Effects of caffeine on neuronal apoptosis in neonatal hypoxic-ischemic brain injury

Kılıçdağ, Hasan; Dağlıoğlu, Yusuf Kenan; Erdoğan, Şeyda; Zorludemir, Suzan

doi:10.3109/14767058.2013.878694

Cited by 41 publications

(24 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rats with ischaemia/reperfusion (I/R) treated with DEX were shown to have decreases in relation to their neurological deficit scores, cerebral infarct volume, brain oedema and neuron death in the CA1 region of hippocampus and cortex area, suggesting that the apoptosis rate may be down‐regulated 34, 35. Studies have held the position that HI could lead to neuronal cell death and neuronal damage, and apoptosis is essential in HI damage of the neonatal brain 36, 37. HI damage in the hippocampus is more sensitive than that in other brain regions, and HI damage results in the death of many neurons, through the vehicle of both the processes of apoptosis and necrosis 38.…”

Section: Discussionmentioning

confidence: 99%

“…34,35 Studies have held the position that HI could lead to neuronal cell death and neuronal damage, and apoptosis is essential in HI damage of the neonatal brain. 36,37 HI damage in the hippocampus is more sensitive than that in other brain regions, and HI damage results in the death of many neurons, through the vehicle of both the processes of apoptosis and necrosis. 38 In our study, we found that the weight and length growth, weight ratio of the left hemisphere to the right hemisphere and the rate of reaching standard were all increased; however, decreases were recorded for total response times, total response duration and neuronal apoptosis rate in the hippocampus, when HIBD rats had been treated with DEX + miR-140-5p mimics or si-Wnt1.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Han

Wen

Wang

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

Hypoxia–ischaemia (HI) remains a major cause of foetal brain damage presented a scarcity of effective therapeutic approaches. Dexmedetomidine (DEX) and microRNA‐140‐5p (miR‐140‐5p) have been highlighted due to its potentially significant role in the treatment of cerebral ischaemia. This study was to investigate the role by which miR‐140‐5p provides cerebral protection using DEX to treat hypoxic–ischaemic brain damage (HIBD) in neonatal rats via the Wnt/β‐catenin signalling pathway. The HIBD rat models were established and allocated into various groups with different treatment plans, and eight SD rats into sham group. The learning and memory ability of the rats was assessed. Apoptosis and pathological changes in the hippocampus CA1 region and expressions of the related genes of the Wnt/β‐catenin signalling pathway as well as the genes responsible of apoptosis were detected. Compared with the sham group, the parameters of weight, length growth, weight ratio between hemispheres, the rate of reaching standard, as well as Bcl‐2 expressions, were all increased. Furthermore, observations of increased levels of cerebral infarction volume, total mortality rate, response times, total response duration, expressions of Wnt1, β‐catenin, TCF‐4, E‐cadherin, apoptosis rate of neurons, and Bax expression were elevated. Following DEX treatment, the symptoms exhibited by HIBD rats were ameliorated. miR‐140‐5p and si‐Wnt1 were noted to attenuate the progression of HIBD. Our study demonstrates that miR‐140‐5p promotes the cerebral protective effects of DEX against HIBD in neonatal rats by targeting the Wnt1 gene through via the negative regulation of the Wnt/β‐catenin signalling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Han

Wen

Wang

et al. 2018

J Cellular Molecular Medi

View full text Add to dashboard Cite

show abstract

“…The phenobarbital‐induced adverse outcomes were partly antagonized by the caffeine. Other findings using similar models indicate that caffeine may be neuroprotective in the developing brain because caffeine has anti‐inflammatory, anti‐oxidant, and anti‐apoptotic properties (Endesfelder, Zaak, Weichelt, Buhrer, & Schmitz, ; Endesfelder et al, ; Kilicdag, Daglioglu, Erdogan, and Zorludemir, ). This neuroprotection may also been seen in later behavioral testing (Kumral et al, ).…”

