Journal: Pharmaceutics

Article Title: Elovanoids Counteract Inflammatory Signaling, Autophagy, Endoplasmic Reticulum Stress, and Senescence Gene Programming in Human Nasal Epithelial Cells Exposed to Allergens

doi: 10.3390/pharmaceutics14010113

Figure Lengend Snippet: ELVN-34 reduce the expression of pro-inflammatory cytokines, chemokines and cell adhesion molecule in HNEpC challenged with LPS or poly(I:C). HNEpC challenged with LPS or poly(I:C) (30 μg/mL) display enhanced production of pro-inflammatory cytokines and chemokines IL-6, IL-1β, IL-8/CXCL8, CCL2/MCP-1, CXCL1/KC/GRO, VEGF, and cell adhesion molecule ICAM1(CD54) compared to non-treated cells. This increase in the production of pro-inflammatory molecules is abrogated by the addition of ELVN-34 (500 nM) 30 min post-challenge. LPS and poly(I:C) induce a reduction of anti-inflammatory IL-10 expression in HNEpC that is restored to normal levels after treatment with ELVN-34 (500 nM). The results showed the averages of three independent experiments. (**** p < 0.0001, NS—not significant).

Article Snippet: In addition, the expression of the following cytokines was analyzed in the supernatant of HNEpC exposed to different allergic inductors: IL-6 (Catalog# 6802, Chondrex) range of detection: (9–600 pg/mL), IL-1β (Catalog# 6805, Chondrex) range of detection: (4–250 pg/mL) IL-8/CXCL8 (Quantikine ELISA Kit, Catalog# D8000C, R&D Systems) range of detection: (31–2000 pg/mL), vascular endothelial growth factor (VEGF) (Catalog# 6810, Chondrex) range of detection: (31–2000 pg/mL), ICAM1(CD54) (ELISA Kit, Catalog# ab100640, Abcam) range of detection: (16–1000 pg/mL), CXCL1/KC/GRO (Catalog# 6825, Chondrex) range of detection: CCL2/MCP-1 (Catalog# 6821, Chondrex) range of detection: (16–1000 pg/mL), and IL-10 (Catalog# 6806, Chondrex) range of detection: (8–500 pg/mL).

Techniques: Expressing

Journal: Pharmaceutics

Article Title: Elovanoids Counteract Inflammatory Signaling, Autophagy, Endoplasmic Reticulum Stress, and Senescence Gene Programming in Human Nasal Epithelial Cells Exposed to Allergens

doi: 10.3390/pharmaceutics14010113

Figure Lengend Snippet: HDM triggered multiple signaling in HNEpC. HNEpC challenged with HDM ( D. farinae + D. pteronyssinus ) (30 μg/mL) induces the expression of several genes related with autophagy (ATG3, ATG5, ATG7, BECLIN-1, and P62), unfolded protein response (UPR) (ATF6, CHOP, and IRE1), and matrix metalloproteinases (MMPs) (MMP8, MMP2, MMP9, MMP3, MMP12, TIMP1, and TIMP2). HDM stressors also induce the expression of senescence (P21, P16, P27, and P53) and inflammation genes (IL-1α, IL-6, and IL-1β) on HNEpC. The treatment with ELVN-34 Na (500 nM) reduces the expression of autophagy, UPR, MMP, senescence (except P53), and inflammation genes induced by HDM extracts. The results showed the averages of three independent experiments. (**** p < 0.0001, NS—not significant).

Article Snippet: In addition, the expression of the following cytokines was analyzed in the supernatant of HNEpC exposed to different allergic inductors: IL-6 (Catalog# 6802, Chondrex) range of detection: (9–600 pg/mL), IL-1β (Catalog# 6805, Chondrex) range of detection: (4–250 pg/mL) IL-8/CXCL8 (Quantikine ELISA Kit, Catalog# D8000C, R&D Systems) range of detection: (31–2000 pg/mL), vascular endothelial growth factor (VEGF) (Catalog# 6810, Chondrex) range of detection: (31–2000 pg/mL), ICAM1(CD54) (ELISA Kit, Catalog# ab100640, Abcam) range of detection: (16–1000 pg/mL), CXCL1/KC/GRO (Catalog# 6825, Chondrex) range of detection: CCL2/MCP-1 (Catalog# 6821, Chondrex) range of detection: (16–1000 pg/mL), and IL-10 (Catalog# 6806, Chondrex) range of detection: (8–500 pg/mL).

