Thymoquinone triggers anti-apoptotic signaling targeting death ligand and apoptotic regulators in a model of hepatic ischemia reperfusion injury

Heikal, Ola A.; Abdel-Aal, Lobna K.; Sharaf, Nadia Mohamed; Mansour, R.; Mahran, Laila

doi:10.1016/j.toxlet.2009.06.686

Cited by 4 publications

(2 citation statements)

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“…The last mentioned function of p53 is mediated largely by the induction of apoptotic genes with functions varying from death receptors, such as Fas, to mitochondrial proteins, such as Puma [75]. In the extrinsic pathway, Fas recruits FADD and procaspase-8 and -10 to the receptor leading to its auto-cleavage and activation, which in turn activates effector caspases such as caspase-3 in causing cell death [76][77][78]. The present study showed that treatment of HT-29 cells with 2 and 3 increased FAS gene expression (Table 2).…”

Section: Intracellular Signalling Cascades and Cell Cycle Analysismentioning

confidence: 99%

“…Consequently, caspase-8, -9, -10 and -3 were activated with an increase in their enzymatic activities (Tables 3, 4). It is possible that caspase-8 and -10 also could cleave the BCL-2 family member Bid, a BH3 interacting domain death agonist, to truncated BID (tBID), which subsequently binds to BAX, resulting in ΔΨ m disruption and the release of cytochrome c [76][77][78]. Moreover, BID is generally considered as a molecular linker bridging death receptor and mitochondria pathways [79].…”

Section: Intracellular Signalling Cascades and Cell Cycle Analysismentioning

confidence: 99%

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Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NC6H4Me-4] for R = Me, Et and iPr, induce apoptosis, cell cycle arrest and inhibit cell invasion of HT-29 colon cancer cells through modulation of the nuclear factor-κB activation pathway and ubiquitination

et al. 2015

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The phosphanegold(I) carbonimidothioates, Ph3PAu{SC(OR)=NC6H4Me-4} for R = Me (1), Et (2) and iPr (3), feature linear P-Au-S coordination geometries and exhibit potent in vitro cytotoxicity against HT-29 colon cancer cells in both monolayer and multi-cellular spheroid models (e.g., IC50 = 11.9 ± 0.4 and 20.3 ± 0.3 μM for 2, respectively). Both intrinsic and extrinsic pathways of apoptosis are demonstrated by human apoptosis PCR array analysis, caspase activities, DNA fragmentation and cell apoptotic assays. Compounds 1-3 induce an extrinsic pathway that leads to down-regulation of NFκB. Compound 2 also exhibits an extrinsic apoptotic pathway involving the activation of both p53 and p73, whereas 3 activates p53 only. Lys48- and Lys63-linked polyubiquitination are also promoted by 1-3. Each of cytotoxic Ph3PAu{SC(OR)=NC6H4Me-4}, for R = Me (1), Et (2) and iPr (3), induce an intrinsic apoptotic pathway as well as an extrinsic pathway leading to down-regulation of NFκB. Lys48- and Lys63-linked polyubiquitination are promoted by 1-3 and these are able to inhibit cell invasion and to suppress the activity of TrxR.

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Section: Intracellular Signalling Cascades and Cell Cycle Analysismentioning

confidence: 99%

Section: Intracellular Signalling Cascades and Cell Cycle Analysismentioning

confidence: 99%

Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NC6H4Me-4] for R = Me, Et and iPr, induce apoptosis, cell cycle arrest and inhibit cell invasion of HT-29 colon cancer cells through modulation of the nuclear factor-κB activation pathway and ubiquitination

et al. 2015

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Continuous Thymoquinone Administration Mitigates Sodium Iodate-Induced Retinal Degeneration in Rats

Erguven,

Sevgin,

Kotil

et al. 2024

Current Eye Research

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Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways

et al. 2018

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Overexposure of the glutamatergic N-methyl-d-aspartate (NMDA) receptor to the excitatory neurotransmitter l-glutamic acid leads to neuronal cell death by excitotoxicity as a result of increased intracellular Ca2+, mitochondrial dysfunction, and apoptosis. Moreover, it was previously reported that prolonged activation of the NMDA receptor increased beta-amyloid (Aβ) levels in the brain. Thymoquinone (TQ), the active constituent of Nigella sativa seeds, has been shown to have potent antioxidant and antiapoptotic effects. The aim of the present study was to explore the neuromodulatory effects of different doses of TQ (2.5 and 10 mg/kg) against apoptotic cell death and Aβ formation resulting from glutamate administration in rats using vitamin E as a positive control. Behavioral changes were assessed using Y-maze and Morris water maze tests for evaluating spatial memory and cognitive functions. Caspase-3, Lactate dehydrogenase, Aβ-42, and cytochrome c gene expression were determined. TQ-treated groups showed significant decreases in the levels of all tested biochemical and behavioral parameters compared with the glutamate-treated group. These findings demonstrated that TQ has a promising neuroprotective activity against glutamate-induced neurotoxicity and this effect is mediated through its anti-amyloidogenic, antioxidant, and antiapoptotic activities.

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Thymoquinone triggers anti-apoptotic signaling targeting death ligand and apoptotic regulators in a model of hepatic ischemia reperfusion injury

Cited by 4 publications

References 0 publications

Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NC6H4Me-4] for R = Me, Et and iPr, induce apoptosis, cell cycle arrest and inhibit cell invasion of HT-29 colon cancer cells through modulation of the nuclear factor-κB activation pathway and ubiquitination

Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NC6H4Me-4] for R = Me, Et and iPr, induce apoptosis, cell cycle arrest and inhibit cell invasion of HT-29 colon cancer cells through modulation of the nuclear factor-κB activation pathway and ubiquitination

Continuous Thymoquinone Administration Mitigates Sodium Iodate-Induced Retinal Degeneration in Rats

Neuromodulatory Effect of Thymoquinone in Attenuating Glutamate-Mediated Neurotoxicity Targeting the Amyloidogenic and Apoptotic Pathways

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