Abstract
Methods Phospho-AMP-activated protein kinase (p-AMPK) and AMP-activated protein kinase (AMPK) were detected by western blot. Immunofluorescence staining was used to validate changes in the levels of nuclear factor kappa B (NF-кB) p65 nuclear translocation. Mice were administered intraperitoneally with calycosin one hour before anaesthesia and endotracheal instillation of PM 2.5. The extent of lung injury was evaluated in the H&E-stained lung sections. Apoptotic cells were detected by TUNEL staining. Results Administration of calycosin was increased in PM 2.5-treated B2B cells in a dose-dependent manner in vitro. Fluorescence signals from anti-NF-кB p65 were increased in nuclei of cells pretreated with calycosin. The level of p-AMPK was increased by calycosin in vitro and in vivo. After pretreatment with compound C, the inhibitory effects of calycosin on cytotoxicity, levels of inflammatory cytokines and p-AMPK, and levels of NF-кB p65 nuclear translocation were not significantly decreased in vitro or in vivo. Conclusions Calycosin effectively decreased the release of inflammatory cytokines and alleviated injury caused by PM 2.5. These effects were mediated through activation of AMPK to suppress NF-κB signalling.
Highlights
Long-term exposure to particulate matter ≤2.5 μm in diameter (PM 2.5) is closely correlated with respiratory and cardiovascular diseases
Calycosin treatment significantly increased the absorbance of PM 2.5-treated B2B cells in a dose-dependent manner compared with cells not receiving calycosin. e differences were statistically significant when the calycosin concentration was 50 μM and 100 μM (p < 0.05 and p < 0.01, Figure 1(b)). e activity and number of B2B cells at 100 μM calycosin were most similar to those of cells not exposed to PM 2.5 based on observation under a microscope at 40× magnification (Figure 1(c))
We found that calycosin significantly alleviated cell damage and reduced the levels of IL-6 and IL-8 induced by PM 2.5 exposure at a concentration of 100 μM, with low cytotoxicity at the same concentration. ese results suggested that calycosin markedly reduced PM 2.5-induced oxidative stress and cell injury
Summary
Long-term exposure to particulate matter ≤2.5 μm in diameter (PM 2.5) is closely correlated with respiratory and cardiovascular diseases. Pun [1] found a positive association between 12month moving average PM 2.5 exposure (per 10 μg/m3 increase) and respiratory, chronic obstructive pulmonary diseases, and pneumonia mortality with risk ratios ranging from 1.10 to 1.24. E researchers identified significant PM 2.5-associated risks for cardiovascular-related and lung cancer mortality in a cohort of 18.9 million Medicare beneficiaries living across the conterminous United States. PM 2.5 is a major component of air pollution in China that is increasingly affecting people’s lives and health [2]. E components of PM 2.5 largely determine its toxicity, including water-soluble inorganic ions, transition metals, and extractable organic matter (EOM) [4]. An isoflavonoid, is a major active component in Astragali radix that has been
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