Related Experiment Video
Updated: Jul 8, 2026
A Silver Nanoparticle Method for Ameliorating Biliary Atresia Syndrome in Mice
Published on: October 13, 2018
Impact of particulate matter 2.5 on the liver function of mice
1Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. zhai0184heyifan2@126.com.
Objective:
The aim of this study was to evaluate the impact of particulate matter 2.5 (PM2.5) on liver function at the animal level and to study its impact targets.
Materials And Methods:
60 male and female BALB/c mice of SPF grade, aged 6-8 weeks, were randomly divided into four groups, with 15 mice in each, including the normal saline control group, the PM2.5 low dose group [2 μg/(100 g/d)], the PM2.5 medium dose group [8 μg/(100 g/d)] and the PM2.5 high dose group [16 μg/(100 g/d)]. Each day, 0.9% saline or PM2.5 particles were administered through the nasal route, and samples were taken after 3 weeks of continuous exposure. Hematoxylin-eosin staining (HE) was used to observe the liver damage caused by PM2.5. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were detected by using an automatic biochemical analyzer to detect the content of liver glycogen and blood glucose. Multiple indicators were observed, including plasma tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) levels, oxidative stress response indicators reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) detection, RT-PCR and Western blot detection of glycogen synthase (GS), glucokinase (GK), nuclear factor erythroid 2-related factor 2 (Nrf2) expression and phosphorylation level of phospho-c-Jun N-terminal kinases (p-JNK).
Results:
PM2.5 can cause damage to the liver by increasing PM2.5 concentrations, raising the metabolic rate of liver cells, resulting in a substantial amount of inflammatory infiltration and vacuolar degeneration of cells, and increasing the liver/body weight. TNF-α and IL-6 inflammatory factor expression increased (p<0.05). An increase in the serum ALT and AST levels were also observed. The blood glucose of mice increased, whereas the content of liver glycogen declined (p<0.05). ROS, MDA, and SOD levels all increased considerably. PM2.5 can drastically lower the expression of GS and GK, increase the expression of Nrf2, and raise the phosphorylation level of p-JNK (p<0.05).
Conclusions:
PM2.5 can induce oxidative stress in mouse liver through the Nrf2/JNK pathway, induce liver inflammation in mice, and inhibit glycogen synthesis.
Insights
Particulate matter 2.5 (PM2.5) exposure damages mouse liver by increasing oxidative stress and inflammation via the Nrf2/JNK pathway, while also inhibiting glycogen synthesis.
Area of Science:
- Environmental Health
- Toxicology
- Hepatology
Background:
- Particulate matter 2.5 (PM2.5) is a major air pollutant with known systemic health effects.
- The specific impact of PM2.5 on liver function and the underlying molecular mechanisms require further elucidation.
Purpose of the Study:
- To investigate the effects of PM2.5 exposure on liver function in a mouse model.
- To identify the molecular targets and pathways involved in PM2.5-induced liver injury.
Main Methods:
- BALB/c mice were exposed to varying doses of PM2.5 via nasal administration for 3 weeks.
- Liver damage was assessed using histopathology (HE staining), serum enzyme levels (ALT, AST), and biochemical assays.
- Inflammatory markers (TNF-α, IL-6), oxidative stress indicators (ROS, MDA, SOD), and key protein expressions (GS, GK, Nrf2, p-JNK) were quantified.
Main Results:
- PM2.5 exposure led to increased liver/body weight ratio, inflammatory infiltration, and vacuolar degeneration in liver cells.
- Elevated serum ALT, AST, TNF-α, IL-6, ROS, MDA, and SOD levels were observed in PM2.5-exposed mice.
- PM2.5 significantly decreased glycogen synthase (GS) and glucokinase (GK) expression, increased Nrf2 expression, and elevated p-JNK phosphorylation.
Conclusions:
- PM2.5 induces liver damage in mice through oxidative stress and inflammation.
- The Nrf2/JNK signaling pathway plays a critical role in mediating PM2.5-induced hepatotoxicity.
- PM2.5 exposure inhibits hepatic glycogen synthesis, contributing to metabolic dysfunction.
More Related Videos
12:15Quantification of three DNA Lesions by Mass Spectrometry and Assessment of Their Levels in Tissues of Mice Exposed to Ambient Fine Particulate Matter
Published on: May 29, 2019
07:35Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
