Effect of Ethyl Acetate Fraction from Eucommia ulmoides Leaves on PM2.5-Induced Inflammation and Cognitive Dysfunction

Abstract

This study aimed to evaluate the protective effect of the ethyl acetate from Eucommia ulmoides leaves (EFEL) on PM2.5-induced cognitive impairment in BALB/c mice. EFEL improved PM2.5-induced cognitive decline by improving spontaneous alternative behavioral and long-term memory ability. EFEL increased ferric reducing activity power (FRAP) in serum. In addition, EFEL increased superoxide dismutase (SOD) and reduced glutathione (GSH) contents and inhibited the production of malondialdehyde (MDA) in lung and brain tissues. EFEL also restored the mitochondrial function by regulating reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) level, and ATP level in lung and brain tissues. EFEL ameliorated the cholinergic system by regulating the acetylcholine (ACh) content and acetylcholinesterase (AChE) activity in the brain tissue and the expression of AChE and choline acetyltransferase (ChAT) in the whole brain and hippocampal tissues. EFEL reduced PM2.5-induced excessive expression of inflammatory protein related to the lung, whole brain, olfactory bulb, and hippocampus. Physiological compounds of EFEL were identified as 5-O-caffeolyquinic acid, rutin, quercetin, and quercetin glycosides. As a result, EFEL has anti-inflammation and anti-amnesic effect on PM2.5-induced cognitive impairment by regulating the inflammation and inhibiting the lung and brain tissue dysfunction, and its effect is considered to be due to the physiological compounds of EFEL.

Eucommia ulmoides Leaves Alleviate Cognitive Dysfunction in Dextran Sulfate Sodium (DSS)-Induced Colitis Mice through Regulating JNK/TLR4 Signaling Pathway

“…Kong et al (2019) reported that the chlorogenic acid contained in E. ulmoides leaves improved MMP and ATP levels in paraquat-induced A549 cells [39]. According to Kim et al (2022), in PM 2.5 -induced mice, the ethyl acetate fraction of E. ulmoides leaves reduced ROS in mouse brain mitochondria and increased MMP and ATP levels [40]. These results demonstrate that AEEL can effectively ameliorate DSS-induced colitis mouse brain mitochondrial dysfunction.…”

Powdered green tea improved particulate matter (PM)2.5 exposure-induced cardiac cytotoxicity via TLR pathway in BALB/c mice

“…causes an in ammatory response in the heart by interaction with TLRs and NF-κB signal [30]. Moreover, in previous studies, it was con rmed that PM 2.5 could produce various in ammatory factors [33][34][35].…”

Codium fragile Suppresses PM2.5-Induced Cognitive Dysfunction by Regulating Gut–Brain Axis via TLR-4/MyD88 Pathway

“…After the pellets and 1 × cell extraction buffer (10% SOD buffer, 0.4% ( v / v ) triton X-100, and 200 μM phenylmethan sulfonyl fluoride) were centrifuged at 4 °C for 10 min at 10,000× g . After processing, SOD contents were measured on absorbance 450 nm (Epoch 2) using the commercial SOD kit (Dojindo Molecular Technologies) [ 5 ].…”

“…Inhaled PM 2.5 can easily pass through blood vessels and circulate throughout the whole body to reach several organs, causing apoptosis and inflammation with the activation of the toll-like receptor-4 (TLR-4)/myeloid differentiation primary response 88 (MyD88) pathway [ 4 ]. In addition, reactive oxygen species (ROS), oxidative stress, and mitochondrial dysfunction caused by exposure to fine dust cause various diseases in the human body [ 5 ]. Additionally, PM 2.5 reaches the gut through pulmonary mucus transport or direct intake; PM 2.5 that enters the gut can cause inflammation by increasing the expression of cytokines and changing the gut microbiome [ 6 ].…”