Int J Med Sci
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Objectives: This study aimed to investigate the involvement of macrophage ferroptosis in chronic apical periodontitis (CAP) and determine if blocking JNK/JUN/NCOA4 axis could alleviate CAP by regulating macrophage ferroptosis. Materials and Methods: Firstly, the in vitro models of apical periodontitis (AP) and in vivo models of CAP, including clinical specimens and rats' periapical lesions, were utilized to investigate the role of macrophage ferroptosis in CAP by detecting the ferroptosis related factors. The activation of the JNK/JUN/NCOA4 axis was observed in CAP in vivo models. ⋯ Conclusions: The occurrence of ferroptosis in macrophages contributes to the development of CAP. Targeting the JNK/JUN/NCOA4 axis is an effective therapeutic strategy to rescue the periapical lesions from inflammation due to its anti-macrophage ferroptosis function. Consequently, the current study provides support for further investigation on the JNK/JUN/NCOA4 axis as a targeted signaling pathway for CAP treatment.
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Introduction: Live microorganisms, named probiotics, can improve overall physical well-being, particularly the oral cavity's health. L. casei Shirota, a popular probiotic, can influence the immune response by increasing the number of macrophages and plasma cells that play a role in traumatic ulcer healing. Aims: To determine the expression of tumor necrosis factor-alpha (TNF-α) and the varied number of plasma cells and macrophages on a traumatic ulcer animal model treated with topical or systemic administration of a probiotic L. casei Shirota. ⋯ Results: The Mann-Whitney and Tukey HSD tests indicated significant differences (p < 0.05) in the results for the three groups. It was observed that topical administration provides more remarkable results than systemic administration for the expression of TNF-α, the number of plasma cells, and the number of macrophages. Conclusion: Topical administration of L. casei Shirota demonstrates better results than systemic administration for healing traumatic ulcers.
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Effective therapies for cognitive impairments induced by brain irradiation are currently lacking. This study investigated the therapeutic potential of hyperbaric oxygen therapy (HBOT) for radiation-induced brain injury in a randomized controlled experimental model using adult male Wistar rats. Adult male Wistar rats were divided into four experimental groups: 0 Gy whole brain radiotherapy (WBRT) with normal baric air (NBA) treatment, 0 Gy WBRT with HBOT, 10 Gy WBRT with NBA, and 10 Gy WBRT with HBOT. ⋯ In addition, HBOT prevented and reversed the increased apoptosis among newborn neural stem cells and neuroblasts caused by 10 Gy WBRT on 7 days. The findings suggest that WBRT disrupts neurogenesis and enhance microgliosis, apoptosis of neuronal progenitors, and lipid peroxidation in the dentate gyrus, potentially leading to cognitive deficits and neuronal death. HBOT may offer a protective effect against these cognitive impairments and their underlying mechanisms in adult male rats following WBRT.
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Background: Myocardial injury is prone to occur during myocardial ischemia-reperfusion, which further causes adverse cardiac events. Cardiomyopeptide (CMP) has been found to protect the heart against ischemia-reperfusion injury. The present study will explore the molecular and signaling mechanisms associated with the therapeutic effects of CMP. ⋯ RNA-seq analysis results showed that PPARγ signaling pathway is a potential signaling pathway for CMP treatment of myocardial injury in rats. The experimental results showed that CMP can significantly up-regulate PPARγ expression in myocardial tissues, inhibit ischemia reperfusion-induced myocardial injury, and alleviate mitochondrial respiratory disorders. Conclusion: CMP can improve myocardial injury in rats by alleviating mitochondrial respiratory dysfunction and reducing myocardial tissue damage and inflammatory infiltration via the regulation of PPARγ signaling pathway.
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Aims: Investigate the role of the apelin/APLNR axis in metabolic dysfunction-associated steatotic liver disease (MASLD), focusing on the progression from metabolic dysfunction-associated simple steatotic liver (MASS) to metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis, with emphasis on liver B cells. Methods: Serum samples from MASLD patients and liver tissues from hepatocellular carcinoma patients were collected to measure apelin and APLNR protein expression. C57BL/6J mouse models of varying MASLD stages were developed using a high-fat diet and CCl4. ⋯ Sequencing and RT-PCR in Raji cells indicate that the apelin/APLNR axis promotes the expression of inflammatory cytokines and extracellular matrix molecules. Conclusion: The apelin/APLNR axis is crucial in MASLD progression. Targeting this axis may offer therapeutic potential to modulate B cell function and mitigate MASLD advancement.