Int J Med Sci
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Embryonic development and tumor genesis share numerous similarities, with OCT4 standing out as a pivotal transcription factor in embryonic development. Expression of OCT4 is associated with poor prognosis of lung adenocarcinoma. VEGF-correlated chemokine-1 (VCC-1), also known as C-X-C motif chemokine ligand 17 (CXCL17), has been suggested to play a role in promoting tumor angiogenesis and metastasis. ⋯ NOD/SCID mice inoculated with VCC-1-knockdown A549 lung cancer cells exhibited significantly smaller tumors than those inoculated with control cells. On the basis of these findings, we highlight the importance of the OCT4-VCC-1 axis in lung cancer progression. Our findings also provide therapeutic targets for lung cancer.
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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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Excessive exercise can lead to fatigue, consequently affect exercise performance, and further have an adverse impact to human health. The synergistic effects of ginsenosides, salidroside, and syringin on improving exercise performance remain unknown. Hence, the effects of Chinese herb powder (CHP) which consisted of bioactive compounds such as ginsenosides (Rg1, Re, and Rb1), salidroside, and syringin on exercise performance, energy metabolism, tissue damage, antioxidant activity, and inflammatory cytokine were investigated in exhaustive exercise rats. ⋯ Abdominal arterial blood, liver, and gastrocnemius muscles were collected 4 hours after exhaustive exercise for further analysis. The high-dose CHP group increased the time to exhaustion, decreased serum lactate level, increased serum superoxide dismutase activity, and decreased liver interleukin-6 concentration. Therefore, CHP exhibits an anti-fatigue effect for prolonging the time to exhaustion through improving lactate clearance, and to a lesser extent, enhancing the capacity of antioxidation and anti-inflammation.
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Nephrotoxicity remains a significant concern associated with tyrosine kinase inhibitors, such as dasatinib (DASA). Previous studies have shown that DASA can induce renal tubular cell death, contributing to its nephrotoxic effects. In contrast, naringenin (NGN) is known for its antioxidant and anti-inflammatory properties. ⋯ Notably, DASA treatment upregulated the gene expression of the pro-apoptotic gene BAX while downregulating the expression of BCL-2 and Caspase-3 in kidney tissues. These findings suggest that NGN exerts nephroprotective effects against DASA-induced nephrotoxicity through its antioxidant, anti-inflammatory, and anti-apoptotic properties. Further investigations are warranted to elucidate the underlying mechanisms involved.
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Receptor-interacting protein 3 (Ripk3) plays a crucial part in acute lung injury (ALI) by regulating inflammation-induced endothelial damage in the lung tissue. The precise mechanisms through which Ripk3 contributes to the endothelial injury in ALI still remain uncertain. In the current research, we employed Ripk3-deficient (Ripk3-/-) mice to examine the role of Ripk3 in ALI progression, focusing on its effects on endothelial cells (ECs), mitochondrial damage and necroptosis. ⋯ Ripk3 upregulation suppressed the AMP-activated protein kinase (AMPK) pathway and activated Drp1-mediated mitochondrial fission, increasing mitochondrial permeability transition pore (mPTP) opening and PMVEC necroptosis. Conversely, Ripk3 deletion activated the AMPK/Drp1-mitochondrial fission pathway, preventing mPTP opening and PMVEC necroptosis in ALI. These findings demonstrated that Ripk3 promotes necroptosis through the AMPK/Drp1/mPTP opening pathway, identifying a potential therapeutic target for ALI treatment.