatory Factor ◽

Hoxa Cluster

Mycoplasma pneumoniae (MP) is the primary cause of community-acquired lung inflammation. The MP-induced manifestations of pneumonia are associated with the release of pro-inflammatory cytokines; however, the mechanisms of MP-induced inflammation have not been fully clarified. The purpose of the present study was to determine whether long noncoding RNA HOXA cluster anti-sense RNA 2 (lncRNA HOXA-AS2) is involved in MP-induced inflammation. A model of MP-induced cellular inflammation was established using the human BEAS-2B lung epithelial cell line and lncRNA HOXA-AS2 levels were detected using reverse transcription-quantitative (RT-q) PCR. MTT and flow cytometric analysis were used to assess cell viability and apoptosis, respectively. The secretion of pro-inflammatory factors including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were measured by ELISA, and protein levels of phosho- (p-)p65 and p-NF-κB inhibitor α (p-IκBα) were detected by western blotting. The results suggest that MP infection significantly decreases the level of lncRNA HOXA-AS2 in BEAS-2B cells. lncRNA HOXA-AS2 overexpression significantly enhanced cell viability, inhibited apoptosis, decreased pro-inflammatory factor expression (TNF-α, IL-β and IL-6) and inhibited NF-κB pathway activation in MP-stimulated BEAS-2B cells. Conversely, lncRNA HOXA-AS2-knockdown resulted in the opposite effects. In conclusion, lncRNA HOXA-AS2 is involved in MP infection-induced inflammation and regulates the NF-κB signaling pathway.

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VGLUT2/Cdk5/p25 Signaling Pathway Contributed to Inflammatory Pain by Complete Freund’s Adjuvant

Pain Research and Management ◽

10.1155/2020/4807674 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9

Author(s):

Yuwen Tang ◽

Zhiyou Peng ◽

Shoujun Tao ◽

Jianliang Sun ◽

Wenyuan Wang ◽

...

Keyword(s):

Spinal Cord ◽

Signaling Pathway ◽

Inflammatory Pain ◽

Glutamate Transporter ◽

Underlying Mechanism ◽

Complete Freund’S Adjuvant ◽

Freund’S Adjuvant ◽

Complete Freund's Adjuvant ◽

Freund's Adjuvant ◽

Heat Hyperalgesia

Vesicular glutamate transporter type 2 (VGLUT2) is known to play an important role in mediating heat hyperalgesia induced by inflammation. However, the underlying mechanism for this activity is poorly understood. Cyclin-dependent kinase 5 (Cdk5), serving as a key regulator in modulating release of glutamate, acted a key player in the formation of heat hyperalgesia of inflammatory pain. However, it remains unknown whether there is a bridge between Cdk5 and VGLUT2 for mediating inflammatory pain. Therefore, we designed the experiment to determine whether VGLUT2 signaling pathway is involved in inflammatory pain mediated by Cdk5 in the inflammatory pain model induced by complete Freund’s adjuvant (CFA). Our results showed that the coexpression of Cdk5/VGLUT2 in small- and medium-sized neuronal cells of the dorsal root ganglion (DRG) and spinal cord between days 1 and 3 following subcutaneous injection of CFA was significantly increased. Moreover, our study revealed that the expression of VGLUT2 protein in the DRG and spinal cord was remarkably increased between days 1 and 3 following CFA injection and was significantly reduced by roscovitine, a selective antagonist of Cdk5. Additionally, p25 but not p35, an activator of Cdk5, protein was significantly increased by CFA and reduced by roscovitine. Our findings suggested that VGLUT2/Cdk5 signaling pathway contributes to inflammatory pain mediated by Cdk5/p25.

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Electroacupuncture Inhibits Spinal Interleukin-17A to Alleviate Inflammatory Pain in a Rat Model

The Open Pain Journal ◽

10.2174/1876386320130624001 ◽

2013 ◽

Vol 6 (1) ◽

pp. 183-189 ◽

Cited By ~ 1

Author(s):

Xianze Meng ◽

Lixing Lao ◽

Xue-Yong Shen ◽

Brian M. Berman ◽

Ke Ren ◽

...