Section: Insights From Animal Studies: What Is the Evidence For Neuromentioning

confidence: 92%

Taurine, caffeine, and energy drinks: Reviewing the risks to the adolescent brain

Curran

Marczinski

2017

Birth Defects Research

View full text Add to dashboard Cite

Energy drinks are emerging as a major component of the beverage market with sales projected to top $60 billion globally in the next five years. Energy drinks contain a variety of ingredients, but many of the top-selling brands include high doses of caffeine and the amino acid taurine. Energy drink consumption by children has raised concerns, due to potential caffeine toxicity. An additional risk has been noted among college-aged consumers of energy drinks who appear at higher risk of over-consumption of alcohol when the two drinks are consumed together. The differential and combinatorial effects of caffeine and taurine on the developing brain are reviewed here with an emphasis on the adolescent brain, which is still maturing. Key data from animal studies are summarized to highlight both reported benefits and adverse effects reported following acute and chronic exposures. The data suggest that age is an important factor in both caffeine and taurine toxicity. Although the aged or diseased brain might benefit from taurine or caffeine supplementation, it appears that adolescents are not likely to benefit from supplementation and may, in fact, suffer ill effects from chronic ingestion of high doses. Additional work is needed though to address gaps in our understanding of how taurine affects females, since the majority of animal studies focused exclusively on male subjects.

show abstract

“…Pre-clinical studies have also reported a neuroprotective effect of caffeine in experimental models of neonatal HI, resulting in behavioural and functional recovery [10][11][12][13]. Previous works from us and others have demonstrated that caffeine reduced a mild lesion in mouse models and/or ameliorated behavioural performances when given before [13] or immediately after injury [10,12], or for multiple days following HI [11]. From a clinical and practical point of view, it is important to know if the single-dose therapy is effective at 6-24 h after injury and at different stages of injury severity.…”

Section: Introductionmentioning

confidence: 99%

Defining a Time Window for Neuroprotection and Glia Modulation by Caffeine After Neonatal Hypoxia-Ischaemia

et al. 2020

View full text Add to dashboard Cite

Hypoxic-ischemic (HI) brain injury remains an important cause of brain damage in neonates with potential lifelong consequences. Caffeine, which is a competitive inhibitor of adenosine receptors, is commonly used as treatment for preterm apnoea in clinical settings. In the current study, we investigated the effects of caffeine given at 0 h, 6 h, 12 h or 24 h after HI in P10 mouse pups. Open field and rotarod behavioural tests were performed 2 weeks after injury, and brain morphology was then evaluated. Gene expression and immunohistological analyses were assessed in mice 1-and 5-day post-HI. A single dose of caffeine directly after HI resulted in a reduction of the lesion in the grey and white matter, judged by immunostaining of MAP2 and MBP, respectively, compared to PBS-treated controls. In addition, the number of amoeboid microglia and apoptotic cells, the area covered by astrogliosis, and the expression of pro-inflammatory cytokines were significantly decreased. Behavioural assessment after 2 weeks showed increased open-field activity after HI, and this was normalised if caffeine was administered immediately after the injury. Later administrations of caffeine did not change the outcomes when compared to the vehicle group. In conclusion, caffeine only yielded neuroprotection and immunomodulation in a neonatal model of brain hypoxia ischaemia if administered immediately after injury.

show abstract

Effects of caffeine on neuronal apoptosis in neonatal hypoxic-ischemic brain injury

Abstract: We show that caffeine administration in hypoxic-ischemic brain injury reduces neuronal apoptosis in the developing brain. We suggest that caffeine may be effective in reducing brain injury.

Cited by 41 publications

References 38 publications

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

Taurine, caffeine, and energy drinks: Reviewing the risks to the adolescent brain

Defining a Time Window for Neuroprotection and Glia Modulation by Caffeine After Neonatal Hypoxia-Ischaemia

Contact Info

Product

Resources

About