Browsing by Subject "Inflammatory response"

Now showing 1 - 4 of 4
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    Aromadendrin alleviates LPS-induced kidney apoptosis and inflammation by inhibiting phosphorylation of MAPK and NF-κB signaling pathways
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Ma, Xiaohong; Liu, Wenhua; Wang, Bin; Shi, Feizhuang
    Background. Excessive inflammation and apoptosis in kidneys are critical players in the pathogenesis of acute kidney injury (AKI). Aromadendrin is a natural flavonoid characterized by anti-inflammatory, anti-apoptotic, and antioxidant actions. Thus, we investigated the roles and mechanisms of aromadendrin in the development of AKI. Methods. Lipopolysaccharide (LPS) was used to induce AKI mice, and one hour after LPS challenge, the mice received oral administration of aromadendrin or vehicle. Renal functions were assessed by measuring blood urea nitrogen and creatinine in serum. Histological changes were determined by hematoxylin and eosin staining. Apoptotic cells of renal tissues were detected by TUNEL staining. Gene expression was measured by western blotting and RT-qPCR. Results. Aromadendrin alleviated LPS-induced renal dysfunctions and histological defects in mice. Additionally, aromadendrin suppressed excessive inflammation and tissue apoptosis in the kidneys of LPS-induced AKI mice. Mechanistically, aromadendrin blocked the activation of NF-κB and MAPK pathways in LPS-induced AKI mice. Conclusion. Aromadendrin alleviates LPS-stimulated inflammation and tissue cell apoptosis in kidneys by inactivating the NF-κB and MAPK pathways
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    Evolution of the inflammatory response in vertebrates: fish TNF-α is a powerful activator of endothelial cells but hardly activates phagocytes
    (2008-10-01) Mulero Méndez, Iván; López-Muñoz, Azucena; Renshaw, Stephen A.; Meseguer Peñalver, J.; Mulero Méndez, Victoriano Francisco; Sepulcre Cortés, María Pilar; Roca Soler, Francisco José; Bioquímica y Biología Molecular B e Inmunología
    TNF-α is conserved in all vertebrate classes and has been identified in all taxonomic groups of teleost fish. However, its biological activities and its role in infection are largely unknown. Using two complementary fish models, gilthead seabream and zebrafish, we report here that the main proinflammatory effects of fish TNF-α are mediated through the activation of endothelial cells. Thus, TNF-α promotes the expression of E-selectin and different CC and CXC chemokines in endothelial cells, thus explaining the recruitment and activation of phagocytes observed in vivo in both species. We also found that TLR ligands, and to some extent TNF-α, were able to increase the expression of MHC class II and CD83 in endothelial cells, which might suggest a role for fish endothelial cells and TNF-α in Ag presentation. Lastly, we found that TNF-α increases the susceptibility of the zebrafish to viral (spring viremia of carp virus) and bacterial (Streptococcus iniae) infections. Although the powerful actions of fish TNF-α on endothelial cells suggest that it might facilitate pathogen dissemination, it was found that TNF-α increased antiviral genes and, more importantly, had little effect on the viral load in early infection. In addition, the stimulation of ZF4 cells with TNF-α resulted in increased viral replication. Together, these results indicate that fish TNF-α displays different sorts of bioactivity to their mammalian counterparts and point to the complexity of the evolution that has taken place in the regulation of innate immunity by cytokines.
