TRPM2 Channel Inhibition Attenuates Amyloid β42-Induced Apoptosis and Oxidative Stress in the Hippocampus of Mice.

ABSTRACT: Alzheimer's disease (AD) is characterized by the increase of hippocampal Ca²⁺ influx-induced apoptosis and mitochondrial oxidative stress (OS). The OS is a stimulator of TRPM2, although N-(p-amylcinnamoyl)anthranilic acid (ACA), 2-aminoethyl diphenylborinate (2/APB), and glutathione (GSH) are non-specific antagonists of TRPM2. In the present study, we investigated the protective roles of GSH and TRPM2 antagonist treatments on the amyloid β42 peptide (Aβ)-caused oxidative neurotoxicity and apoptosis in the hippocampus of mice with AD model. After the isolation of hippocampal neurons from the newborn mice, they were divided into five incubation groups as follows: control, ACA, Aβ, Aβ+ACA, and Aβ+GSH. The levels of apoptosis, hippocampus death, cytosolic ROS, cytosolic Zn²⁺

SUBMITTER: Cınar R 

PROVIDER: S-EPMC11414446 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature