Inhibitory effects of curcumin on H2O2-induced cell damage and APP expression and processing in SH-SY5Y cells transfected with APP gene with Swedish mutation

Song, Xiaoyu; Zhou, He-Yan; Sun, Yijian; Huang, Han-Chang

doi:10.1007/s11033-020-05305-w

Cited by 12 publications

(5 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Transfection with the APP695 Swedish mutant gene did not affect cell morphology and resulted in neurotoxicity [ 20 ]. The model is then considered useful to study AD pathogenesis [ 21 ] and to test novel therapeutic strategies [ 22 ], but the modeling of AD with induced pluripotent stem cell (iPSC)-derived neurons (iNeurons) brought new potentials in the recapitulation of molecular mechanisms of AD. Indeed, iNeurons better mimic the in vivo conditions and hold great promise to assess neurotoxic mechanisms, though they show differences in spontaneous neuronal activity [ 23 , 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

Neuronal Dynamics and miRNA Signaling Differ between SH-SY5Y APPSwe and PSEN1 Mutant iPSC-Derived AD Models upon Modulation with miR-124 Mimic and Inhibitor

Garcia

Pinto

Cunha

et al. 2021

Cells

View full text Add to dashboard Cite

Neuronal miRNA dysregulation may have a role in the pathophysiology of Alzheimer’s disease (AD). miRNA(miR)-124 is largely abundant and a critical player in many neuronal functions. However, the lack of models reliably recapitulating AD pathophysiology hampers our understanding of miR-124’s role in the disease. Using the classical human SH-SY5Y-APP695 Swedish neuroblastoma cells (SH-SWE) and the PSEN1 mutant iPSC-derived neurons (iNEU-PSEN), we observed a sustained upregulation of miR-124/miR-125b/miR-21, but only miR-124 was consistently shuttled into their exosomes. The miR-124 mimic reduced APP gene expression in both AD models. While miR-124 mimic in SH-SWE neurons led to neurite outgrowth, mitochondria activation and small Aβ oligomer reduction, in iNEU-PSEN cells it diminished Tau phosphorylation, whereas miR-124 inhibitor decreased dendritic spine density. In exosomes, cellular transfection with the mimic predominantly downregulated miR-125b/miR-21/miR-146a/miR-155. The miR-124 inhibitor upregulated miR-146a in the two experimental cell models, while it led to distinct miRNA signatures in cells and exosomes. In sum, though miR-124 function may be dependent on the neuronal AD model, data indicate that keeping miR-124 level strictly controlled is crucial for proper neuronal function. Moreover, the iNEU-PSEN cellular model stands out as a useful tool for AD mechanistic studies and perhaps for the development of personalized therapeutic strategies.

show abstract

Section: Introductionmentioning

confidence: 99%

Neuronal Dynamics and miRNA Signaling Differ between SH-SY5Y APPSwe and PSEN1 Mutant iPSC-Derived AD Models upon Modulation with miR-124 Mimic and Inhibitor

Garcia

Pinto

Cunha

et al. 2021

Cells

View full text Add to dashboard Cite

show abstract

“…The mutated APP is primarily processed by β-secretase and therefore causes elevated level of Aβ and the transcriptional regulator AICD via the amyloidogenic processing pathway [ 56 , 57 , 58 , 59 ]. SH-SY5Y cells expressing the APPswe mutation are a commonly accepted cellular AD-model and frequently used in AD research, for example in the context of oxidative stress [ 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 ]. Importantly, this cell line has been characterized for its suitability to be used as a familial AD model, for details please see [ 61 ].…”

Section: Discussionmentioning

confidence: 99%

Vitamin B12 Attenuates Changes in Phospholipid Levels Related to Oxidative Stress in SH-SY5Y Cells

Theiss

Griebsch

Lauer

et al. 2022

Cells

View full text Add to dashboard Cite

Oxidative stress is closely linked to Alzheimer’s disease (AD), and is detected peripherally as well as in AD-vulnerable brain regions. Oxidative stress results from an imbalance between the generation and degradation of reactive oxidative species (ROS), leading to the oxidation of proteins, nucleic acids, and lipids. Extensive lipid changes have been found in post mortem AD brain tissue; these changes include the levels of total phospholipids, sphingomyelin, and ceramide, as well as plasmalogens, which are highly susceptible to oxidation because of their vinyl ether bond at the sn-1 position of the glycerol-backbone. Several lines of evidence indicate that a deficiency in the neurotropic vitamin B12 is linked with AD. In the present study, treatment of the neuroblastoma cell line SH-SY5Y with vitamin B12 resulted in elevated levels of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and plasmalogens. Vitamin B12 also protected plasmalogens from hydrogen peroxide (H2O2)-induced oxidative stress due to an elevated expression of the ROS-degrading enzymes superoxide-dismutase (SOD) and catalase (CAT). Furthermore, vitamin B12 elevates plasmalogen synthesis by increasing the expression of alkylglycerone phosphate synthase (AGPS) and choline phosphotransferase 1 (CHPT1) in SH-SY5Y cells exposed to H2O2-induced oxidative stress.

