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Updated: Jul 28, 2025
Author Spotlight: Advancing Diabetes Research with Static Exercise Training in Mice
Published on: March 29, 2024
Swimming training reduced inflammation and apoptotic changes in pulmonary tissue in type 1 diabetic mice
Nasim Azizi1, Afshin Rahbarghazi2, Fariba Mirzaei Bavil2
1Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Background:
Despite the vulnerability of pulmonary tissue to diabetic conditions, there are few reports related to the detrimental effects of hyperglycemia and therapeutic modalities on lung parenchyma. Here, the apoptotic changes were monitored in the diabetic pulmonary tissue of mice (DM1) subjected to a four‒week swimming plan.
Methods:
The mice were randomly allocated into Control; Control + Swimming (S); Diabetic group (D); and Diabetic + Swimming (D + S) groups (each in 8 mice). In the D and D + S groups, mice received intraperitoneally 50 mg/kg of streptozotocin (STZ). After 14 days, swimming exercise was done for four weeks. The expression of il-1β, bcl-2, bax, and caspase-3 was investigated using real-time PCR analysis. A histological examination was performed using H&E staining.
Results:
DM1 significantly upregulated il-1β, bax, and caspase-3, and down-regulated bcl-2 compared to the non-diabetic mice (p < 0.05). We noted that swimming exercises reversed the expression pattern of all genes in the diabetic mice and closed to basal levels (p < 0.05). Data indicated that swimming exercise could diminish emphysematous changes, and interstitial pneumonitis induced by STZ. Along with these changes, swimming exercise had protective effects to reduce the thickness of the inter-alveolar septum and mean alveolar area in diabetic mice.
Conclusion:
These data demonstrated that swimming exercises could decrease DM1-related pathologies in mouse lungs by regulating apoptosis and inflammatory response.
Insights
Swimming exercise benefits diabetic mice lungs by reducing inflammation and apoptosis. This intervention helps reverse hyperglycemia-induced lung damage, improving overall pulmonary health in diabetic conditions.
Area of Science:
- Pulmonary Medicine
- Endocrinology
- Exercise Physiology
Background:
- Pulmonary tissue is vulnerable to diabetic complications, yet research on hyperglycemia's lung effects is limited.
- Diabetic conditions can detrimentally impact lung parenchyma, leading to cellular damage and inflammation.
Purpose of the Study:
- To investigate the effects of swimming exercise on apoptotic changes in the lung tissue of diabetic mice.
- To evaluate the therapeutic potential of exercise in mitigating hyperglycemia-induced pulmonary damage.
Main Methods:
- Diabetic mice (DM1) were induced using streptozotocin (STZ) and subjected to a four-week swimming regimen.
- Gene expression of inflammatory and apoptotic markers (il-1β, bcl-2, bax, caspase-3) was analyzed using real-time PCR.
- Histological examination of lung tissue was performed using Hematoxylin and Eosin (H&E) staining.
Main Results:
- Diabetes significantly upregulated pro-apoptotic genes (il-1β, bax, caspase-3) and downregulated anti-apoptotic gene (bcl-2).
- Swimming exercise reversed these gene expression patterns in diabetic mice, bringing them closer to basal levels.
- Exercise diminished emphysematous changes and interstitial pneumonitis, reducing inter-alveolar septum thickness and mean alveolar area.
Conclusions:
- Swimming exercise demonstrates protective effects against diabetic lung pathologies in mice.
- Exercise mitigates hyperglycemia-induced lung damage by regulating apoptosis and inflammatory responses.
