TY - JOUR
T1 - Protective Effects of Chlorogenic Acid Against Amyloid-Beta-Induced Oxidative Stress and Ion Transport Dysfunction in SH-SY5Y Cells
AU - Singh, Abhishek Kumar
AU - Singh, Ishika
AU - Pai, Varsha
N1 - Publisher Copyright:
© 2024 Wiley Periodicals LLC.
PY - 2024/11
Y1 - 2024/11
N2 - Caloric restriction mimetics mimic the beneficial effects of dietary restriction approaches, such as caloric restriction approaches, without limiting the dietary intake. Chlorogenic acid (CGA) acts as a caloric restriction mimetic; however, its neuroprotective mechanisms remain ambiguous. Therefore, in this study, we aimed to elucidate the neuroprotective effects of CGA on SH-SY5Y cells treated with amyloid-beta (Aβ)1-42. Aβ1-42 (1.25 μM) induced oxidative stress by significantly increasing the pro-oxidant levels and decreasing the antioxidant levels in the cells. Additionally, it decreased the Na+/K+-ATPase and Ca2+-ATPase ion transporter activities and enhanced the acetylcholinesterase activity. However, CGA (100 μM) reversed these Aβ1-42-induced changes in SH-SY5Y cells. Overall, CGA exerted neuroprotective effects against Aβ1-42-induced oxidative stress and impaired ion transporter and acetylcholinesterase activities, serving as a promising therapeutic candidate for neurodegenerative diseases, such as Alzheimer's disease.
AB - Caloric restriction mimetics mimic the beneficial effects of dietary restriction approaches, such as caloric restriction approaches, without limiting the dietary intake. Chlorogenic acid (CGA) acts as a caloric restriction mimetic; however, its neuroprotective mechanisms remain ambiguous. Therefore, in this study, we aimed to elucidate the neuroprotective effects of CGA on SH-SY5Y cells treated with amyloid-beta (Aβ)1-42. Aβ1-42 (1.25 μM) induced oxidative stress by significantly increasing the pro-oxidant levels and decreasing the antioxidant levels in the cells. Additionally, it decreased the Na+/K+-ATPase and Ca2+-ATPase ion transporter activities and enhanced the acetylcholinesterase activity. However, CGA (100 μM) reversed these Aβ1-42-induced changes in SH-SY5Y cells. Overall, CGA exerted neuroprotective effects against Aβ1-42-induced oxidative stress and impaired ion transporter and acetylcholinesterase activities, serving as a promising therapeutic candidate for neurodegenerative diseases, such as Alzheimer's disease.
UR - https://www.scopus.com/pages/publications/85208143103
UR - https://www.scopus.com/pages/publications/85208143103#tab=citedBy
U2 - 10.1002/jbt.70046
DO - 10.1002/jbt.70046
M3 - Article
C2 - 39474852
AN - SCOPUS:85208143103
SN - 1095-6670
VL - 38
JO - Journal of Biochemical and Molecular Toxicology
JF - Journal of Biochemical and Molecular Toxicology
IS - 11
M1 - e70046
ER -