Effects of propofol on proliferation and anti-apoptosis of neuroblastoma SH-SY5Y cell line: New insights into neuroprotection

Wu, Gong-Jhe; Chen, Wu Fu; Hung, Han Chun; Jean, Yen-Hsuan; Sung, Chun Sung; Chakraborty, Chiranjib; Lee, Hsin Pai; Chen, Nan Fu; Wen, Zhi Hong

doi:10.1016/j.brainres.2011.02.004

Cited by 34 publications

(28 citation statements)

References 51 publications

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“…Similar results have been obtained by Tu et al who investigated the effects of propofol on neuropathogenesis in newborn rats under hypoxic conditions and showed that neither propofol nor hypoxia influenced apoptosis [38]. Employing the neuroblastoma cell line SH-SY5Y, Wu et al demonstrated that 10 lM propofol improved cell proliferation and inhibited dynorphin A induced cytotoxicity [17], an observation that is in concordance with our in vitro results obtained with 30 lM propofol.…”

Section: Discussionsupporting

confidence: 82%

“…Propofol, a widely used intravenous anaesthetic, has been demonstrated to have neuroprotective properties in several in-vivo [11][12][13][14] and in-vitro [15][16][17] models of cerebral hypoxia re-oxygenation injury. Propofol contains a phenolic hydroxyl group and thus its structure resembles that of a-tocopherol (vitamin E) [18], a natural antioxidant.…”

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confidence: 99%

“…In the brain, hypoxia re-oxygenation often leads to severe cellular damage resulting in a loss of neurological function and a poor clinical outcome [6][7][8]. The underlying mechanisms of hypoxia re-oxygenation injury are multifaceted, but recent studies point towards a central role of reactive oxygen species, which are generated during the hypoxia re-oxygenation [9] and may harm cells by damaging DNA, lipid peroxidation and oxidation of proteins [10].Propofol, a widely used intravenous anaesthetic, has been demonstrated to have neuroprotective properties in several in-vivo [11][12][13][14] and in-vitro [15][16][17] models of cerebral hypoxia re-oxygenation injury. Propofol contains a phenolic hydroxyl group and thus its structure resembles that of a-tocopherol (vitamin E) [18], a natural antioxidant.…”

mentioning

confidence: 99%

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Effect of propofol on hypoxia re‐oxygenation induced neuronal cell damage in vitro*

Huang

Zitta²,

Bein

et al. 2012

Anaesthesia

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SummaryPropofol may protect neuronal cells from hypoxia re-oxygenation injury, possibly via an antioxidant actions under hypoxic conditions. This study investigated the molecular effects of propofol on hypoxia-induced cell damage using a neuronal cell line. Cultured human IMR-32 cells were exposed to propofol (30 lM) and biochemical and molecular approaches were used to assess cellular effects. Propofol significantly reduced hypoxia-mediated increases in lactate dehydrogenase, a marker of cell damage (mean (SD) for normoxia: 0.39 (0.07) a.u.; hypoxia: 0.78 (0.21) a.u.; hypoxia + propofol: 0.44 (0.17) a.u.; normoxia vs hypoxia, p < 0.05; hypoxia vs hypoxia + propofol, p < 0.05), reactive oxygen species and hydrogen peroxide. Propofol also diminished the morphological signs of cell damage. Increased amounts of catalase, which degrades hydrogen peroxide, were detected under hypoxic conditions. Propofol decreased the amount of catalase produced, but increased its enzymatic activity. Propofol protects neuronal cells from hypoxia reoxygenation injury, possibly via a combined direct antioxidant effect along with induced cellular antioxidant mechanisms. Hypoxia and re-oxygenation events occur under various clinical conditions including intra-and peri-operative brain ischaemia [1][2][3][4][5]. In the brain, hypoxia re-oxygenation often leads to severe cellular damage resulting in a loss of neurological function and a poor clinical outcome [6][7][8]. The underlying mechanisms of hypoxia re-oxygenation injury are multifaceted, but recent studies point towards a central role of reactive oxygen species, which are generated during the hypoxia re-oxygenation [9] and may harm cells by damaging DNA, lipid peroxidation and oxidation of proteins [10].Propofol, a widely used intravenous anaesthetic, has been demonstrated to have neuroprotective properties in several in-vivo [11][12][13][14] and in-vitro [15][16][17] models of cerebral hypoxia re-oxygenation injury. Propofol contains a phenolic hydroxyl group and thus its structure resembles that of a-tocopherol (vitamin E) [18], a natural antioxidant. The antioxidant activity of propofol results partly from this phenolic chemical structure and may be responsible for its cytoprotective effects [19]. Moreover, propofol has been shown to induce and regulate intracellular signalling pathways [20,21] and the neuroprotective effects of propofol may also be mediated indirectly via the induction of cell-based antioxidant mechanisms.In the study presented, we employed an in-vitro model of human neuronal cells to mimic hypoxia reoxygenation events and evaluate the effects of anaesthetic

