Abstract
Ambient air particulate matter (PM) represents a class of heterogeneous substances present in polluted air, which contains many harmful components. Exposure to ambient particulate matter in fine rages (PM2.5) is associated with non-alcoholic fatty liver disease (NAFLD). Loquat Leaf possesses pharmacological actions on NAFLD. As the main biological active ingredients, the potential therapeutic role of total flavonoids (TF) isolated from Loquat Leaf in PM2.5-induced NAFLD model remains unclear. The present study was designed to explore the hepatoprotective effect of TF in PM2.5-induced NAFLD mice with its related mechanisms of action. Mice were exposed to PM2.5 to induce NAFLD, and body weight, the ratio of liver to body weight, and blood lipids increased significantly compared with the control group. It was found that TF significantly reduced the above parameters in PM2.5-induced NAFLD mice. TF treatment alleviated oxidative stress by preventing the accumulation of oxidative product malondialdehyde (MDA) and by strengthening the anti-oxidative capacity of superoxide dismutase (SOD). TF was also found to reduce the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity in the PM2.5 group. In addition, TF repaired the PM2.5-induced decline of insulin receptor substrate-1 (IRs-1) and protein kinase B (Akt) phosphorylation. Meanwhile, the data showed TF suppressed the expression of cytochrome P450 2E1(CYP2E1) and the phosphorylation of c-jun N-terminal kinase (JNK) in PM2.5-induced NAFLD. Taken together, these findings show that TF alleviate PM2.5-induced NAFLD via regulation of IRs-1/Akt and CYP2E1/JNK pathways, which may have potential for further development as novel therapeutic agents for NAFLD.
Highlights
Ambient air particulate matter (PM) represents a class of heterogeneous substances present in polluted air, especially the ambient fine particulate matter, which has been associated with the increasing prevalence of many diseases, such as pulmonary, cardiovascular, and hepatic diseases and metabolic syndrome [1,2,3,4]
We demonstrated that PM2.5 exposure for 35 days caused significant lipid metabolism disorder, liver damage, and oxidative stress
We further found that exposure to PM2.5 can inhibit insulin resistance (IR)/Akt signaling, which participated in IR promotion
Summary
Ambient air particulate matter (PM) represents a class of heterogeneous substances present in polluted air, especially the ambient fine particulate matter (aerodynamic diameter < 2.5 μm, PM2.5), which has been associated with the increasing prevalence of many diseases, such as pulmonary, cardiovascular, and hepatic diseases and metabolic syndrome [1,2,3,4]. The chemical and biological elements of PM2.5 include metals, salts, volatile organic compounds, hydrocarbons, and even endotoxins [6,7]. These PM2.5 particles can deposit in alveolar regions of the lung, and can penetrate into the distal airway units and enter into the circulatory system with diminishing sizes, bringing health risks [8]. Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by hepatic steatosis, and it is regarded as a manifestation of metabolic syndrome in the liver. Multiple studies have shown that PM2.5 exposure induces integrated lipid accumulation, oxidative stress, insulin resistance, and inflammatory responses in the liver, leading to NAFLD in animal models [2,3,11,12,13]
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