Protective effect of N-acetylcysteine on acute lung injury in septic rats by inhibiting inflammation, oxidation, and apoptosis | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 9، دوره 25، شماره 7، مهر 2022، صفحه 859-864 اصل مقاله (802.72 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2022.65350.14384 | ||
| نویسندگان | ||
| Jian-wei Le؛ Min Sun؛ Jian-hua Zhu؛ Heng Fan* | ||
| Department of Intensive Care Unit, Ningbo First Hospital, Ningbo, Zhejiang Province, P.R China | ||
| چکیده | ||
| Objective(s): Acute lung injury (ALI) is a common comorbidity in patients with sepsis, and finding drugs that can effectively reduce its mortality is a hot spot in current research. The purpose of this study is to explore the protective mechanism of N-acetylcysteine (NAC) on ALI in septic rats. Materials and Methods: We used NAC to intervene in septic rats to evaluate the plasma inflammatory factors and lung tissue pathological damage. Biochemical methods were used to determine the levels of oxidases in lung tissue, the expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) proteins, and observed lung tissue cell apoptosis. Results: NAC pretreatment decreased the mortality of septic rats, improved lung tissue pathological damage, reduced the levels of tumor necrosis factor-α, interleukin-1β, interleukin-6, interleukin-8, and malondialdehyde, and increased activity of superoxide dismutase, glutathione peroxidase, and catalase. Moreover, NAC pretreatment significantly decreased iNOS protein expression and increased eNOS protein expression in lung tissue. Meanwhile, NAC significantly decreased the number of apoptosis and the levels of Bax and Caspase-3 mRNA and increased the level of Bcl-2 mRNA in the lung tissue of septic rats. Conclusion: NAC protects ALI in septic rats by inhibiting inflammation, oxidative stress, and apoptosis. | ||
| کلیدواژهها | ||
| Acute lung injury؛ Apoptosis؛ Inflammation؛ N-acetylcysteine؛ Oxidative stress؛ Sepsis | ||
| مراجع | ||
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