Effects of Intrathecal Caffeic Acid Phenethyl Ester and Methylprednisolone on Oxidant/Antioxidant Status in Traumatic Spinal Cord Injuries

Göçmez, Cüneyt; Çelik, Feyzi; Kamaşak, Kağan; Kaplan, Metin; Uzar, Ertuğrul; Arıkanoğlu, Adalet; Evliyaoğlu, Osman

doi:10.1055/s-0034-1371513

Cited by 9 publications

(4 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ROS is a collective term that broadly describes O 2 -derived free radicals that can induce extrinsic apoptosis through the activation of JNK or attack DNA directly (reviewed in [25,26]). We and others have demonstrated the potential of CAPE structures to modulate the cell’s redox state [48,49,50]. We also observe that 10 is among the weakest antioxidants in our panel of analogs, suggesting a pro-oxidative potential that sensitizes cancer cells to extrinsic apoptotic events.…”

Section: Resultssupporting

confidence: 63%

CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells

et al. 2015

View full text Add to dashboard Cite

Breast cancer is the second leading cause of death amongst women worldwide. As a result, many have turned their attention to new alternative approaches to treat this disease. Caffeic acid phenylethyl ester (CAPE), a well-known active compound from bee propolis, has been previously identified as a strong antioxidant, anti-inflammatory, antiviral and anticancer molecule. In fact, CAPE is well documented as inducing cell death by inhibiting NFκB and by inducing pro-apoptotic pathways (i.e., p53). With the objective of developing stronger anticancer compounds, we studied 18 recently described CAPE derivatives for their ability to induce apoptosis in breast cancer cell lines. Five of the said compounds, including CAPE, were selected and subsequently characterised for their anticancer mechanism of action. We validated that CAPE is a potent inducer of caspase-dependent apoptosis. Interestingly, some newly synthesized CAPE derivatives also showed greater cell death activity than the lead CAPE structure. Similarly to CAPE, analog compounds elicited p53 activation. Interestingly, one compound in particular, analog 10, induced apoptosis in a p53-mutated cell line. These results suggest that our new CAPE analog compounds may display the capacity to induce breast cancer apoptosis in a p53-dependent and/or independent manner. These OPEN ACCESSMolecules 2015, 20 12577 CAPE analogs could thus provide new therapeutic approaches for patients with varying genotypic signatures (such as p53 mutations) in a more specific and targeted fashion.

show abstract

Section: Resultssupporting

confidence: 63%

CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells

et al. 2015

View full text Add to dashboard Cite

show abstract

“…In experimental SCI models related to quercetin, a flavonoid, the neuroprotective effect of this agent was shown based on reduced MDA and increased TAS levels. [33] In an experimental SCI study, Gocmez et al [34] performed an intrathecal injection of caffeic acid, a phenol component, and showed that it inhibited lipid peroxidation and the increase of oxidants.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Annona muricata (graviola) in experimental spinal cord injury: biochemical and histopathological analysis

Keskin¹

2021

Ulus Travma Acil Cerrahi Derg

View full text Add to dashboard Cite

BACKGROUND: Annona muricata (AM) (graviola) is a plant that grows in tropical regions and is thought to be good for many diseases by local people. Unfortunately, there is no acceptable medical treatment for spinal cord injury (SCI) yet. In our study, we investigated the neuropeotective effects of AM leaf extract on SCI in an experimental rat model. METHODS:A total of 40 Wistar albino rats were randomly divided into five equal groups (n=8). Group 1 was the control group in which only laminectomy was performed. Trauma was induced in four groups after laminectomy. Group 2 (untreated trauma group) was given no medication. In Group 3, a single intraperitoneal dose of methylprednisolone (30 mg/kg) was administered after trauma. The rats in Groups 4 received a low dose (100 mg/kg) of AM leaf extracts by oral gavage one week before trauma while the rats in Group 5 received a high-dose (300 mg/kg) of these extracts by oral gavage one week before trauma. All rats, including the control group, were sacrificed 24 h after the trauma was created.RESULTS: Tissue samples taken to evaluate the neuroprotective effect were examined biochemically and histopathologically. Inflammatory findings in the trauma group were significantly better in both groups treated with AM. There was no difference between the groups in terms of clinical motor examination and inclined plane test results. CONCLUSION:Our histopathological and biochemical results showed that AM is an agent with neuroprotective effects in traumatic SCI.

show abstract

“…To examine the role of nuclear factor‐κB (NF‐κB) in stress‐caused effect, an NF‐κB inhibitor caffeic acid phenethyl ester (CAPE, 50 μM, 50 μL; Selleck) was given at the start of WAS and continuously i.t. administered via an osmotic minipump 25 …”

Section: Methodsmentioning

confidence: 99%

ZBTB20 mediates stress‐induced visceral hypersensitivity via activating the NF‐κB/transient receptor potential channel pathway

Luo,

Cheng,

Wang

et al. 2023

Neurogastroenterology Motil

View full text Add to dashboard Cite

BackgroundPsychological stress is a major trigger for visceral hypersensitivity (VH) in irritable bowel syndrome. The zinc finger protein ZBTB20 (ZBTB20) is implicated in somatic nociception via modulating transient receptor potential (TRP) channels, but its role in the development of VH is unclear. This study aimed to investigate the role of ZBTB20/TRP channel axis in stress‐induced VH.MethodsRats were subjected to water avoidance stress (WAS) for 10 consecutive days. Small interfering RNA (siRNA) targeting ZBTB20 was intrathecally administered. Inhibitors of TRP channels, stress hormone receptors, and nuclear factor kappa‐B (NF‐κB) were administered. Visceromotor response to colorectal distension was recorded. Dorsal root ganglia (DRGs) were dissected for Western blot, coimmunoprecipitation, and chromatin immunoprecipitation. The DRG‐derived neuron cell line was applied for specific research.Key ResultsWAS‐induced VH was suppressed by the inhibitor of TRPV1, TRPA1, or TRPM8, with enhanced expression of these channels in L6‐S2 DRGs. The inhibitor of glucocorticoid receptor or β2‐adrenergic receptor counteracted WAS‐induced VH and TRP channel expression. Concurrently, WAS‐induced stress hormone‐dependent ZBTB20 expression and NF‐κB activation in DRGs. Intrathecally injected ZBTB20 siRNA or an NF‐κB inhibitor repressed WAS‐caused effect. In cultured DRG‐derived neurons, stress hormones promoted nuclear translocation of ZBTB20, which preceded p65 nuclear translocation. And, ZBTB20 siRNA suppressed stress hormone‐caused NF‐κB activation. Finally, WAS enhanced p65 binding to the promoter of TRPV1, TRPA1, or TRPM8 in rat DRGs.Conclusions and InferencesZBTB20 mediates stress‐induced VH via activating NF‐κB/TRP channel pathway in nociceptive sensory neurons.

show abstract

Effects of Intrathecal Caffeic Acid Phenethyl Ester and Methylprednisolone on Oxidant/Antioxidant Status in Traumatic Spinal Cord Injuries

Abstract: Intrathecal injection of both CAPE and MP inhibits lipid peroxidation and increase of oxidants in SCIs.

Cited by 9 publications

References 29 publications

CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells

CAPE Analogs Induce Growth Arrest and Apoptosis in Breast Cancer Cells

Efficacy of Annona muricata (graviola) in experimental spinal cord injury: biochemical and histopathological analysis

ZBTB20 mediates stress‐induced visceral hypersensitivity via activating the NF‐κB/transient receptor potential channel pathway

Contact Info

Product

Resources

About