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Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
SAM protects against alveolar septal cell apoptosis in autoimmune emphysema rats
Dan Li1,2, Ben-Xue Li1,3, Ye Zhang1,2
1Department of Respiratory Medicine, Guizhou Provincial People's Hospital, No. 83, Zhongshan East Road, Guiyang, Guizhou, China.
Background:
Hypomethylation of the perforin gene promoter in CD4 + T cells, inflammation and oxidative stress, might be involved in alveolar septal cell apoptosis associated with emphysema in rats. This study aimed to investigate the effects of S-adenosylmethionine (SAM) on this kind of apoptosis in rats with autoimmune emphysema.
Methods:
Twenty-four rats were randomly divided into three groups: a normal control group, a model group, and a SAM group. Pathological changes in lung tissues were observed, and the mean linear intercept (MLI) and mean alveolar number (MAN) were measured. The levels of anti-endothelial cell antibodies (AECA) in serum, alveolar septal cell apoptosis, perforin gene promotor methylation in CD4 + T cells in the spleen, and the levels of cytokines, malondialdehyde (MDA), and glutathione (GSH) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in bronchoalveolar lavage fluid (BALF) were investigated.
Results:
The MLI, apoptosis index (AI) of alveolar septal cells, levels of AECA in serum, and levels of tumour necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9) and MDA in BALF were increased, while the MAN, methylation levels, and the activities of GSH, SOD and GSH-Px in BALF were decreased in the model group compared with those in the normal control group and the SAM group (all P < 0.05). The levels of interleukin-8 (IL-8) in BALF were greater in the model group than in the normal control group (P < 0.05).
Conclusions:
SAM protects against alveolar septal cell apoptosis, airway inflammation and oxidative stress in rats with autoimmune emphysema possibly by partly reversing the hypomethylation of the perforin gene promoter in CD4 + T cells.
Insights
S-adenosylmethionine (SAM) treatment reduced alveolar septal cell apoptosis and inflammation in rats with autoimmune emphysema. SAM may protect by reversing perforin gene hypomethylation in CD4+ T cells.
Area of Science:
- Pulmonary Medicine
- Immunology
- Molecular Biology
Background:
- Autoimmune emphysema in rats involves CD4+ T cell perforin gene promoter hypomethylation, inflammation, and oxidative stress, leading to alveolar septal cell apoptosis.
- S-adenosylmethionine (SAM) is investigated for its potential therapeutic effects on these pathological processes.
Purpose of the Study:
- To investigate the effects of SAM on alveolar septal cell apoptosis in rats with experimentally induced autoimmune emphysema.
- To explore the potential role of perforin gene promoter methylation in CD4+ T cells as a mechanism of SAM's action.
Main Methods:
- Twenty-four rats were divided into normal control, model (autoimmune emphysema), and SAM treatment groups.
- Evaluated lung pathology, mean linear intercept (MLI), mean alveolar number (MAN), serum anti-endothelial cell antibodies (AECA), alveolar septal cell apoptosis, and perforin gene promoter methylation in CD4+ T cells.
- Assessed cytokines (TNF-α, MMP-9, IL-8), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in bronchoalveolar lavage fluid (BALF).
Main Results:
- The model group showed increased MLI, apoptosis index, AECA, TNF-α, MMP-9, MDA, and IL-8, with decreased MAN, perforin gene methylation, GSH, SOD, and GSH-Px compared to controls (P<0.05).
- SAM treatment significantly improved these parameters, bringing them closer to normal control levels.
- SAM group exhibited reduced apoptosis, inflammation, and oxidative stress markers compared to the model group.
Conclusions:
- SAM demonstrates protective effects against alveolar septal cell apoptosis, airway inflammation, and oxidative stress in autoimmune emphysema models.
- These protective effects are potentially mediated by the partial reversal of perforin gene promoter hypomethylation in CD4+ T cells.
- SAM represents a potential therapeutic agent for autoimmune emphysema.