Techniques: Expressing

Journal: BMC Gastroenterology

Article Title: Inhibition of TLR4 enhances oxaliplatin chemotherapy sensitivity in esophageal squamous cell carcinoma by suppressing inflammation and glycolysis

doi: 10.1186/s12876-026-04663-2

Figure Lengend Snippet: OXA activated TLR4 signaling in ESCC cells. The cells were treated by OXA (25 µM) for 24 h. A , B . The mRNA expressions of TLR4 and MYD88 in ESCC cell lines and normal esophageal cells were detected by qRT-PCR. C . ICC showed the immunocytochemical activity of NF-κB p65, p-NF-κB p65, COX-2, and MYD88. Scale bar: 50 μm. D . qRT-PCR analysis of mRNA levels of IL-1β, IL-6, COX-2, CXCL5, and CXCL8. *p < 0.05, **p < 0.01, ***p < 0.001 vs. Control group

Article Snippet: Serum concentrations of IL-6 (JL20268, Jonin) and IL-1β (KE10003, Proteintech) were quantified using commercial ELISA kits according to manufacturers’ protocols.

Techniques: Quantitative RT-PCR, Activity Assay, Control

Journal: BMC Gastroenterology

Article Title: Inhibition of TLR4 enhances oxaliplatin chemotherapy sensitivity in esophageal squamous cell carcinoma by suppressing inflammation and glycolysis

doi: 10.1186/s12876-026-04663-2

Figure Lengend Snippet: TLR4 knockout enhances the sensitivity of OXA chemotherapy in ESCC in vivo. A . Number of tumors. B . HE staining of esophageal epithelial tissues. Scale bar: 50 μm. C . Body weight of mice. D , E . the levels of serum IL-1β and IL-6 in mice from different groups were detected by ELISA. F . The immunohistochemical activities of PCNA, CK14, Cyclin D1, COX-2, S100A8 and S100A9 in the esophageal tissue were detected. Scale bar: 100 μm. G , H . The mRNA levels of inflammatory cytokines and glycolysis-related proteins in esophageal tissue were detected by qRT-PCR. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. WT group; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. WT + 4NQO + OXA group

Article Snippet: Serum concentrations of IL-6 (JL20268, Jonin) and IL-1β (KE10003, Proteintech) were quantified using commercial ELISA kits according to manufacturers’ protocols.

Techniques: Knock-Out, In Vivo, Staining, Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Quantitative RT-PCR

Journal: BMC Gastroenterology

Article Title: Inhibition of TLR4 enhances oxaliplatin chemotherapy sensitivity in esophageal squamous cell carcinoma by suppressing inflammation and glycolysis

doi: 10.1186/s12876-026-04663-2

Figure Lengend Snippet: Schematic diagram illustrating the mechanism by which TLR4 inhibition enhances oxaliplatin (OXA) chemosensitivity in esophageal squamous cell carcinoma (ESCC). OXA treatment upregulates TLR4 and its downstream adaptor protein MYD88, which activates the phosphorylation of NF-κB p65. This activation drives two parallel pathways: (1) the inflammatory response, characterized by the upregulation of pro-inflammatory factors such as IL-6, COX-2, and CXCL5; (2) the glycolytic metabolic reprogramming, mediated by the HIF-1α/GLUT1 axis and enhanced expression of glycolytic enzymes including PFKM and LDHB. These two pathways synergistically promote ESCC cell proliferation, migration, and invasion, ultimately reducing OXA chemosensitivity. Inhibition of TLR4 (via genetic knockout, shRNA knockdown, or pharmacological inhibitor TAK-242) or its downstream mediator MYD88 (via shRNA knockdown or inhibitor ST2825) blocks NF-κB p65 phosphorylation, thereby suppressing both the inflammatory response and glycolytic activity. This dual inhibition disrupts the adaptive survival mechanisms of ESCC cells, potentiating the anti-tumor efficacy of OXA

Article Snippet: Serum concentrations of IL-6 (JL20268, Jonin) and IL-1β (KE10003, Proteintech) were quantified using commercial ELISA kits according to manufacturers’ protocols.

Techniques: Inhibition, Phospho-proteomics, Activation Assay, Expressing, Migration, Knock-Out, shRNA, Knockdown, Activity Assay