Fraxin, isolated from Acer tegmentosum, exert potent anti-oxidative stress action. Treatment with fraxin significantly lowered the serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in a CCl₄-induced hepatotoxicity rat model. In the fraxin-treated group, glutathione (GSH) significantly increased, while the malondialdehyde (MDA) in the liver significantly decreased. Fraxin also showed radical-scavenging activity. Fraxin protected HepG2 cells through Nrf2 pathway-dependent HO-1 expression[3]. Fraxin showed free radical scavenging effect at high concentration (0.5 mM) and cell protective effect against H2O2-mediated oxidative stress. Fraxin recovered viability of HUVECs damaged by H2O2-treatment and reduced the lipid peroxidation and the internal reactive oxygen species level elevated by H2O2 treatment[4]. Fraxin reduced LPS-induced TNF-α, IL-6 and IL-1β production in A549 cells and alleviated the LPS-induced wet/dry (W/D) weight ratio and the effects observed via histopathological examination of the lung in vivo. Furthermore, fraxin reduced the protein concentrations in the broncho-alveolar lavage (BAL) fluid and cytokine production in the sera. Fraxin played a protective role in LPS-induced lung injury by inhibiting the NF-κB and NLRP3 signalling pathways[5]. Fraxin elicited protective effects on mice with LPS-induced ARDS (Acute respiratory distress syndrome) and might be used as a drug to cure ARDS induced by Gram-negative bacterial infection[6].
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