Swimming training reduced inflammation and apoptotic changes in pulmonary tissue in type 1 diabetic mice

Azizi, Nasim; Rahbarghazi, Afshin; Bavil, Fariba Mirzaei; Rahbarghazi‬, Reza; Ghaffari-Nasab, Arshad; Rezaie, Jafar; Delkhosh, Aref; Ahmadi, Mahdi

doi:10.1007/s40200-023-01202-8

Cited by 2 publications

(1 citation statement)

References 37 publications

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“…Apoptosis might also be a central mechanism through which exercise training confers benefits against lung injury. For instance, swimming exercise was shown to mitigate lung-related lesions in type I diabetic mice through the regulation of apoptosis 44 . Consistently, treadmill training has been observed to counteract lung tissue damage during PM exposure in mice by eliminating damaged mitochondria and reducing apoptosis; it similarly ameliorated COPD-induced lung injury through apoptosis reduction and sirt1 activation 14 , 45 .…”

Section: Discussionmentioning

confidence: 99%

Treadmill training improves lung function and inhibits alveolar cell apoptosis in spinal cord injured rats

Wang,

Fu,

Yang

et al. 2024

Sci Rep

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Secondary lung injury after SCI is a major cause of patient mortality, with apoptosis playing a key role. This study aimed to explore the impact of treadmill training and miR145-5p on the MAPK/Erk signaling pathway and apoptosis in rats with complete SCI. SD rats were used to establish T10 segmental complete SCI models and underwent treadmill training 3, 7, or 14 days postinjury. Various techniques including arterial blood gas analysis, lung wet/dry weight ratio, HE staining, immunofluorescence staining, immunohistochemical staining, qRT-PCR, and Western blotting were employed to assess alterations in lung function and the expression levels of crucial apoptosis-related factors. In order to elucidate the specific mechanism, the impact of miR145-5p on the MAPK/Erk pathway and its role in apoptosis in lung cells were confirmed through miR145-5p overexpression and knockdown experiments. Following spinal cord injury (SCI), an increase in apoptosis, activation of the MAPK/Erk pathway, and impairment of lung function were observed in SCI rats. Conversely, treadmill training resulted in a reduction in alveolar cell apoptosis, suppression of the MAPK/Erk pathway, and enhancement of lung function. The gene MAP3K3 was identified as a target of miR145-5p. The influence of miR145-5p on the MAPK/Erk pathway and its impact on apoptosis in alveolar cells were confirmed through the manipulation of miR145-5p expression levels. The upregulation of miR145-5p in spinal cord injury (SCI) rats led to a reduction in MAP3K3 protein expression within lung tissues, thereby inhibiting the MAPK/Erk signaling pathway and decreasing apoptosis. Contrarily, rats with miR145-5p knockdown undergoing treadmill training exhibited an increase in miR145-5p expression levels, resulting in the inhibition of MAP3K3 protein expression in lung tissues, suppression of the MAPK/Erk pathway, and mitigation of lung cell apoptosis. Ultimately, the findings suggest that treadmill training may attenuate apoptosis in lung cells post-spinal cord injury by modulating the MAP3K3 protein through miR145-5p to regulate the MAPK/Erk signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Treadmill training improves lung function and inhibits alveolar cell apoptosis in spinal cord injured rats

Wang,

Fu,

Yang

et al. 2024

Sci Rep

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Lung molecular and histological changes in type 2 diabetic rats and its improvement by high-intensity interval training

Rajizadeh,

Khoramipour,

Joukar

et al. 2024

BMC Pulm Med

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Background Type 2 diabetes (T2D) leads to serious respiratory problems. This study investigated the effectiveness of high-intensity interval training (HIIT) on T2D-induced lung injuries at histopathological and molecular levels. Methods Forty-eight male Wistar rats were randomly allocated into control (CTL), Diabetes (Db), exercise (Ex), and Diabetes + exercise (Db + Ex) groups. T2D was induced by a high-fat diet plus (35 mg/kg) of streptozotocin (STZ) administration. Rats in Ex and Db + Ex performed HIIT for eight weeks. Tumor necrosis factor-alpha (TNFα), Interleukin 10 (IL-10), BAX, Bcl2, Lecithin, Sphingomyelin (SPM) and Surfactant protein D (SPD) levels were measured in the bronchoalveolar lavage fluid (BALF) and malondialdehyde (MDA) and total antioxidant capacity (TAC) levels were measured in lung tissue. Lung histopathological alterations were assessed by using H&E and trichrome mason staining. Results Diabetes was significantly associated with imbalance in pro/anti-inflammatory, pro/anti-apoptosis and redox systems, and reduced the SPD, lecithin sphingomyelin and alveolar number. Performing HIIT by diabetic animals increased Bcl2 (P < 0.05) and IL10 (P < 0.01) levels as well as surfactants components and TAC (P < 0.05) but decreased fasting blood glucose (P < 0.001), TNFα (P < 0.05), BAX (P < 0.05) and BAX/Bcl2 (P < 0.001) levels as well as MDA (P < 0.01) and MDA/TAC (P < 0.01) compared to the diabetic group. Furthermore, lung injury and fibrosis scores were increased by T2D and recovered in presence of HIIT. Conclusion These findings suggested that the attenuating effect of HIIT on diabetic lung injury mediated by reducing blood sugar, inflammation, oxidative stress, and apoptosis as well as improving pulmonary surfactants components. Graphical Abstract Type 2 diabetes increased inflammation, oxidative stress and apoptosis and reduced pulmonary surfactants , while high intensity training improved these negative effects

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Swimming training reduced inflammation and apoptotic changes in pulmonary tissue in type 1 diabetic mice

Cited by 2 publications

References 37 publications

Treadmill training improves lung function and inhibits alveolar cell apoptosis in spinal cord injured rats

Treadmill training improves lung function and inhibits alveolar cell apoptosis in spinal cord injured rats

Lung molecular and histological changes in type 2 diabetic rats and its improvement by high-intensity interval training

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