Protective effects of PARP inhibitor, PJ34, is related to down-regulation of calpain and NF-<i>κ</i>B in a mouse model of TBI

Xue, Tao; Chen, Xuetao; Mao, Xiang; Hou, Zhiyong; Hao, Shuyu; Tian, Runfa; Zhu, Zhendan; Sun, Ming; Liu, Baiyun

doi:10.3109/02699052.2016.1160151

Cited by 3 publications

(3 citation statements)

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“…Therefore, strong activation of PARP-1 due to TBI may convert PARP-1 from being an agent of DNA repair to a trigger of neuronal injury and neuroinflammation. In support of PARP-1 contributing to CNS damage in TBI, PARP-1 inhibition reduces microglial activation and functional impairment and increases neuron survival in experimental models of TBI 38– 40 . The activation of mGluR5 decreases microglial activation and reduces microglial release of pro-inflammatory factors, which reduces neuronal loss and improves functional recovery after experimental TBI 41 .…”

Section: Traumatic Brain Injury-induced Neuroinflammationmentioning

confidence: 95%

“…Additionally, PARP-1 may initiate neuronal death through the release of apoptosis-inducing factor and impairing mitochondrial function and glycolytic metabolism 32, 35, 36 . PARP-1-dependent nuclear factor-kappa-B activation induces the expression of pro-inflammatory genes and activates microglia 37, 38 . Activated microglia release multiple types of neurotoxic molecules.…”

Section: Traumatic Brain Injury-induced Neuroinflammationmentioning

confidence: 99%

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Pathophysiological links between traumatic brain injury and post-traumatic headaches

Ruff

Blake

2016

F1000Res

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This article reviews possible ways that traumatic brain injury (TBI) can induce migraine-type post-traumatic headaches (PTHs) in children, adults, civilians, and military personnel. Several cerebral alterations resulting from TBI can foster the development of PTH, including neuroinflammation that can activate neural systems associated with migraine. TBI can also compromise the intrinsic pain modulation system and this would increase the level of perceived pain associated with PTH. Depression and anxiety disorders, especially post-traumatic stress disorder (PTSD), are associated with TBI and these psychological conditions can directly intensify PTH. Additionally, depression and PTSD alter sleep and this will increase headache severity and foster the genesis of PTH. This article also reviews the anatomic loci of injury associated with TBI and notes the overlap between areas of injury associated with TBI and PTSD.

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Section: Traumatic Brain Injury-induced Neuroinflammationmentioning

confidence: 95%

Section: Traumatic Brain Injury-induced Neuroinflammationmentioning

confidence: 99%

Pathophysiological links between traumatic brain injury and post-traumatic headaches

Ruff

Blake

2016

F1000Res

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“…Similarly, post-traumatic administration of the novel p53 inactivator pifithrin-α oxygen analogue offers protection against brain injury-induced neuronal apoptotic loss in hippocampal and improves cognitive deficits in rats [ 293 ]. PARP inhibitors (such as PJ34, CV1013, GPI 6150 etc .,) have also shown beneficial effects in TBI mediated cell death and neurological outcome in preclinical as well as clinical studies [ 294 , 295 ]. Although, several other classes of molecules (such as inhibitors of toll-like receptor pathway/mTOR pathway/p53 etc .,) have been tested for their therapeutic potential in brain injury-induced secondary cell death and apoptosis, details description of each is out of scope within this manuscript [ 296 ].…”

Section: Therapeutic Approaches In the Treatment Of Tbimentioning

confidence: 99%

The Complexity of Secondary Cascade Consequent to Traumatic Brain Injury: Pathobiology and Potential Treatments

Khatri

‬‬‬‬‬‬‬Bommaraju

Kumar

et al. 2021

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: According to the World Health Organization, Traumatic brain injury (TBI) is the major cause of death and disability and will surpass the other diseases by the year 2020. Patients who suffer TBI face many difficulties which negatively affect their social and personal life. TBI patients suffer from changes in mood, impulsivity, poor social judgment and memory deficits. Both open and closed head injuries have their own consequences. Open head injury associated problems are specific in nature e.g. loss of motor functions whereas closed head injuries are diffused in nature like poor memory, problems in concentration etc. Brain injury may have a detrimental effect on the biochemical processes responsible for the homeostatic and physiological disturbances in the brain. Although significant research has been done in order to decrease the overall TBI-related mortality, many individuals suffer from a life-long disability. In this article, we have discussed the causes of TBI, its consequence and the pathobiology of secondary injury. We have also tried to discuss the evidence-based strategies which are shown to decline the devastating consequences of TBI.

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Dual-targeting AAV9P1-mediated neuronal reprogramming in a mouse model of traumatic brain injury

Liu¹,

Xin²,

Sun³

et al. 2023

Neural Regeneration Research

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JOURNAL/nrgr/04.03/01300535-202403000-00038/inline-graphic1/v/2023-08-11T153926Z/r/image-tiff Traumatic brain injury results in neuronal loss and glial scar formation. Replenishing neurons and eliminating the consequences of glial scar formation are essential for treating traumatic brain injury. Neuronal reprogramming is a promising strategy to convert glial scars to neural tissue. However, previous studies have reported inconsistent results. In this study, an AAV9P1 vector incorporating an astrocyte-targeting P1 peptide and glial fibrillary acidic protein promoter was used to achieve dual-targeting of astrocytes and the glial scar while minimizing off-target effects. The results demonstrate that AAV9P1 provides high selectivity of astrocytes and reactive astrocytes. Moreover, neuronal reprogramming was induced by downregulating the polypyrimidine tract-binding protein 1 gene via systemic administration of AAV9P1 in a mouse model of traumatic brain injury. In summary, this approach provides an improved gene delivery vehicle to study neuronal programming and evidence of its applications for traumatic brain injury.

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Protective effects of PARP inhibitor, PJ34, is related to down-regulation of calpain and NF-κB in a mouse model of TBI

Abstract: PARP inhibition by PJ34 suppresses the over-activation of calpain and the production of inflammatory factors that are caused by NF-κB activation and it improves neurological functioning, decreases the contusion volume and attenuates neuronal cell death in a mouse model of CCI.

Cited by 3 publications

References 69 publications

Pathophysiological links between traumatic brain injury and post-traumatic headaches

Pathophysiological links between traumatic brain injury and post-traumatic headaches

The Complexity of Secondary Cascade Consequent to Traumatic Brain Injury: Pathobiology and Potential Treatments

Dual-targeting AAV9P1-mediated neuronal reprogramming in a mouse model of traumatic brain injury

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