Keyword(s):

Spinal Cord ◽

Inflammatory Pain ◽

Thermal Hyperalgesia ◽

Lumbar Spinal Cord ◽

Thermal Stimulus ◽

Sham Control ◽

Interleukin 17A ◽

Neuronal Interactions ◽

Lumbar Spinal ◽

Essential Subunit

Although acupuncture analgesia has been reported in clinical trials, its mechanisms have been unclear. It was recently reported that spinal astrocytes-produced interleukin-17A (IL-17A) facilitates inflammatory pain. Hypothesizing that electroacupuncture (EA) would suppress inflammation-enhanced IL-17A synthesis to inhibit pain, we induced hyperalgesia, as measured by decreased paw withdrawal latency (PWL) to a noxious thermal stimulus, by subcutaneously injecting complete Freund's adjuvant (CFA, 0.08 ml, 40 μg Mycobacterium tuberculosis) into the hind paws of rats, or intrathecal (i.t.) IL-17A (400 ng in 10 μl) into the lumbar spinal cord. We then gave EA at acupoint GB30 for two 20-min periods, once immediately after CFA or IL-17A administration and again 2 h post-injection. For sham control, EA needles were inserted into GB30 without stimulation. PWL was measured before and 2.5 and 24 h after injection. Spinal IL-17A, IL-17 receptor A (IL-17RA), and phosphorylated NR1, an essential subunit of the N-methyl D-aspartate receptor (NMDAR), were determined 24 h post-CFA or –IL-17A using immunohistochemistry and western blot. Compared to sham control, EA inhibited CFA-caused thermal hyperalgesia 2.5 and 24 h post-CFA and concurrently suppressed inflammation-enhanced IL-17A and IL-17RA synthesis and NR1 phosphorylation in the ipsilateral spinal cord. EA inhibited IL-17A-produced thermal hyperalgesia, IL-17RA synthesis and NR1 phosphorylation. Our data suggest that EA inhibits inflammatory pain by blocking spinal IL-17A synthesis. Since previous study shows that IL-17A is located in astrocytes and IL-17RA and NR1 are in neurons, the data suggest that EA alleviates pain by modulating glia-neuronal interactions that involve IL-17A, IL-17RA, and NR1 phosphorylation.

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Antioxidative and anti-inflammatory effects of Cichorium intybus L. seed extract in ischemia/reperfusion injury model of rat spinal cord

Journal of Contemporary Medical Sciences ◽

10.22317/jcms.v4i4.493 ◽

2018 ◽

Vol 4 (4) ◽

Keyword(s):

Spinal Cord ◽

Treatment Group ◽

Aqueous Extract ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Spinal Cord Ischemia ◽

Cichorium Intybus ◽

Inflammatory Factors ◽

The Mean ◽

Anti Inflammatory

Objectives: The antioxidant and anti-inflammatory effects of aqueous extract of chicory seed (CSE, Cichorium intybus L. seed) following spinal cord ischemia/reperfusion (SCI/R) injury in rat model were evaluated. Methods: In this study 36 male Wistar rats were randomly divided to six groups: control (Co), sham (Sh), CSE, SCI/R, CSE+SCI/R (7 days pretreatment with CSE group+inducing I/R injury), SCI/R +CSE (induced I/R injury group+3 days treatment with CSE). SCI/R injury was induced by creating a longitudinal incision on the midline of abdominal region and clamping the aorta just below renal artery for 30 minutes. After 3 days, SC was removed and used for evaluation of antioxidant enzymes (including Superoxide dismutase [SOD] and catalase [CAT]), oxidative stress markers (malondialdehyde [MDA]), inflammatory factors (IL1β, IL18 & TNFα) and histopathological changes. Before sacrificing the animals, the motional score were assessed. Results: Our results demonstrated that, in the SCI/R group, the mean levels of SOD, and CAT were significantly decreased (P<0.05), while the mean level of MDA was significantly increased (P<0.05) in comparison to Co and Sh groups. Also, the mean levels of SOD and CAT in the treatment group were higher than the SCI/R group (P<0.05), while, the mean MDA content in the treatment group was significantly less than the SCI/R group (P <0.05). In addition, comparison between SCI/R and treatment groups demonstrated a significant decrease in tissue damage in the treatment group. Conclusions: Our study demonstrated that, the neuroprotective effects of aqueous extract of Cichorium intybus L. seed on SCI/R injury in rat by anti-oxidative and anti-inflammatory activities. Additionally, comparing the treatment and pretreatment groups shows that the pretreatment usage of the extract is more effective than treatment group.

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