The Effects of Caffeic Acid Phenethyl Ester on Inflammatory Cytokines after Acute Spinal Cord Injury

Ak, Hakan; Gülşen, İsmail; Karaaslan, Tamer; Alaca, İlker; Candan, Aydın; Koçak, Havva; Atalay, Tugay; Çelikbilek, Asuman; Demir, Ismail; Yılmaz, Tevfik

doi:10.5505/tjtes.2015.33848

Cited by 10 publications

(10 citation statements)

References 17 publications

(34 reference statements)

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“…At present, the NF-κB pathway has been most extensively studied. However, the inflammatory pathway is a multi-channel reticular structure (18), as a result, it is not determined by a certain pathway. The mechanism underlying inflammation will become increasingly clear with research on each pathway, and the reticular structure of the inflammatory pathway will be elucidated (19); therefore, it will be more easily controlled.…”

Section: Discussionmentioning

confidence: 99%

SIRT1 inhibits apoptosis in in�vivo and in�vitro models of spinal cord injury via microRNA-494

Zhang

Zhao

et al. 2019

Int J Mol Med

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The aim of the present study was to investigate the function and mechanism of sirtuin 1 (SIRT1) in spinal cord injury (SCI). Reverse transcription-quantitative polymerase chain reaction was used to measure the expression levels of microRNA (miR)-494. MTT assay, lactate dehydrogenase activity assay and flow cytometry were used to analyze the effects of miR-494 on cell growth and apoptosis in a model of SCI. The present study demonstrated that SIRT1 expression was reduced; whereas miR-494 expression was increased in a rat model of SCI. Overexpression of miR-494 suppressed the protein expression levels of SIRT1, and induced p53 protein expression. Conversely, knockdown of miR-494 induced SIRT1 protein expression in an in vitro model of SCI. Furthermore, overexpression of miR-494 promoted cell apoptosis and decreased cell growth in an in vitro model of SCI; however, miR-494 knockdown enhanced cell growth and inhibited cell apoptosis. Administration of a SIRT1 agonist reduced the effects of miR-494 overexpression on cell apoptosis in an SCI model, whereas treatment with a p53 agonist reduced the effects of miR-494 knockdown on cell apoptosis in an SCI model. Together, these findings suggested that SIRT1 may inhibit apoptosis of SCI in vivo and in vitro through the p53 signaling pathway, whereas miR-494 suppressed SIRT1 and induced apoptosis.

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Section: Discussionmentioning

confidence: 99%

SIRT1 inhibits apoptosis in in�vivo and in�vitro models of spinal cord injury via microRNA-494

Zhang

Zhao

et al. 2019

Int J Mol Med

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“…This impairment is at least partially mediated by the release of pro‐inflammatory cytokines. These cytokines will induce cellular apoptosis, axonal destruction and extensive demyelination during secondary spinal cord injury .…”

Section: Introductionmentioning

confidence: 99%

Melatonin antagonizes interleukin‐18‐mediated inhibition on neural stem cell proliferation and differentiation

Chan

et al. 2017

J Cellular Molecular Medi

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Neural stem cells (NSCs) are self‐renewing, pluripotent and undifferentiated cells which have the potential to differentiate into neurons, oligodendrocytes and astrocytes. NSC therapy for tissue regeneration, thus, gains popularity. However, the low survivals rate of the transplanted cell impedes its utilities. In this study, we tested whether melatonin, a potent antioxidant, could promote the NSC proliferation and neuronal differentiation, especially, in the presence of the pro‐inflammatory cytokine interleukin‐18 (IL‐18). Our results showed that melatonin per se indeed exhibited beneficial effects on NSCs and IL‐18 inhibited NSC proliferation, neurosphere formation and their differentiation into neurons. All inhibitory effects of IL‐18 on NSCs were significantly reduced by melatonin treatment. Moreover, melatonin application increased the production of both brain‐derived and glial cell‐derived neurotrophic factors (BDNF, GDNF) in IL‐18‐stimulated NSCs. It was observed that inhibition of BDNF or GDNF hindered the protective effects of melatonin on NSCs. A potentially protective mechanism of melatonin on the inhibition of NSC's differentiation caused IL‐18 may attribute to the up‐regulation of these two major neurotrophic factors, BNDF and GNDF. The findings indicate that melatonin may play an important role promoting the survival of NSCs in neuroinflammatory diseases.

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“…with a proportion >20-50% (23). Although pre-hospital first aid and clinical therapy has received continuous innovation and improvement, early mortality from acute SCI caused by respiratory failure remains at a high level (23). The results of the present study indicated that sparstolonin B significantly recovered the decrease in BBB score and the increase in the water content of the spinal cord in SCI rat.…”

Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Sparstolonin B attenuates spinal cord injury‑induced inflammation in rats by modulating TLR4‑trafficking

Yuan¹,

Zhang²,

Zhu³

et al. 2018

Mol Med Report

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The present study used a spinal cord injury (SCI) model to evaluate whether sparstolonin B was able to prevent SCI, and to investigate the underlying signaling mechanism. Sparstolonin B attenuated the SCI‑induced Batto, Beattie and Bresnahan score and water content in rats. Sparstolonin B attenuated the mRNA expression of proinflammatory cytokines interleukin (IL)‑18, IL‑6, IL‑1β, and IL‑23, decreased the levels of tumor necrosis factor‑α and interferon‑γ, and decreased caspase‑3 activity and apoptosis regulator Bax protein expression in SCI rats. Similarly, sparstolonin B inhibited monocyte chemoattractant protein‑1 mRNA levels, and Toll‑like receptor (TLR) 4, myeloid differentiation primary response protein MyD88 (MyD88) and nuclear factor (NF)‑κB protein levels in SCI rats. The present results suggested that sparstolonin B may attenuate SCI‑induced inflammation and apoptosis in rats by modulating the TLR4/MyD88/NF‑κB signaling pathway.

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The Effects of Caffeic Acid Phenethyl Ester on Inflammatory Cytokines after Acute Spinal Cord Injury

Abstract: BACKGROUND:The purpose of this study was to investigate the effects of Caffeic Acid Phenethyl Ester (CAPE) on proinflammatory cytokines, IL-1β and TNF-α, and explore its healing effect after acute spinal cord injury.

Cited by 10 publications

References 17 publications

SIRT1 inhibits apoptosis in in�vivo and in�vitro models of spinal cord injury via microRNA-494

SIRT1 inhibits apoptosis in in�vivo and in�vitro models of spinal cord injury via microRNA-494

Melatonin antagonizes interleukin‐18‐mediated inhibition on neural stem cell proliferation and differentiation

Sparstolonin B attenuates spinal cord injury‑induced inflammation in rats by modulating TLR4‑trafficking

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