Low concentrations of estradiol reduce β-amyloid (25–35)-induced toxicity, lipid peroxidation and glucose utilization in human SK-N-SH neuroblastoma cells

1997 ◽  
Vol 778 (1) ◽  
pp. 158-165 ◽  
Author(s):  
Kelly E Gridley ◽  
Pattie S Green ◽  
James W Simpkins
1999 ◽  
Vol 155 (2) ◽  
pp. 252-259 ◽  
Author(s):  
C. Fabrizi ◽  
R. Businaro ◽  
G.M. Lauro ◽  
G. Starace ◽  
L. Fumagalli

Author(s):  
Hasriadi . ◽  
Matusorn Wong-on ◽  
Phakhamon Lapphanichayakool ◽  
Nanteetip Limpeanchob

Objective: Artocarpus lakoocha Roxb. is a traditional medical plant native to Southeast Asia and used as a dried aqueous extract so-called puag haad. Its role (and its major ingredient, oxyresveratrol) as an antioxidant neuroprotectant were explored.Methods: Differentiated SH-SY5Y neuroblastoma cells in 96-well plates were challenged with 200 µM H2O2 for 4 h and either Trolox (100 µM), oxyresveratrol (5-100 µM), or puag haad (1.2-25 µg/ml) applied 2 h before H2O2 or for 20 h after H2O2 washout. Cell viability, mitochondrial function, intracellular ROS, and lipid peroxidation were assessed.Results: Continuous presence of both H2O2 and antioxidant reduced mitochondrial function by ~50% but only by 30% with antioxidant. Sustained 24 h H2O2 showed no recoveries with antioxidants. Cell viability was modestly restored when antioxidants accompanied H2O2 for 4 h and both washed for another 20 h, but little recovery of mitochondrial function even though antioxidants removed ROS and prevent lipid peroxidation. Antioxidants added for 20 h after H2O2 marginally improve mitochondria and modestly restore cell viability, but lipid peroxidation was completely reversed.Conclusion: These results show that mitochondrial protection was illusive, yet both tested compounds, puag haad and oxyresveratrol, improved cell viability and especially ROS levels and lipid peroxidation. The potency oxyresveratrol on the redox-sensitive expression of antioxidant enzymes and its pharmacokinetics suggests that oral puag haad could provide effective protection in transient neurodegenerative disease. 


Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1539 ◽  
Author(s):  
Bussiere ◽  
Oulès ◽  
Mary ◽  
Vaillant-Beuchot ◽  
Martin ◽  
...  

Dysregulation of the Endoplasmic Reticulum (ER) Ca2+ homeostasis and subsequent ER stress activation occur in Alzheimer Disease (AD). We studied the contribution of the human truncated isoform of the sarco-endoplasmic reticulum Ca2+ ATPase 1 (S1T) to AD. We examined S1T expression in human AD-affected brains and its functional consequences in cellular and transgenic mice AD models. S1T expression is increased in sporadic AD brains and correlates with amyloid β (Aβ) and ER stress chaperone protein levels. Increased S1T expression was also observed in human neuroblastoma cells expressing Swedish-mutated β-amyloid precursor protein (βAPP) or treated with Aβ oligomers. Lentiviral overexpression of S1T enhances in return the production of APP C-terminal fragments and Aβ through specific increases of β-secretase expression and activity, and triggers neuroinflammation. We describe a molecular interplay between S1T-dependent ER Ca2+ leak, ER stress and βAPP-derived fragments that could contribute to AD setting and/or progression.


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