Gallic acid attenuates blood-spinal cord barrier disruption by inhibiting Jmjd3 expression and activation after spinal cord injury

Park, Chan Sol; Lee, Jee Youn; Choi, Hae Young; Lee, Sang Hoon; Heo, Yeonju; Ju, Bong Gun; Choo, Hae-Young Park; Yune, Tae Young

doi:10.1016/j.nbd.2020.105077

Cited by 26 publications

(20 citation statements)

References 42 publications

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“…The antioxidant effects of some other polyphenols/phenolic compounds, including apocynin [268,269], baicalin [270,271], gastrodin [272], mangiferin [19], mulberrin [273], salvianolic acid [274,275], gallic acid [276,277], kaempferol [278], luteolin [279], naringenin [280], oleuropein [281,282], pycnogenol [283], silymarin [284], and protocatechuic acid [94], have been shown in Table 1. From the chemical point of view, Figure 2 presents the candidate chemical structures of neuroprotective polyphenols against SCI.…”

Section: Caffeic Acid Phenethylmentioning

confidence: 99%

Effects of Polyphenols on Oxidative Stress, Inflammation, and Interconnected Pathways during Spinal Cord Injury

Fakhri

Abbaszadeh

Moradi

et al. 2022

Oxidative Medicine and Cellular Longevity

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Despite the progression in targeting the complex pathophysiological mechanisms of neurodegenerative diseases (NDDs) and spinal cord injury (SCI), there is a lack of effective treatments. Moreover, conventional therapies suffer from associated side effects and low efficacy, raising the need for finding potential alternative therapies. In this regard, a comprehensive review was done regarding revealing the main neurological dysregulated pathways and providing alternative therapeutic agents following SCI. From the mechanistic point, oxidative stress and inflammatory pathways are major upstream orchestras of cross-linked dysregulated pathways (e.g., apoptosis, autophagy, and extrinsic mechanisms) following SCI. It urges the need for developing multitarget therapies against SCI complications. Polyphenols, as plant-derived secondary metabolites, have the potential of being introduced as alternative therapeutic agents to pave the way for treating SCI. Such secondary metabolites presented modulatory effects on neuronal oxidative stress, neuroinflammatory, and extrinsic axonal dysregulated pathways in the onset and progression of SCI. In the present review, the potential role of phenolic compounds as critical phytochemicals has also been revealed in regulating upstream dysregulated oxidative stress/inflammatory signaling mediators and extrinsic mechanisms of axonal regeneration after SCI in preclinical and clinical studies. Additionally, the coadministration of polyphenols and stem cells has shown a promising strategy for improving post-SCI complications.

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Section: Caffeic Acid Phenethylmentioning

confidence: 99%

Effects of Polyphenols on Oxidative Stress, Inflammation, and Interconnected Pathways during Spinal Cord Injury

Fakhri

Abbaszadeh

Moradi

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…The BSCB, which is a highly selective brain endothelial structure between the peripheral circulation and central nervous system, provides a particular homeostasis for the spinal cord [39]. Under different pathological conditions such as SCIRI, spinal cord injury, multiple sclerosis and epilepsy, the integrity of BSCB is damaged and immune cells in ltrate into the spinal cord, contributing to secondary injuries.…”

Section: Discussionmentioning

confidence: 99%

TSG–6 Released from Adipose‐Derived Stem Cells Derived Small Extracellular Vesicle Protects Against Spinal Cord Ischemia Reperfusion Injury by Inhibiting Endoplasmic Reticulum Stress

Xiao¹,

Zhao

et al. 2021

Preprint

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BackgroundSpinal cord ischemia reperfusion injury (SCIRI) is a complication of aortic aneurysm repair or spinal cord surgery that is associated with permanent neurological deficits. Mesenchymal stem cell (MSC)-derived small extracellular vesicles (sEVs) have been shown to be potential therapeutic options for improving motor functions after SCIRI. Due to their easy access and multi-directional differentiation potential, adipose‐derived stem cells (ADSCs) are preferable for this application. However, the effects of ADSC-derived sEVs (ADSC-sEVs) on SCIRI have not been reported.ResultsWe found that ADSC-sEVs inhibited SCIRI induced neuronal apoptosis, degradation of tight junction proteins and suppressed endoplasmic reticulum (ER) stress. However, in the presence of the ER stress inducer, tunicamycin, its anti-apoptotic and blood-spinal cord barrier (BSCB) protective effects were significantly reversed. We found that ADSC-sEVs contain tumor necrosis factor-(TNF) stimulated gene-6 (TSG-6) whose overexpression inhibited ER stress in vivo by modulating the PI3K/AKT pathway.ConclusionsADSC-sEVs inhibit neuronal apoptosis and BSCB disruption in SCIRI by transmitting TSG-6, which suppresses ER stress by modulating the PI3K/AKT pathway.