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    Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate Helicobacter pylori-associated gastritis
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Li Ze; Chen Ruirui; Tang Weihong; Zheng Xiaoya; Jin Xuefeng; Wang Zhongmin; Wu Qiao; Biología Celular e Histología
    Background. Helicobacter pylori (HP)-associated gastritis is an important factor in development of stomach cancer. Components of Sheng-Jiang-Yi-You decoction (SJYYD) exert gastroprotective effects. However, the effects and mechanism of SJYYD in HP-associated gastritis remain uncertain. Methods. HP bacterial solution (1×109 CFU/mL) was gavaged every other day for 14 days to construct an HP-associated gastritis mouse model. Male BALB/c mice were randomized into Sham, HP, HP+Standardized triple therapy (HP+Triplet), HP+SJYYD (0.4 mL/20 g), HP+Triplet+SJYYD, HP+anisomycin (ANI) (2.5 mg/kg/d, p38MAPK agonist, HP+ANI), and HP+ SJYYD+ANI groups (n=6). Gastric mucosal injury detection and rapid urease test for HP infection were conducted. HE staining for pathological damage and ELISA for pro-inflammatory factors and immuno-globulin G (IgG) content were performed. Measurement of p38 mitogen-activated protein kinase (p38MAPK) pathway-related factor expression was performed by qRT-PCR and western blot. Results. The increased IgG content and HP colonization rate indicated successful modeling. SJYYD caused attenuated gastric mucosal damage, with decreased ulcer index (UI), HP colonization rate, inflammatory cell infiltration, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β levels in HP-associated gastritis mice. Moreover, SJYYD reduced p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinase (ERK) mRNA expression, as well as p-p38MAPK/p38MAPK, p-JNK/JNK, and p-ERK/ERK protein expression in gastric mucosa tissues of HP-associated gastritis mice. The above effects were reversed by further ANI treatment. Conclusion. SJYYD may attenuate HP-associated gastritis by inhibiting inflammatory response by down-regulating p38MAPK pathway, providing scientific evidence for clinical application of SJYYD in HP-associated gastritis treatment and promoting the development of therapeutic approaches in HP-associated gastritis
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    Shensiqigui tablets alleviate bleomycin-induced pulmonary fibrosis by inhibiting the hedgehog/wnt-β-catenin pathway
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Ma Rui; Xie Yupeng; Dong Yuan; Yin Fan; Yang Jiong; Xu Fenghua; Biología Celular e Histología
    Background. Pulmonary fibrosis (PF) is a refractory disease characterized by inflammation and fibrosis. Shensiqigui Tablets (SSQGT), a combination of Codonopsis pilosula, Astragalus, and Angelica, is a traditional Chinese medicine with anti-inflammatory and antioxidant properties. Therefore, SSQGT may be a potential therapeutic agent for managing PF. This study aimed to investigate the effects of SSQGT on PF and its potential mechanisms. Methods. This study established a mouse model of PF through a single intratracheal injection of bleomycin (BLM) and used a TGF-β1-induced HFL-1 cell model. The experiment included control, model (BLM/TGF-β1), and treatment groups (pirfenidone, compound Biejiaruangan tablet (BJRGT), low-dose SSQGT, medium-dose SSQGT, and high-dose SSQGT). Histopathological changes and collagen deposition in lung tissues were observed using Hematoxylin-Eosin (HE) and Masson staining. Inflammatory exudation in bronchoalveolar lavage fluid (BALF) was assessed using ELISA, including TNF-α, IL-1β, IL-6, and NO. Oxidative stress markers SOD, GSH, and Malondi-aldehyde (MDA) were measured using commercial kits. mRNA and protein expression levels in lung tissues and in vitro models, including α-SMA, vimentin, collagen I, caspase-3, TGF-β, and the Hedgehog/Wnt-β-catenin pathway, were evaluated using qRT-PCR and western blot analysis. Results. SSQGT significantly alleviated BLM-induced weight loss and lung injury in mice and reduced HYP levels and collagen deposition. Additionally, SSQGT improved oxidative stress markers (decreased MDA levels and increased SOD and GSH activity) and mitigated inflammatory responses (reduced TNF-α, IL-1β, IL-6, and NO levels) and (downregulated α-SMA, collagen I, caspase-3, and TGF-β). Further mechanistic analysis showed that SSQGT inhibited the Hedgehog/ Wnt-β-catenin pathway. Conclusion. SSQGT alleviates BLM- or TGF-β1-induced PF by reducing oxidative stress and inhibiting inflammation through the suppression of the Hedgehog/ Wnt-β-catenin pathway, suggesting its potential as a therapeutic agent for PF