Ameliorative effects of echinacoside against spinal cord injury via inhibiting NLRP3 inflammasome signaling pathway

Gao, Shutao; Xu, Tao; Guo, Hailong; Deng, Qiang; Xun, Chuanhui; Li, Weidong; Sheng, Weibin

doi:10.1016/j.lfs.2019.116978

Cited by 28 publications

(20 citation statements)

References 42 publications

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“…PAMPs activate the NF-kB signaling pathway and induce the NLRP3, other inflammasomes as well as inflammatory cytokines including pro-IL-1β and pro-IL-18 release. Moreover, DAMPs activate the NLRP3 inflammasome by recruiting pro-caspase-1 in large quantities via ASC adaptor protein activation, which results in the formation of an autocatalytic process that predominantly stimulates the caspase-1 in SCI animal models [66] , [67] , [68] . Mounting pieces of evidence have documented that NF-κB pathway can tremendously trigger the NLRP3 inflammasome activation and inflammatory factors release after SCI [69] .…”

Section: Role Of Pyroptosis-regulated Cell Death Mechanisms In Scimentioning

confidence: 99%

“…Further investigations have documented that ECH has significant neuroprotective activities [102] , [103] . In a study, Gao and colleagues focused on exploring the potential therapeutic effects of ECH to impede the NLRP3 and other inflammasome components in microglia injury and SCI rat model [68] . The authors demonstrated that ECH administration efficaciously blocked the NEK7, NLRP3, caspase-1, ASC, as well as inflammatory mediators such as IL-1β, and IL-18 protein expression levels in the injured spinal cord on day 3 after the injury [68] .…”

Section: Inhibiting the Pyroptosis-regulated Cell Death And Inflammasmentioning

confidence: 99%

“…In a study, Gao and colleagues focused on exploring the potential therapeutic effects of ECH to impede the NLRP3 and other inflammasome components in microglia injury and SCI rat model [68] . The authors demonstrated that ECH administration efficaciously blocked the NEK7, NLRP3, caspase-1, ASC, as well as inflammatory mediators such as IL-1β, and IL-18 protein expression levels in the injured spinal cord on day 3 after the injury [68] . Administration of ECH in various concentrations largely impeded the expression of NEK7, NLRP3, ASC, caspase-1 as well as pro-inflammatory factors including IL-18 and IL-1β levels in LPS/ATP-induced BV-2 cells.…”

Section: Inhibiting the Pyroptosis-regulated Cell Death And Inflammasmentioning

confidence: 99%

See 2 more Smart Citations

Role of pyroptosis in spinal cord injury and its therapeutic implications

Mamun

Monalisa

et al. 2021

Journal of Advanced Research

107

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Section: Role Of Pyroptosis-regulated Cell Death Mechanisms In Scimentioning

confidence: 99%

Section: Inhibiting the Pyroptosis-regulated Cell Death And Inflammasmentioning

confidence: 99%

Section: Inhibiting the Pyroptosis-regulated Cell Death And Inflammasmentioning

confidence: 99%

See 1 more Smart Citation

Role of pyroptosis in spinal cord injury and its therapeutic implications

Mamun

Monalisa

et al. 2021

Journal of Advanced Research

107

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“…27,28 The activation of the NLRP3 inflammasome, which initiates an inflammatory cascade and triggers inflammatory death, plays a crucial role in the pathogenesis of SCI. 29 Wu et al believed that the NLRP3 inflammasome is a vital contributor to the secondary damage of SCI. 30 However, whether the activation of the NLRP3 inflammasome complex contributes to inflammation after duraplasty following SCI has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…Local pressure and edema play an important role in inflammation after SCI 27,28 . The activation of the NLRP3 inflammasome, which initiates an inflammatory cascade and triggers inflammatory death, plays a crucial role in the pathogenesis of SCI 29 . Wu et al believed that the NLRP3 inflammasome is a vital contributor to the secondary damage of SCI 30 .…”

Section: Introductionmentioning

confidence: 99%

Duraplasty of PHBV/PLA/Col membranes promotes axonal regeneration by inhibiting NLRP3 complex and M1 macrophage polarization in rats with spinal cord injury

Zhao

et al. 2020

FASEB j.

