Phytochemical Ginkgolide B Attenuates Amyloid-β1-42 Induced Oxidative Damage and Altered Cellular Responses in Human Neuroblastoma SH-SY5Y Cells

Gill, Iqbal; Kaur, Sukhchain; Kaur, Navrattan; Dhiman, Monisha; Mantha, Anil K.

doi:10.3233/jad-161086

Cited by 55 publications

(35 citation statements)

References 73 publications

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“…We observed an alteration in cell morphology, as well as an increase in NeuN levels (a marker for mature neurons) after RA treatment, as previously reported (Cheung et al, ; Lopes et al, ). Various studies have described the characteristics of differentiated cells, and they seem to be an appropriate model to study Aβ peptide‐induced toxicity (Bang et al, ; da Rocha, da Cruz e Silva, & Vieira, 2015; Gill, Kaur, Kaur, Dhiman, & Mantha, ). Here we have used Aβ 25–35 peptide, which has similar toxic effects with respect to cell death, as well as on cell signaling pathway, as the Aβ 1–42 in in vitro models (Frozza et al, ).…”

Section: Discussionmentioning

confidence: 99%

Genistein protects against amyloid‐beta‐induced toxicity in SH‐SY5Y cells by regulation of Akt and Tau phosphorylation

Petry

Coelho

Gaelzer

et al. 2019

Phytotherapy Research

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Alzheimer's disease is a neurodegenerative disorder characterized by extracellular deposition of amyloid‐β (Aβ) peptide and hyperphosphorylation of Tau protein, which ultimately leads to the formation of intracellular neurofibrillary tangles and cell death. Increasing evidence indicates that genistein, a soy isoflavone, has neuroprotective effects against Aβ‐induced toxicity. However, the molecular mechanisms involved in its neuroprotection are not well understood. In this study, we have established a neuronal damage model using retinoic‐acid differentiated SH‐SY5Y cells treated with different concentrations of Aβ25–35 to investigate the effect of genistein against Aβ‐induced cell death and the possible involvement of protein kinase B (PKB, also termed Akt), glycogen synthase kinase 3β (GSK‐3β), and Tau as an underlying mechanism to this neuroprotection. Differentiated SH‐SY5Y cells were pre‐treated for 24 hr with genistein (1 and 10 nM) and exposed to Aβ25–35 (25 μM), and we found that genistein partially inhibited Aβ induced cell death, primarily apoptosis. Furthermore, the protective effect of genistein was associated with the inhibition of Aβ‐induced Akt inactivation and Tau hyperphosphorylation. These findings reinforce the neuroprotective effects of genistein against Aβ toxicity and provide evidence that its mechanism may involve regulation of Akt and Tau proteins.

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Section: Discussionmentioning

confidence: 99%

Genistein protects against amyloid‐beta‐induced toxicity in SH‐SY5Y cells by regulation of Akt and Tau phosphorylation

Petry

Coelho

Gaelzer

et al. 2019

Phytotherapy Research

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“…GB, a major monomer of extracts from leaves of Ginkgo biloba traditionally used in Chinese herbal medicine, displays a wide range of biological activities, including anti-inflammatory and anti-oxidant effects (26). It has been reported that GB could exert neuroprotective effects against cerebral ischemia/reperfusion injury (CI/RI) via suppressing inflammatory response and scavenging oxygen free radical (27, 28). Both MI/RI and CI/RI are hypoxic and anoxic diseases, which have similar characteristics in pathogenesis and treatment, suggesting that GB may possess a potential value in the treatment strategy of MI/RI.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotection of Ginkgolide B on Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Regulation of A20-NF-κB Pathway

Zhang

et al. 2018

Front. Immunol.

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Inflammation urges most of the characteristics of plaques involved in the pathogenesis of myocardial ischemia/reperfusion injury (MI/RI). In addition, inflammatory signaling pathways not only mediate the properties of plaques that precipitate ischemia/reperfusion (I/R) but also influence the clinical consequences of the post-infarction remodeling and heart failure. Here, we studied whether Ginkgolide B (GB), an effective anti-inflammatory monomer, improved MI/RI via suppression of inflammation. Left anterior descending (LAD) coronary artery induced ischemia/reperfusion (I/R) of rats or A20 silencing mice, as well as hypoxia/reoxygenation (H/R) induced damages of primary cultured rat neonatal ventricular myocytes or A20 silencing ventricular myocytes, respectively, served as MI/RI model in vivo and in vitro to discuss the anti-I/R injury properties of GB. We found that GB significantly alleviated the symptoms of MI/RI evidently by reducing infarct size, preventing ultrastructural changes of myocardium, depressing Polymorphonuclears (PMNs) infiltration, lessening histopathological damage and suppressing the excessive inflammation. Further study demonstrated that GB remarkably inhibited NF-κB p65 subunit translocation, IκB-α phosphorylation, IKK-β activity, as well as the downstream inflammatory cytokines and proteins expressions via zinc finger protein A20. In conclusion, GB could alleviate MI/RI-induced inflammatory response through A20-NF-κB signal pathway, which may give us new insights into the preventive strategies for MI/RI disease.

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“…The 8‐hydroxydeoxyguanosine (8‐OHdG) levels were determined using an enzyme‐linked immunosorbent assay kit (Cloud‐Clone, Katy, TX, USA) (Gill, Kaur, Kaur, Dhiman, & Mantha, 2017). Supernatants were collected from the differentially treated cells and subjected to the assay according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

Lycopene protects neuroblastoma cells against oxidative damage via depression of ER stress

Fang

Tang

et al. 2020

Journal of Food Science

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Lycopene is a pigment derived from tomatoes and other red fruits, and has potent antioxidant and antitumor effects. However, its potential role in alleviating oxidative damage in neuronal cells is not well defined. In this study, we investigated the effects of lycopene on H 2 O 2-induced damage in neuroblastoma cells, as well as the underlying mechanisms. Exposure to H 2 O 2 markedly decreased the viability of SH-SY5Y cells and increased LDH release, both of which were reversed by lycopene pretreatment. Lycopene also ameliorated H 2 O 2-induced damage and reduced the expression of apoptotic markers, such as Bcl-2, Bax, and cleaved caspase 3. In addition, the H 2 O 2-induced oxidative markers, including MDA, 8-OHdG, and protein carbonyls, were also downregulated by lycopene. Exogenous H 2 O 2 activated the GRP78/PERK/eIF2α signaling pathway, which was inhibited by pretreatment with lycopene. Finally, lycopene significantly ameliorated ER stress-induced activation and nuclear translocation of CHOP. Overexpression of CHOP markedly reversed the antiapoptotic effects of lycopene, indicating that it is essential for the latter's protective effects. Taken together, lycopene protects neuroblastoma cells from oxidative stress and ER stress-induced damage by inhibiting the PERK-CHOP signaling pathway, which is a potential therapeutic target in neurodegenerative diseases.

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Phytochemical Ginkgolide B Attenuates Amyloid-β1-42 Induced Oxidative Damage and Altered Cellular Responses in Human Neuroblastoma SH-SY5Y Cells

Cited by 55 publications

References 73 publications

Genistein protects against amyloid‐beta‐induced toxicity in SH‐SY5Y cells by regulation of Akt and Tau phosphorylation

Genistein protects against amyloid‐beta‐induced toxicity in SH‐SY5Y cells by regulation of Akt and Tau phosphorylation

Cardioprotection of Ginkgolide B on Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Regulation of A20-NF-κB Pathway

Lycopene protects neuroblastoma cells against oxidative damage via depression of ER stress

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