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1.
J Burn Care Res ; 45(3): 777-789, 2024 05 06.
Artigo em Inglês | MEDLINE | ID: mdl-38245850

RESUMO

Postburn hypermetabolism remains an important clinical problem. During this phase, there is a significant loss of diaphragmatic proteins. Better understanding of respiratory muscle dynamics and potential mechanisms affecting respiratory muscle function is necessary for the development of effective therapeutic approaches. Male Wistar rats were subjected to 50% TBSA burns and sham injuries, and respiratory muscle function was assessed with 0, 1, 4, 7, and 14 days postinjury, including pulmonary function, blood gas analysis, transdiaphragmatic pressure, diaphragm ultrasonography, isolated diaphragm contractility, fatigue index, protein oxidative stress content, and ATP levels. Burned rats had significantly reduced inspiratory time, expiratory time, and tidal volume and significantly increased respiratory rate and minute ventilation. At the same time, the isolated diaphragm contractility, specific force during fatigue, and fatigue index were significantly decreased in the burned rats. Pdi, Pdimax, diaphragm thickness, diaphragm thickening fraction, and diaphragm excursion also decreased significantly postburn, whereas the Pdi/Pdimax ratio increased significantly. Finally, the content of protein carbonyls and lactic acid of burned rats was increased, and ATP levels of burned rats were decreased. The present study demonstrates the dynamic changes in diaphragm contractile properties postburn from both in vivo and in vitro perspectives, while cursorily exploring the possibility that protein oxidative stress and reduced ATP production may be the cause of diaphragm dysfunction. This understanding contributes to the development of methods to mitigate the extent of diaphragmatic function loss after severe burns.


Assuntos
Queimaduras , Contração Muscular , Ratos Wistar , Animais , Masculino , Ratos , Queimaduras/fisiopatologia , Queimaduras/complicações , Queimaduras/metabolismo , Contração Muscular/fisiologia , Estresse Oxidativo , Diafragma/fisiopatologia , Músculos Respiratórios/fisiopatologia , Modelos Animais de Doenças , Carbonilação Proteica , Trifosfato de Adenosina/metabolismo , Fadiga Muscular/fisiologia
2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-484510

RESUMO

Objective:To investigate the damage effect of bisphenol A (BPA)on the testis tissue of adult mice, and to reveal the reproductive toxicity of BPA in the body of animal and mechanism.Methods:40 KM mice aged 8 weeks were randomly divided into control group (according to the weight ratio of corn oil gavage), low dose of BPA group (100 mg·kg-1BPA),moderate dose of BPA group (200 mg·kg-1 BPA),and high dose of BPA group (400 mg·kg-1 BPA).4 weeks laster,the testis tissue was taken.The apoptotic rates in the testis tissue were detected by flow cytometry;the distribution and expression of Fas and FADD were measured by immunohistochemistry.Results:Compared with control group,the apoptotic rate,the expression rates of Fas and FADD in testis tissue of the mice in low dose of BAP group had no changes (P>0.05),while the apoptotic rates in the testis tissue and the positive expressions rates of Fas and FADD in moderate and high doses of BPA groups were increased (P<0.05).Compared with low dose of BPA group,the apoptotic rates and the positive expression rates of FAS and FADD in tests tissue of the mice in moderate and high doses of BPA groups were significantly increased (P<0.05).Compared with moderate dose of BPA group,the apoptotic rate and the positive expression rates of FAS and FADD in testis tissue of the mice in high dose of BPA group was significantly increased (P<0.05).The overexpression of Fas and FADD was positively correlated to the apoptotic rate in testis tissue in moderate dose of BPA group (r=0.430,P<0.05;r=0.238,P<0.01)and high dose of BPA group (r=0.637,P<0.01;r=0.359,P<0.01).Conclusion:BPA with content dose can increase the apoptotic rates of cells in testis tissue and the expressions of Fas and FADD.BPA’s reproductive toxicity may be closely associated with the activation of Fas signal pathway and resulting in massive apoptosis.

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