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“…American Type Culture Collection (Manassas, VA) provided a mouse brain endothelial cell line (bEnd.3), which was cultured as previously described [20,21]. bEnd.3 cells was seeded onto 6-well plate with 5 x 10 5 cells in each well and subjected to oxygen glucose deprivation (OGD) in a humidi ed anaerobic chamber (APM-30D, Astec, Fukuoka, Japan) as previously described (Park et al, 2020). Then, cells were replaced under normoxic conditions and the media was changed with 25 mM glucose containing DMEM.…”

Section: Endothelial Cell Culture and Ogd/reperfusionmentioning

confidence: 99%

“…As previously described, the permeability of the BSCB was measured using Evans blue dye extravasation [22]. In brief, Evans blue dye (Sigma) was dissolved in 0.9% saline and 5 ml of dye (2 %) was injected via i.p.…”

Section: Measurement Of Bscb Disruptionmentioning

confidence: 99%

Suppression of Transient Receptor Potential Melastatin 7 by Carvacrol Protects against Injured Spinal Cord by Inhibiting Blood–Spinal Cord Barrier Disruption

Park

Lee

Choi

et al. 2022

Journal of Neurotrauma

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When the blood-spinal cord barrier (BSCB) is disrupted after a spinal cord injury (SCI), several pathophysiological cascades occur, including in ammation and apoptotic cell death of neurons and oligodendrocytes, resulting in permanent neurological de cits. Transient receptor potential melastatin 7 (TRPM7) is involved in the pathological processes in many neuronal diseases, including traumatic brain injury, amyotrophic lateral sclerosis, parkinsonism dementia, and Alzheimer's disease. Furthermore, carvacrol (CAR), a TRPM7 inhibitor, is known to protect against SCI by reducing oxidative stress and inhibiting the endothelial nitric oxide synthase pathway. However, the functions of TRPM7 in the regulation of BSCB homeostasis after SCI have not been examined. Here, we demonstrated that TRPM7, a calcium-mediated non-selective divalent cation channel, plays a critical role after SCI in rat. Rats were contused at T9 and given CAR (50 mg/kg) via intraperitoneally immediately and 12 hours after SCI, and then given the same dose once a day for 7 days. TRPM7 was found to be up-regulated after SCI in both in vitro and in vivo studies, and it was expressed in blood vessels alongside neurons and oligodendrocytes. Additionally, CAR treatment suppressed BSCB disruption by inhibiting the loss of TJ proteins and preserved TJ integrity. CAR also reduced apoptotic cell death and improved functional recovery after SCI by preventing BSCB disruption caused by blood in ltration and in ammatory responses. Based on these ndings, we propose that blocking the TRPM7 channel can inhibit the destruction of the BSCB and it is a potential target in therapeutic drug development for use in SCI.

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Gallic acid attenuates blood-spinal cord barrier disruption by inhibiting Jmjd3 expression and activation after spinal cord injury

Cited by 26 publications

References 42 publications

Effects of Polyphenols on Oxidative Stress, Inflammation, and Interconnected Pathways during Spinal Cord Injury

Effects of Polyphenols on Oxidative Stress, Inflammation, and Interconnected Pathways during Spinal Cord Injury

TSG–6 Released from Adipose‐Derived Stem Cells Derived Small Extracellular Vesicle Protects Against Spinal Cord Ischemia Reperfusion Injury by Inhibiting Endoplasmic Reticulum Stress

Suppression of Transient Receptor Potential Melastatin 7 by Carvacrol Protects against Injured Spinal Cord by Inhibiting Blood–Spinal Cord Barrier Disruption

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