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Introduction: Ischemia-reperfusion (IR) injury is a major concern that frequently occurs during vascular surgeries. Hydrogen-rich saline (HRS) solution exhibits antioxidant and anti-inflammatory properties. This study aimed to examine the effects of HRS applied before ischemia in the lungs of rats using a lower extremity IR model.
Material And Methods: After approval was obtained from the ethics committee, 18 male Wistar albino rats weighing 250-280 g were randomly divided into three groups: control (C), IR and IR-HRS. In the IR and IR-HRS groups, an atraumatic microvascular clamp was used to clamp the infrarenal abdominal aorta, and skeletal muscle ischemia was induced. After 120 min, the clamp was removed, and reperfusion was achieved for 120 min. In the IR-HRS group, HRS was administered intraperitoneally 30 min before the procedure. Lung tissue samples were examined under a light microscope and stained with hematoxylin-eosin (H&E). Malondialdehyde (MDA) levels, total sulfhydryl (SH) levels, and histopathological parameters were evaluated in the tissue samples.
Results: MDA and total SH levels were significantly higher in the IR group than in the control group ( < 0.0001 and = 0.001, respectively). MDA and total SH levels were significantly lower in the IR-HRS group than in the IR group ( < 0.0001 and = 0.013, respectively). A histopathological examination revealed that neutrophil infiltration/aggregation, alveolar wall thickness, and total lung injury score were significantly higher in the IR group than in the control group ( < 0.0001, = 0.001, and < 0.0001, respectively). Similarly, alveolar wall thickness and total lung injury scores were significantly higher in the IR-HRS group than in the control group ( = 0.009 and = 0.004, respectively). A statistically significant decrease was observed in neutrophil infiltration/aggregation and total lung injury scores in the IR-HRS group compared to those in the IR group ( = 0.023 and = 0.022, respectively).
Conclusion: HRS at a dose of 20 mg/kg, administered intraperitoneally 30 min before ischemia in rats, reduced lipid peroxidation and oxidative stress, while also reducing IR damage in lung histopathology. We believe that HRS administered to rats prior to IR exerts a lung-protective effect.
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http://dx.doi.org/10.1177/00368504241257060 | DOI Listing |
Am J Forensic Med Pathol
September 2025
Department of Pathology, St Louis University School of Medicine, Office of the Medical Examiner - City of St. Louis, St. Louis, MO.
Myotonic dystrophy type 1, or dystrophia myotonica type 1 (DM1), is a multisystem disorder inherited in an autosomal dominant manner. It is caused by a CTG tri-nucleotide expansion in the 3'-untranslated region (3'-UTR) of the dystrophia myotonia protein kinase (DMPK) gene. Core clinical features include progressive skeletal muscle weakness, myotonia, and systemic complications, with premature mortality most often due to respiratory or cardiac dysfunction.
View Article and Find Full Text PDFNeuropathol Appl Neurobiol
October 2025
Division of Rheumatology and Systemic Inflammatory Diseases, III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Aims: Sarcoid myopathy (SaM) is characterised by granulomatous myositis (GM) and can overlap with inclusion body myositis (IBM), a late-onset chronic idiopathic inflammatory myopathy with a still enigmatic pathogenesis. As GM can occur in different clinical contexts, we aimed to examine the histomorphologic features and gene expression profiles in cases of definite SaM that may inform diagnostic and therapeutic considerations.
Methods: We performed a multidimensional characterisation of muscle biopsy specimens from patients with 'pure SaM' (n=17), SaM with concomitant IBM (SaM-IBM) (n=2), including histopathologic and ultrastructural analysis in addition to quantitative real-time polymerase chain reaction.
J Cachexia Sarcopenia Muscle
October 2025
Department of Sports Science, College of Natural Science, Jeonbuk National University, Jeonju, Republic of Korea.
Background: Fine particulate matter has developmental toxicity, and midgestation is an important period for the development of foetal skeletal muscle. The ability of exercise to modulate skeletal muscle damage in mice exposed to PM during gestation remains unclear.
Methods: Pregnant C57BL/6 mice were exposed to 50 μg/m PM for 2 h on five consecutive days starting at embryonic day 12.
J Endocrinol
September 2025
University of Missouri, Columbia, MO.
Purpose: CL316,243 (CL), a beta 3 adrenergic receptor (B3-AR) agonist has 'exercise mimetic' effects in adipose tissue (AT). CL may also positively affect skeletal muscle (SM), yet the role of estrogen receptor beta (ERβ) in mediating SM-specific effects of CL is not known. We investigated the effects of CL on SM metabolism, as well as the role played by ERβ.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
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