Selective cyclooxygenase 2 inhibition lowers spinal cord prostaglandin concentrations after injury

Resnick, Daniel K.; Nguyen, Peter H.; Cechvala, Catherine F.

doi:10.1016/s1529-9430(01)00117-6

Cited by 12 publications

(5 citation statements)

References 20 publications

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“…Animals were injured using the MASCIS impactor as described previously. [13][14][15][16][17] In summary, T9 laminectomy was performed under halothane anesthesia and spinal cord contusion was induced by dropping a 10-g weight from a height of 12.5 mm. Animals were only included in the study if the actual impact velocity was within 5% of the predicted ideal impact velocity and only if they exhibited anticipated neurologic deficits during the immediate post injury period.…”

Section: Methodsmentioning

confidence: 99%

B1 and TRPV-1 Receptor Genes and Their Relationship to Hyperalgesia Following Spinal Cord Injury

Dombourian¹,

Turner²,

Gerovac³

et al. 2006

Spine

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B1 and TRPV-1 receptor genes are overexpressed in the injured spinal cord of animals manifesting thermal hyperalgesia following SCI compared with similarly injured animals without hyperalgesia. This finding is consistent with past work regarding the role of these receptors in nociception and indicates that ongoing modifiable processes are occurring in the spinal cord that lead to clinical pain syndromes.

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Section: Methodsmentioning

confidence: 99%

B1 and TRPV-1 Receptor Genes and Their Relationship to Hyperalgesia Following Spinal Cord Injury

Dombourian¹,

Turner²,

Gerovac³

et al. 2006

Spine

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“…PGE 2 and TXB 2 , a stable metabolite of TXA 2 , have been found to be significantly increased over the first 72 h in the injured spinal cord (Resnick et al 2001a), indicating that COX-2 is metabolically active after SCI. COX-2 inhibition reduces this increase in PGE 2 and TXB 2 by three-to four-fold at 4 h and 24 h after SCI (Resnick et al 2001b). Schwab and colleagues have reported a persistent accumulation of COX-1-expressing microglia/macrophages and the expression of COX-1 in endothelial cells in SCI (Schwab et al 2000a) and brain lesions in rats (Schwab et al 2001) and humans (Schwab et al 2000b(Schwab et al , 2002.…”

Section: Aa Derivativesmentioning

confidence: 97%

Role of phospholipase A2s and lipid mediators in secondary damage after spinal cord injury

2012

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Inflammation is considered to be an important contributor to secondary damage after spinal cord injury (SCI). This secondary damage leads to further exacerbation of tissue loss and functional impairments. The immune responses that are triggered by injury are complex and are mediated by a variety of factors that have both detrimental and beneficial effects. In this review, we focus on the diverse effects of the phospholipase A(2) (PLA(2)) superfamily and the downstream pathways that generate a large number of bioactive lipid mediators, some of which have pro-inflammatory and demyelinating effects, whereas others have anti-inflammatory and pro-resolution properties. For each of these lipid mediators, we provide an overview followed by a discussion of their expression and role in SCI. Where appropriate, we have compared the latter with their role in other neurological conditions. The PLA(2) pathway provides a number of targets for therapeutic intervention for the treatment of SCI and other neurological conditions.

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“…Indomethacin, a nonsteroidal anti-inflammatory (NSAID) drug, acts as a nonselective cyclooxygenase inhibitor. It has shown that it inhibits the synthesis of prostaglandins and ameliorates the effects of secondary injuries like tissue necrosis in SCI [55][56][57]. RhoA is a convergent intracellular pathway that limits axonal growth; its inhibition with indomethacin prevents oligodendrocyte loss and induces myelination across damaged white matter [58].…”

Section: Treatment Outcomementioning

confidence: 99%

Trends in Neuroprotective Strategies after Spinal Cord Injury: State of the Art

Rodríguez-Barrera¹,

Garibay-López²,

Ibarra³

2020

Neuroprotection - New Approaches and Prospects

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Spinal cord injury (SCI) is an important pathology leading to possibly fatal consequences. The most common repercussions are those affecting motor and sensitivity skills. SCI-damage occurs in its first phase-as a result of the lesion mechanism (contusion, compression, transection, and primary lesion). After this primary damage, there is a second phase with further deleterious effects on neural degeneration and tissue restoration. At the moment, several investigation groups are working on developing therapeutic strategies to induce neuroprotection. This chapter pretends to introduce the reader to a wide range of these therapies, particularly those with promising results and tested in preclinical and clinical studies. In the first section, physiopathology of SCI will be addressed. Afterwards, the chapter will review neuroprotective strategies such as cyclooxygenase, calpain, and apoptosis inhibitors. Finally, the effect of immunophilin ligands, neural-derived peptides, antioxidants, hypoglycemic agent, gonadal hormones, Na channel blockers, and transplant of cultured cells will also be reviewed.

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Selective cyclooxygenase 2 inhibition lowers spinal cord prostaglandin concentrations after injury

Cited by 12 publications

References 20 publications

B1 and TRPV-1 Receptor Genes and Their Relationship to Hyperalgesia Following Spinal Cord Injury

B1 and TRPV-1 Receptor Genes and Their Relationship to Hyperalgesia Following Spinal Cord Injury

Role of phospholipase A2s and lipid mediators in secondary damage after spinal cord injury

Trends in Neuroprotective Strategies after Spinal Cord Injury: State of the Art

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