Objectives: The current study compared the impact of pretreatment with melatonin and N-acetylcysteine (NAC) on the prevention of rat lung damage following intestinal ischemia-reperfusion (iIR).
Methods: Twenty-eight Wistar rats were subjected to intestinal ischemia induced by a 60 min occlusion of the superior mesenteric artery, followed by reperfusion for 120 min. Animals were divided into the following groups (n=7 per group): sham, only abdominal incision; SS+iIR, pretreated with saline solution and iIR; NAC+iIR, pretreated with NAC (20 mg/kg) and iIR; MEL+iIR, pretreated with melatonin (20 mg/kg) and iIR. Oxidative stress and inflammatory mediators were measured and histological analyses were performed in the lung tissues.
Results: Data showed a reduction in malondialdehyde (MDA), myeloperoxidase (MPO), and TNF-alpha in the animals pretreated with NAC or MEL when compared to those treated with SS+iIR (p<0.05). An increase in superoxide dismutase (SOD) levels in the NAC- and MEL-pretreated animals as compared to the SS+iIR group (34±8 U/g of tissue; p<0.05) was also observed. TNF-α levels were lower in the MEL+iIR group (91±5 pg/mL) than in the NAC+iIR group (101±6 pg/mL). Histological analysis demonstrated a higher lung lesion score in the SS+iIR group than in the pretreated groups.
Conclusion: Both agents individually provided tissue protective effect against intestinal IR-induced lung injury, but melatonin was more effective in ameliorating the parameters analyzed in this study.
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http://dx.doi.org/10.6061/clinics/2021/e2513 | DOI Listing |
Front Immunol
December 2024
Physical Examination Center, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China.
Organ transplantation is a vital intervention for end-stage organ failure; however, ischemia-reperfusion injury is a complication of transplantation, affecting the prognosis and survival of transplant recipients. As a complex ecosystem, recent research has highlighted the role of the intestinal microecology in transplantation, revealing its significant interplay with ischemia-reperfusion injury. This review explores the interaction between ischemia-reperfusion injury and intestinal microecology, with a special focus on how ischemia-reperfusion injury affects intestinal microecology and how these microecological changes contribute to complications after organ transplantation, such as infection and rejection.
View Article and Find Full Text PDFZhonghua Wei Zhong Bing Ji Jiu Yi Xue
November 2024
Department of Hepatobiliary Pancreatic Surgery, Quzhou City People's Hospital, Quzhou 324002, Zhejiang, China. Corresponding author: Lu Genlin, Email:
Objective: To investigate whether hydrogen sulfide (HS) protects against intestinal ischemia/reperfusion (I/R) injury in rats by regulating c-Jun N-terminal kinase/activator protein-1 (JNK/AP-1) signaling pathway.
Methods: Thirty male Wistar rats were divided into sham operated group (Sham group), I/R group, and HS donor sodium hydrosulfide (NaHS) intervention group (I/R+NaHS group), with 10 rats in each group. The I/R injury model was established by blocking the superior mesenteric artery with a non-traumatic vascular clip, with 60 minutes of ischemia followed by 120 minutes of reperfusion.
Front Cell Infect Microbiol
December 2024
Department of Anesthesiology, Zigong Fourth People's Hospital, Zigong, Sichuan, China.
Ischemia-reperfusion injury (IRI) is a common and clinically significant form of tissue damage encountered in medical practice. This pathological process has been thoroughly investigated across a variety of clinical settings, including, but not limited to, sepsis, organ transplantation, shock, myocardial infarction, cerebral ischemia, and stroke. Intestinal IRI, in particular, is increasingly recognized as a significant clinical entity due to marked changes in the gut microbiota and their metabolic products, often described as the body's "second genome.
View Article and Find Full Text PDFJ Thorac Dis
November 2024
Key Laboratory of Immune Microenvironment and Inflammatory Disease Research in Universities of Shandong Province, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, China.
Background And Objective: Farnesoid X receptor (FXR), which is encoded by the gene, is a ligand-activated transcription factor and a member of the nuclear receptor (NR) superfamily. As a receptor for bile acid (BA), FXR has been shown to play a key role in the regulation of BA metabolism, lipid metabolism, and the inflammatory response. This article reviews the roles of FXR in the pathogenesis of various lung diseases, and identifies potential diagnostic indicators or therapeutic targets for these diseases.
View Article and Find Full Text PDFImmunol Res
December 2024
Department of Nephrology, Liuzhou Workers Hospital, the Fourth Affiliated Hospital of Guangxi Medical University, No. 156, Heping Road, Liunan District, Liuzhou, 545000, Guangxi Zhuang Autonomous Region, P.R. China.
After stroke, there is a high incidence of acute lung injury and impairment of intestinal barrier function. In this research, the effects of pinocembrin on organ injuries induced by cerebral ischemia-reperfusion were investigated in mice with middle cerebral artery occlusion/reperfusion (MCAO/R) and further explored the possible mechanism. The potential targets of pinocembrin against MCAO/R were obtained by online tools.
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