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of propofol on hypoxia re‐oxygenation induced neuronal cell damage in vitro*

Huang

Zitta²,

Bein

et al. 2012

Anaesthesia

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“…One example of this has been demonstrated in prostatic cancer cells (Guo et al, 2007). The specificity of the effects of quercetin on cancer cells, particularly in regard to cellular metabolism, requires caution when interpreting the results from the neuroprotection studies that use tumor-derived cells, such as the human neuroblastoma cell line SH-SY5Y (Kim et al, 2008;Lee et al, 2010a;Wu et al, 2011). Another important aspect of the anticancer effects of quercetin is its interaction with cell cycle regulatory proteins.…”

Section: Anticancer Mechanisms Of Quercetinmentioning

confidence: 96%

Life or death: Neuroprotective and anticancer effects of quercetin

Dajas¹

2012

Journal of Ethnopharmacology

327

177

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“…Immunocytochemistry was performed using modified methods as previously described [56]. After treatment, RAW 264.7 cells were fixed with 4% paraformaldehyde in PBS buffer for 8 min and then washed 3 times with PBS buffer.…”

Section: Methodsmentioning

confidence: 99%

Dihydroaustrasulfone Alcohol (WA-25) Impedes Macrophage Foam Cell Formation by Regulating the Transforming Growth Factor-β1 Pathway

Wang

Hung

Feng

et al. 2015

IJMS

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Atherosclerosis is considered an inflammatory disease. However, clinically used anti-atherosclerotic drugs, such as simvastatin, have many side effects. Recently, several unique marine compounds have been isolated that possess a variety of bioactivities. In a previous study, we found a synthetic precursor of the marine compound (austrasulfone), which is dihydroaustrasulfone alcohol (WA-25), has anti-atherosclerotic effects in vivo. However, the detailed mechanisms remain unclear. Therefore, to clarify the mechanisms through which WA-25 exerts anti-atherosclerotic activity, we used RAW 264.7 macrophages as an in vitro model to evaluate the effects of WA-25. In lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, WA-25 significantly inhibited expression of the pro-inflammatory proteins, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In contrast, simvastatin increased the COX-2 expression compared to WA-25. In addition, WA-25 impedes foam cell formation and up-regulated the lysosomal and cyclic adenosine monophosphate (cAMP) signaling pathway. We also observed that transforming growth factor β1 (TGF-β1) was up-regulated by WA-25 and simvastatin in LPS-induced RAW 264.7 cells, and the promising anti-atherosclerosis effects of WA-25 were disrupted by blockade of TGF-β1 signaling. Besides, WA-25 might act through increasing lipolysis than through alteration of lipid export. Taken together, these data demonstrate that WA-25 may have potential as an anti-atherosclerotic drug with anti-inflammatory effects.

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Effects of propofol on proliferation and anti-apoptosis of neuroblastoma SH-SY5Y cell line: New insights into neuroprotection

Cited by 34 publications

References 51 publications

Effect of propofol on hypoxia re‐oxygenation induced neuronal cell damage in vitro*

Effect of propofol on hypoxia re‐oxygenation induced neuronal cell damage in vitro*

Life or death: Neuroprotective and anticancer effects of quercetin

Dihydroaustrasulfone Alcohol (WA-25) Impedes Macrophage Foam Cell Formation by Regulating the Transforming Growth Factor-β1 Pathway

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