Abstract
To evaluate the effects of Ecklonia cava (E. cava) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM2.5). The intake of water extract from E. cava (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM2.5 exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM2.5-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM2.5-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol.
Highlights
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The number of total arm entries showed a similar result for all groups (Figure 1b) The black lines indicate the movement of mice in Figure 1c, and the normal control (NC) showed a similar path tracing in each arm
The PM2.5 -exposed group tended to lean toward one arm and distracted movement within the arm, and similar movements to the NC group were found in the water extract from E. cava (WEE) groups
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Air pollution is a current and growing global problem [1]. Fine dust (particulate matter; PM2.5 ) smaller than 2.5 μm in aerodynamic diameter can cause various health hazards and other systemic dysfunctions. PM2.5 is derived from various origins and is composed of primary emissions from anthropogenic and natural sources and secondary formation by chemical reactions (e.g., NO3− , SO4− , NH4− , polyaromatic hydrocarbon (PAHs), quinone et al.) [1]. Absorbed PM2.5 is not removed from the body and has immediate effects such as oxidative stress and inflammatory-mediated reaction. The accumulated PM2.5 directly causes pulmonary dysfunction by the systemic oxidative damage and an inflammatory reaction [1]
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