show abstract

“…cells were treated with PM 2.5 at concentrations of 0, 12.5, 25, 50 and 100 mg/ml for 24 h to analyze the intracellular response. cells were treated with curcumin at concentrations of 0, 1, 2.5, 5, 7.5, 10, 20 and 50 µM for 48 h for ccK-8 assay (11,12). To evaluate the effects of curcumin, the cells were incubated in dMEM without or with curcumin (10 µM) for 1 h (10) and treated with PM 2.5 at 25 and 50 µg/ml for 24 h.…”

Section: Methodsmentioning

confidence: 99%

Curcumin protects BEAS‑2B cells from PM_2.5‑induced oxidative stress and inflammation by activating NRF2/antioxidant response element pathways

et al. 2021

View full text Add to dashboard Cite

Fine particulate matter (PM 2.5 ) with an average aerodynamic diameter of <2.5 µm can cause severe lung injury. Oxidative stress and inflammation are considered the main outcomes of PM 2.5 exposure. curcumin is a well-known antioxidant; however, its effect on PM 2.5 -induced oxidative injury in airway epithelial cells remains unclear. In the present study, it was demonstrated that pre-treatment with curcumin significantly reduced the PM 2.5 -induced apoptosis of BEAS-2B human bronchial epithelial cells by decreasing the level of intercellular reactive oxygen species. Western blot analysis revealed that curcumin increased the expression of nuclear factor erythroid 2-related factor 2 (NRF2) and regulated the transcription of downstream genes, particularly those encoding antioxidant enzymes. Moreover, curcumin reduced the PM 2.5 -induced expression and production of inflammatory factors, and induced the expression of the anti-inflammatory factors, interleukin (IL)-5 and IL-13. Taken together, the present study demonstrates that curcumin protects BEAS-2B cells against PM 2.5 -induced oxidative damage and inflammation, and prevents cell apoptosis by increasing the activation of NRF2-related pathways. It is thus suggested that curcumin may be a potential compound for use in the prevention of PM 2.5 -induced tissue injury.

show abstract

Inhibitory effects of curcumin on H2O2-induced cell damage and APP expression and processing in SH-SY5Y cells transfected with APP gene with Swedish mutation

Cited by 12 publications

References 39 publications

Neuronal Dynamics and miRNA Signaling Differ between SH-SY5Y APPSwe and PSEN1 Mutant iPSC-Derived AD Models upon Modulation with miR-124 Mimic and Inhibitor

Neuronal Dynamics and miRNA Signaling Differ between SH-SY5Y APPSwe and PSEN1 Mutant iPSC-Derived AD Models upon Modulation with miR-124 Mimic and Inhibitor

Vitamin B12 Attenuates Changes in Phospholipid Levels Related to Oxidative Stress in SH-SY5Y Cells

Curcumin protects BEAS‑2B cells from PM_2.5‑induced oxidative stress and inflammation by activating NRF2/antioxidant response element pathways

Contact Info

Product

Resources

About

Inhibitory effects of curcumin on H2O2-induced cell damage and APP expression and processing in SH-SY5Y cells transfected with APP gene with Swedish mutation

Cited by 12 publications

References 39 publications

Neuronal Dynamics and miRNA Signaling Differ between SH-SY5Y APPSwe and PSEN1 Mutant iPSC-Derived AD Models upon Modulation with miR-124 Mimic and Inhibitor

Neuronal Dynamics and miRNA Signaling Differ between SH-SY5Y APPSwe and PSEN1 Mutant iPSC-Derived AD Models upon Modulation with miR-124 Mimic and Inhibitor

Vitamin B12 Attenuates Changes in Phospholipid Levels Related to Oxidative Stress in SH-SY5Y Cells

Curcumin protects BEAS‑2B cells from PM2.5‑induced oxidative stress and inflammation by activating NRF2/antioxidant response element pathways

Contact Info

Product

Resources

About

Curcumin protects BEAS‑2B cells from PM_2.5‑induced oxidative stress and inflammation by activating NRF2/antioxidant response element pathways