Purpose: This study aimed to discuss the effects and relative mechanisms of astragaloside (AST) on diaphragm cell apoptosis in mice with chronic obstructive pulmonary disease (COPD).
Materials and methods: The mouse models of COPD were established by passive smoking. The pathological changes in lung and diaphragm tissues were observed by hematoxylin and eosin staining and evaluating the number of apoptotic cells of the diaphragm via a terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. The relative protein expression levels of AKT, p-AKT, caspase-3, and caspase-9 were measured through immunohistochemistry and Western blot assay.
Results: In comparison with the normal control mice, the pathological change and number of apoptotic cells deteriorated in the lung and diaphragm tissues of COPD model mice. With AST supplement, the pathological change and the number of apoptotic cells significantly improved (p < .05). With AKT inhibitor intervention, the effects of AST treatment disappeared. p-AKT, caspase-3, and caspase-9 protein expression was stimulated in the model group but was depressed in the AST-treated groups.
Conclusion: Our in vivo study revealed that AST improved COPD-induced diaphragm apoptosis by regulating and depressing AKT activities.
Keywords: apoptosis; astragaloside; caspase‐3; caspase‐9; chronic obstructive pulmonary disease; diaphragm; p‐AKT.
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