Neuroprotective effects of Kukoamine B against hydrogen peroxide-induced apoptosis and potential mechanisms in SH-SY5Y cells.

Oxidative stress mediates the cell damage in several neurodegenerative diseases, including multiple sclerosis, Alzheimer's disease (AD) and Parkinson's disease (PD). This study aimed at investigating the protective effects of Kukoamine B (KuB) against hydrogen peroxide (H2O2) induced cell injury and potential mechanisms in SH-SY5Y cells. Our results revealed that treatment with KuB prior to H2O2 exposure effectively increased the cell viability, and restored the mitochondria membrane potential (MMP).

Compound MQA, a Caffeoylquinic Acid Derivative, Protects Against NMDA-Induced Neurotoxicity and Potential Mechanisms In Vitro.

Aims: Compound MQA (1,5-O-dicaffeoyl-3-O-[4-malic acid methyl ester]-quinic acid) is a natural derivative of caffeoylquinic acid isolated from Arctium lappa L. roots. However, we know little about the effects of MQA on the central nervous system.

Neuroprotection by Kukoamine A against oxidative stress may involve N-methyl-D-aspartate receptors.

Background: Accumulative evidences have indicated that oxidative-stress and over-activation of N-methyl-d-aspartate receptors (NMDARs) are important mechanisms of brain injury. This study investigated the neuroprotection of Kukoamine A (KuA) and its potential mechanisms.

Methods: Molecular docking was used to discover KuA that might have the ability of blocking NMDARs.