Browsing by Subject "TLR4"

Now showing 1 - 4 of 4
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    Expression of Foxp3 and TLR4 in human papillary thyroid carcinoma and its clinical significance
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Xin, Jingwei; Fu, Haiying; Zhang, Jiaping; Zou, Hongrui; Li, Qi; Yang, Wei; Sun, Hui
    This study aimed to explore the association of Foxp3 and TLR4 with clinical pathological characteristics in papillary thyroid carcinoma (PTC) patients. Methods 78 cases of PTC were used as experimental group and 20 cases of normal thyroid tissue were used as control group. The expression of Foxp3 and TLR4 in thyroid tissue from the two groups was detected by immunohistochemistry, and the experimental group was divided into several groups on the basis of different clinicopathological indicators. The association between Foxp3 and TLR4 expression and clinicopathological parameters was statistically analyzed. Results Foxp3 and TLR4 were expressed in higher levels in PTC than in normal thyroid tissue (P<0.05). Foxp3 was mainly localized in the cytoplasm and nucleus of PTC cells, while TLR4 was found in the cytoplasm and cell membrane of cancer cells. The expression of both proteins associated with lymph node metastasis and TNM clinical stage (P<0.05). The expression of Foxp3 correlated with the expression of TLR4 in tested PTC tissues (P<0.05). In addition, the result of confocal fluorescence microscopy showed that Foxp3 and TLR4 co-localized in PTC cells. Conclusion Foxp3 and TLR4 were upregulated and associated with lymph node metastasis and advanced TNM stage in PTC tissues. Together they may act as valuable factors for the identification of high-risk PTC patients.
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    Functional mechanism of baicalein in alleviating severe acute pancreatitis-acute lung injury by blocking the TLR4/MyD88/TRIF signaling pathway
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Yang, Qingjing; Yue, Chao; Huang, Xing; Wang, Zihe; Li, Zhenlu; Hu, Weiming; Lu, Huimin
    y. Severe acute pancreatitis-acute lung injury (SAP-ALI) is a disease with high mortality. This study aims to explore the mechanism of baicalein on SAP-ALI in rats by blocking toll-like receptor-4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88)/TIRdomain-containing adapter-inducing interferon-β (TRIF) signal pathway. The SAP-ALI rat model was established by intraperitoneal injection of 3% pentobarbital sodium (30 mg/kg), with pancreas and intestines turned over, injected with 3.5% sodium taurocholate backward into the bile-pancreatic duct at 0.1 mL/100 g for 12h, and treated with baicalein, lipopolysaccharide (LPS), miR182 agomir, or miR-182 antagomir. The TLR4/MyD88/ TRIF pathway was activated using LPS in SAP-ALI rats after baicalein treatment. Baicalein attenuated inflammatory cell infiltration, alveolar wall edema, decreased W/D ratio and levels of TLR4, MyD88, and TRIF in the lung tissues, reduced levels of inflammatory factors in pancreatic and lung tissues and BALF, diminished ROS, and elevated GSH, SOD and CAT in pancreatic and lung tissues of SAP-ALI rats. Activation of the TLR4/MyD88/TRIF pathway partly abrogated baicalein-mediated improvements in inflammation and oxidative stress in SAP-ALI rats. miR-182 targeted TLR4. miR-182 suppressed inflammation and oxidative stress in SAP-ALI rats by targeting TLR4. Inhibition of miR-182 partly nullified baicalein-mediated attenuation on inflammation and oxidative stress in SAP-ALI rats. In conclusion, baicalein can inhibit the TLR4/MyD88/ TRIF pathway and alleviate inflammatory response and oxidative stress in SAP-ALI rats by upregulating miR182 and suppressing TLR4, thus ameliorating SAP-ALI.
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    Mechanism of Weiwei granules in the treatment of chronic active Helicobacter pylori gastritis with atrophy based on the TLR4/NF-κB/COX-2 inflammatory signaling pathway
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Zhang, Haipeng; Liu, Hongyan
    Objective. Our paper aimed to elucidate the mechanism of Weiwei granules in the treatment of Helicobacter pylori (Hp)-positive chronic atrophic gastritis (CAG) based on the TLR4/NF-κB/COX-2 inflammatory signaling pathway. Methods. Hp-positive CAG patients were randomized into the control group (treated with quadruple therapy) or the observation group (treated with Weiwei granules based on the control group). The clinical efficacy, Hp clearance rate, and efficacy of traditional Chinese medicine (TCM) symptoms were compared between the two groups after six months of treatment. The scores of various histopathology variables, serum levels of inflammatory factors (interleukin-6 [IL-6], interleukin-8 [IL-8], and tumor necrosis factor-alpha [TNF-α]), gastrin-17 (G-17) and motilin (MTL), pepsinogen (PG) I and PG II, as well as serum levels of gastrointestinal hormone endothelin (ET), epidermal growth factor (EGF), and calcitonin gene-related peptide (CGRP), were compared between the two groups before and after treatment. TLR4, NF-κB, and COX-2 mRNA levels were compared in gastric mucosal tissues before and after treatment in the two groups. Results. After treatment, the clinical efficacy, Hp clearance rate, and efficacy of TCM symptoms of patients in the observation group were higher than those in the control group. After treatment, the scores of various histopathology variables, serum levels of inflammatory factors (IL-6, IL-8, and TNF-α), gastrointestinal hormones (ET and EGF), and the expression levels of TLR4, NF-κB, and COX-2 mRNA in the gastric mucosal tissues were lower and G-17, MTL, CGRP, and PG I levels were higher in the observation group than in the control group. Conclusion. Weiwei granules can effectively improve Hp-positive CAG patients and reduce the expression levels of TLR4, NF-κB, and COX-2
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    Penning decoction ameliorated pyroptosis in mice with lipopolysaccharide-induced endometritis through inhibition of the TLR4/NF-κB/NLRP3 pathway
    (2026) Chen Chen; Yuqiong Yuan; Zhihui Liu; Qianru Zhou; Jiani Shi; Biología Celular e Histología; Universidad de Murcia, Departamento de Biología Celular e Histología
    Objectives. Endometritis, stemming from bacterial infection, manifests as persistent inflammation and may cause infertility. Penning decoction (PND) has been approved for clinical treatment of patients with endometritis. However, the mechanism by which it prevents endometritis remains unknown. This study aimed to examine the impact of PND on lipopoly saccharide (LPS)-induced endometritis and elucidate the underlying mechanisms involved. Methods. Firstly, ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF-MS) analysis, in which both positive and negative ion modes were used to identify the chemical compounds in PND, was performed. The antipyroptotic effects of PND were validated in LPS-induced endometritis mice. Additionally, mouse endometrial epithelial cells (MEECs) were used to explore the molecular mechanism of PND in serum in vitro. Results. A total of 145 chemical compounds, including flavones, saponins, polysaccharides, alkaloids, and glycosides, were identified in positive and negative ion modes. The results showed that LPS could induce pyroptosis in endometritis in vivo and in vitro. Treatment with PND or serum containing PND could significantly ameliorate LPS-induced pyroptosis by inhibiting the activation of the TLR4/NF-κB/NLRP3 signaling pathway. Conclusion. Our results demonstrated that PND may improve LPS-induced endometritis by inhibiting the TLR4/NF-κB/NLRP3 pathway, which provides a potentially effective drug for the clinical treatment of endometritis.