Maackiain Reduces Neuroinflammation by Modulating Inflammatory Signals in LPS-Induced In Vitro and In Vivo Models

Neuroinflammation, an immune process in the central nervous system (CNS), is a key contributor to a range of neurological diseases, including neurodegenerative disorders (e.g., Alzheimer's and Parkinson's disease), stroke, and depression, underscoring its significant pathological relevance. While maackiain (MAA) exhibits potent anti-inflammatory activity, its potential to mitigate neuroinflammation remains poorly understood. This study investigated the therapeutic effects of MAA on lipopolysaccharide (LPS)-induced neuroinflammation and its underlying mechanisms. In vitro, MAA significantly improved BV2 cell viability and reduced nitric oxide (NO) expression in LPS-treated cells, decreased the expression of Reactive Oxygen Species (ROS), and it also inhibited the accumulation of Ferrous ion (Fe²⁺) and lipid peroxides as well as the damage to mitochondria. Higher concentrations of MAA were more effective, consistent with subsequent animal experiments. In vivo, mice treated with MAA showed improved memory in the Morris water maze compared to the LPS group. Nissl staining revealed fewer IBA-1 positive cells and a decrease in COX-2 and IL-6 levels in the hippocampus and cortex. This compound also increased the number of normal neurons in the cortex and CA3 region. The results of this study highlight the inhibitory effects of MAA on neuroinflammation, suggesting its potential as an effective therapeutic agent for treating neuroinflammation.

BV2; Inflammation; Lipopolysaccharide; Maackiain; Neuroinflammation.