Engeletin Attenuates A β1–42-Induced Oxidative Stress and Neuroinflammation by Keap1/Nrf2 Pathway

AbstractAlzheimer ’s disease (AD) is a serious neuropathologic disease characterized by aggregation of amyloid-β (Aβ) peptide. Aβ-mediated oxidative stress and neuroinflammation play crucial role in the development of AD. Engeletin is a flavononol glycoside that possesses anti-inflammatory effect. However, the e ffects of engeletin on AD have not been investigated. In the present study, we investigated the role of engeletin in AD using anin vitro AD model. Murine microglia BV-2 cells were stimulated with A β1–42 (5 μM) for 24 h to induce oxidative stress and inflammation. Our results showed that treatment with engeletin suppressed Aβ1–42-induced viability reduction and lactate dehydrogenase (LDH) release in BV-2 cells. Engeletin attenuated Aβ1–42-induced oxidative stress in BV-2 cells, as proved by decreased production of reactive oxygen species (ROS) and malonaldehyde (MDA) and increased glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities. Aβ1–42-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression were inhibited by enge letin treatment. Besides, engeletin inhibited Aβ1–42-induced production and mRNA levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6). Engeletin enhanced Aβ1–42-induced activation of Kelch-like ECH-associated protein 1 (Keap1)/nuclear transcription fa ctor E2-related factor 2 (Nrf2) signaling pathway in BV-2 cells. Inhibition of Ke...
Source: Inflammation - Category: Allergy & Immunology Source Type: research