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Duraplasty after decompression decreases the lesion size and scar formation, promoting better functional recovery, but the underlying mechanism has not been clarified. Here, we fabricated a series of poly(hydroxybutyrate‐co‐hydroxyvalerate)/polylactic acid/collagen (PHBV/PLA/Col) membranes and cultured them with VSC4.1 motor neurons. The material characteristics and in vitro biological characteristics were evaluated. In the subcutaneous implantation test, PHBV/PLA/COl scaffolds supported the cellular infiltration, microvasculature formation, and decreased CD86‐positive macrophage aggregation. Following contusion spinal cord injury at T10 in Sprague‐Dawley rats, durotomy was performed with allograft dura mater or PHBV/PLA or PHBV/PLA/Col membranes. At 3 days post‐injury, Western blot assay showed decreased the expression of the NLRP3, ASC, cleaved‐caspase‐1, IL‐1β, TNF‐α, and CD86 expression but increased the expression of CD206. Immunofluorescence demonstrated that duraplasty with PHBV/PLA/Col membranes reduced the infiltration of CD86‐positive macrophages in the lesion site, decreased the glial fibrillary acidic protein expression, and increased the expression of NF‐200. Moreover, duraplasty with PHBV/PLA/Col membranes improved locomotor functional recovery at 8 weeks post‐injury. Thus, duraplasty with PHBV/PLA/Col membranes decreased the glial scar formation and promoted axon growth by inhibiting inflammasome activation and modulating macrophage polarization in acute spinal cord injury.

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The effect of the “segment” of spinal cord injury on the activity of the nucleotide‐binding domain‐like receptor protein 3 inflammasome and response to hormonal therapy

Majidpoor

Mortezaee

Khezri

et al. 2020

Cell Biochemistry & Function

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Spinal cord injury (SCI) is a common devastating condition that causes neuronal loss and dysfunction. Neuroinflammation takes cardinal roles in the pathogenesis of SCI, and nucleotide‐binding domain‐like receptor protein 3 (NLRP3) inflammasome is a mediator of inflammatory reactions occurring in SCI patients. The present study was designed to survey possible relation between thoracic segments whereby injury occurs with the activity of NLRP3 inflammasome complex, and to find the influence of hormonal therapy on the outcomes. Adult male Wistar rats underwent contusion SCI model at three different thoracic segments T1, T6 and T12, then receiving subcutaneous injection of either 10 mg/kg melatonin or 25 μg/kg 17‐β estradiol (E2) every 12 hours until 72 hours post‐SCI. Inflammasome activity was assessed before and at the end of hormonal therapy. SCI rats showed decreased locomotor activity and myelination, and increased activity of the NLRP3, apoptosis‐associated speck‐like protein (ASC) and caspase‐1 at gene and protein levels. Release of interleukins (ILs) 18 and 1β was also augmented after SCI (P < 0.0.5). Hormonal therapy was most effective for targeting mRNA activity at T6 segment. Treatment with either melatonin or E2 caused a decrease in the protein activity of NLRP3 inflammasome at all segments (P < 0.0.5), except for T6 that NLRP3 protein had no response to melatonin. IL‐1β showed decreased activity in response to hormonal therapy at all segments, whilst IL‐18 protein had no change at T1 segment. It is understood that although no alteration in the activity of NLRP3 was found for SCI at different segments, the response to hormonal therapy was influenced by segment. Significance of the study From our results, the NLRP3 inflammasome activity is not influenced by segment, but there are differences in the effect of hormonal therapy on inflammasome activity at different segments in response to melatonin or E2. These findings also provide the beneficial effects of melatonin or E2 on inflammation caused by spinal cord injury in different thoracic segments. Finally, these data can have therapeutic importance for hormone therapy of spinal cord injury.

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Ameliorative effects of echinacoside against spinal cord injury via inhibiting NLRP3 inflammasome signaling pathway

Cited by 28 publications

References 42 publications

Role of pyroptosis in spinal cord injury and its therapeutic implications

Role of pyroptosis in spinal cord injury and its therapeutic implications

Duraplasty of PHBV/PLA/Col membranes promotes axonal regeneration by inhibiting NLRP3 complex and M1 macrophage polarization in rats with spinal cord injury

The effect of the “segment” of spinal cord injury on the activity of the nucleotide‐binding domain‐like receptor protein 3 inflammasome and response to hormonal therapy

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