Effect of Selective COX-2 Inhibitor on IL-1β and Glasgow Coma Scale (GCS) Score in Moderate Traumatic Brain Injury Patients

Bisri, Dewi Yulianti; Arifin, Zafrulah; Redjeki, Ike Sri; Bisri, Tatang

doi:10.4172/2155-6148.1000855

Cited by 1 publication

(2 citation statements)

References 13 publications

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“…Although serotonin deficiency is one of the hallmarks in the pathophysiology of PTSD, explicit research is anticipated to confirm the contribution of the serotonergic system in the significant inflammatory imbalance scenario of PTSD. Taken together, altered 5HT COX-2 inhibition had a brain-protective effect via reducing glutamate levels (Bisri et al 2017). In vitro studies also confirmed that glutamate NMDA receptor coupling results in Ca + entry and propels neuronal nitric oxide synthase (nNOS) activation.…”

Section: Glutamatergic System Inflammation and Ptsdmentioning

confidence: 67%

“…A randomized controlled trial involving individuals who had surgery for minor head injuries revealed that selective COX-2 inhibition had a brain-protective effect via reducing glutamate levels (Bisri et al 2017 ). In vitro studies also confirmed that glutamate NMDA receptor coupling results in Ca + entry and propels neuronal nitric oxide synthase (nNOS) activation.…”

Section: Channelization Of Neural Systems Towards Ptsd Symptomologymentioning

confidence: 99%

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Emphasizing the Crosstalk Between Inflammatory and Neural Signaling in Post-traumatic Stress Disorder (PTSD)

Govindula

Ranadive

Nampoothiri

et al. 2023

J Neuroimmune Pharmacol

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Post-traumatic stress disorder (PTSD) is a chronic incapacitating condition with recurrent experience of trauma-related memories, negative mood, altered cognition, and hypervigilance. Agglomeration of preclinical and clinical evidence in recent years specified that alterations in neural networks favor certain characteristics of PTSD. Besides the disruption of hypothalamus-pituitary-axis (HPA) axis, intensified immune status with elevated pro-inflammatory cytokines and arachidonic metabolites of COX-2 such as PGE2 creates a putative scenario in worsening the neurobehavioral facet of PTSD. This review aims to link the Diagnostic and Statistical Manual of mental disorders (DSM-V) symptomology to major neural mechanisms that are supposed to underpin the transition from acute stress reactions to the development of PTSD. Also, to demonstrate how these intertwined processes can be applied to probable early intervention strategies followed by a description of the evidence supporting the proposed mechanisms. Hence in this review, several neural network mechanisms were postulated concerning the HPA axis, COX-2, PGE2, NLRP3, and sirtuins to unravel possible complex neuroinflammatory mechanisms that are obscured in PTSD condition.

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Section: Glutamatergic System Inflammation and Ptsdmentioning

confidence: 67%

Section: Channelization Of Neural Systems Towards Ptsd Symptomologymentioning

confidence: 99%

Emphasizing the Crosstalk Between Inflammatory and Neural Signaling in Post-traumatic Stress Disorder (PTSD)

Govindula

Ranadive

Nampoothiri

et al. 2023

J Neuroimmune Pharmacol

View full text Add to dashboard Cite

show abstract

Effect of Selective COX-2 Inhibitor on IL-1β and Glasgow Coma Scale (GCS) Score in Moderate Traumatic Brain Injury Patients

Cited by 1 publication

References 13 publications

Emphasizing the Crosstalk Between Inflammatory and Neural Signaling in Post-traumatic Stress Disorder (PTSD)

Emphasizing the Crosstalk Between Inflammatory and Neural Signaling in Post-traumatic Stress Disorder (PTSD)

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