Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death

Lee, Sang Hwon; Choi, Bo Young; Lee, Song Hee; Kho, A Ra; Jeong, Jeong Hyun; Hong, Dae Ki; Suh, Sang Won

doi:10.3390/ijms18122510

Cited by 33 publications

(22 citation statements)

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“…Neuronal apoptosis occurs through multiple cellular mechanisms, following secondary neuronal injury, after a primary brain injury [61]. It was found that RAGE activation induces inflammation, oxidative stress, and apoptosis via upregulation of NF-κB [62,63].…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury

Alam

Rehman

Kim

2019

JCM

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Brain injuries are a serious global health issue and are the leading cause of neurodegeneration. To date, there is no proper cure and treatment for brain-injury-induced neuropathological conditions because of a lack of sufficient knowledge and the failure to develop a drug due to the multi-pathological conditions in the brain. Herein, we explored the neurotherapeutic effects of Nicotinamide (NAM), against brain injury-induced neurodegeneration and behavioral problems. Treating injured mouse brains with NAM, for 7 days, significantly ameliorated several pathological events. Interestingly, NAM treatment significantly inhibited the injury-induced activation of receptor for advanced glycation end-products (RAGE), c-Jun N-terminal kinases (JNK), and neuroinflammatory mediators, such as NF-κB, TNF-α, IL-1β, and NOS2 in the brain, and it also regulated the levels of apoptotic markers, including Bax, caspase-3, and Bcl-2. Furthermore, treatment using NAM in TBI mice, significantly reversed synaptic protein loss and improved memory impairments and behavioral outcomes. Our findings suggested that NAM treatment reduced injury-induced secondary neurodegenerative pathology by modulating RAGE/JNK/NF-κB signaling in mice. Therefore, we recommend that NAM would be a safe and efficient therapeutic agent against brain-injury-induced neurodegeneration.

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Section: Discussionmentioning

confidence: 99%

Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury

Alam

Rehman

Kim

2019

JCM

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“…46 Similar enhancement of microglial/astrocytes population after traumatic injury has been shown in several studies. [54][55][56]61 Gradual decrease in the number of degenerating neurons in injured and treated with IFN-γ (I + IFN-γ) and IL-1β (I + IL-1β) groups from first day to seventh day postinjury may be due to specific trophic neuroprotective effects of IFN-γ and IL-1β directly or through enhancement of microglia and astrocytes, thereby enhancing the neurotrophic factors such as BDNF as observed in this study, which may be one of the many neurotrophic factors provided neuroprotection. We have reported similar enhancement of astrocytes, microglia and BDNF by dibutyryl cyclic adenosine monophosphate (dBcAMP), a synthetic analogue of cAMP.…”

Section: Il-1β Are Able To Increase Secretion Of Bdnf Through Astrocymentioning

confidence: 99%

Interferon-Gamma and Interleukin-1Beta Enhance the Secretion of Brain-Derived Neurotrophic Factor and Promotes the Survival of Cortical Neurons in Brain Injury

2020

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Neuro-inflammation is associated with the production of cytokines, which influence neuronal and glial functions. Although the proinflammatory cytokines interferon-γ (IFN-γ) and interleukin-1Beta (IL-1β) are thought to be the major mediators of neuro-inflammation, their role in brain injury remains ill-defined. The objective of this study was to examine the effect of IFN-γ and IL-1β on survival of cortical neurons in stab wound injury in mice. A stab wound injury was made in the cortex of male BALB/c mice. Injured mice (I) were divide into IFN-γ and IL-1β treatment experiments. Mice in I + IFN-γ group were treated with IFN-γ (ip, 10 µg/kg/day) for 1, 3 and 7 days and mice in I + IL-1β group were treated with 5 IP injection of IL-1β (0.5 µg /12 h). Appropriate control mice were maintained for comparison. Immunostaining of frozen brain sections for astrocytes (GFAP), microglia (Iba-1) and Fluoro-Jade B staining for degenerating neurons were used. Western blotting and ELISA for brain-derived neurotrophic factor (BDNF) were done on the tissues isolated from the injured sites. Results showed a significant increase in the number of both astrocytes and microglia in I + IFN-γ and I + IL-1β groups. There were no significant changes in the number of astrocytes or microglia in noninjury groups (NI) treated with IFN-γ or IL-1β. The number of degenerating neurons significantly decreased in I + IFN-γ and I + IL-1β groups. GFAP and BDNF levels were significantly increased in I + IFN-γ and I + IL-1β groups. Interferon-γ and IL-1β induce astrogliosis, microgliosis, enhance the secretion of BDNF, one of the many neurotrophic factors after brain injury, and promote the survival of cortical neurons in stab wound brain injury.

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“…In the present study, we used PCA (30 mg/kg, i.p.) [ 21 ] on a pilocarpine-induced animal seizure model. Here, we found that treatment with PCA after a seizure decreased oxidative injury, microglia activation, and neurodegeneration.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Protocatechuic Acid on Seizure-Induced Neuronal Death

Lee

Choi

Kho

et al. 2018

IJMS

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Protocatechuic acid (PCA) is a type of phenolic acid found in green tea and has been shown to have potent antioxidant and anti-inflammatory properties. However, the effect of PCA on pilocarpine seizure-induced neuronal death in the hippocampus has not been evaluated. In the present study, we investigated the potential therapeutic effects of PCA on seizure-induced brain injury. Epileptic seizure was induced by intraperitoneal (i.p.) injection of pilocarpine (25 mg/kg) in adult male rats, and PCA (30 mg/kg) was injected into the intraperitoneal space for three consecutive days after the seizure. Neuronal injury and oxidative stress were evaluated three days after a seizure. To confirm whether PCA increases neuronal survival and reduced oxidative injury in the hippocampus, we performed Fluoro-Jade-B (FJB) staining to detect neuronal death and 4-hydroxynonenal (4HNE) staining to detect oxidative stress after the seizure. In the present study, we found that, compared to the seizure vehicle-treated group, PCA administration reduced neuronal death and oxidative stress in the hippocampus. To verify whether a decrease of neuronal death by PCA treatment was due to reduced glutathione (GSH) concentration, we measured glutathione with N-ethylmaleimide (GS-NEM) levels in hippocampal neurons. A seizure-induced reduction in the hippocampal neuronal GSH concentration was preserved by PCA treatment. We also examined whether microglia activation was affected by the PCA treatment after a seizure, using CD11b staining. Here, we found that seizure-induced microglia activation was significantly reduced by the PCA treatment. Therefore, the present study demonstrates that PCA deserves further investigation as a therapeutic agent for reducing hippocampal neuronal death after epileptic seizures.

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Administration of Protocatechuic Acid Reduces Traumatic Brain Injury-Induced Neuronal Death

Cited by 33 publications

References 50 publications

Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury

Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury

Interferon-Gamma and Interleukin-1Beta Enhance the Secretion of Brain-Derived Neurotrophic Factor and Promotes the Survival of Cortical Neurons in Brain Injury

Protective Effects of Protocatechuic Acid on Seizure-Induced Neuronal Death

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