thp 1 cells (Beijing Solarbio Science)
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Thp 1 Cells, supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 98/100, based on 2116 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/thp 1 cells/product/Beijing Solarbio Science
Average 98 stars, based on 2116 article reviews
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1) Product Images from "Triptolide exerts antiviral effects and alleviates influenza A-induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells"
Article Title: Triptolide exerts antiviral effects and alleviates influenza A-induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells
Journal: International Journal of Molecular Medicine
doi: 10.3892/ijmm.2026.5829
Figure Legend Snippet: H1N1 infection affects cell viability, inflammatory cytokine secretion and interactions between HBEpiCs and THP-1 cells. (A) CCK-8 assay revealed that HBEpiC viability decreased in a concentration-dependent manner following H1N1 infection. (B) ELISA revealed that the levels of IL-1β, IL-6, TNF-α, and IL-8 in HBEpiCs decreased with increasing H1N1 infection. (C) CCK-8 assay indicated that supernatants from H1N1-infected HBEpiC cultures reduced the viability of THP-1 cells in a dose-dependent manner. (D) ELISA results suggested that the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-8) in THP-1 cells were decreased following exposure to supernatants from H1N1-infected HBEpiC cultures. (E) Cell adhesion assay revealed that the number of THP-1 cells adhering to HBEpiCs increased with increasing H1N1 concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) Transwell assay suggested that H1N1 infection enhanced the migration capacity of THP-1 cells, with increased migration observed at higher virus concentrations (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; ** P<0.01, *** P<0.001 vs. control. H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; ELISA, enzyme-linked immunosorbent assay; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control; MOI, multiplicity of infection.
Techniques Used: Infection, CCK-8 Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Cell Adhesion Assay, Transwell Assay, Migration, Virus, Standard Deviation, Control
Figure Legend Snippet: Differential activation of AIM2 signaling in THP-1 cells and HBEpiCs following H1N1 infection. (A) RT-qPCR analysis revealed that H1N1 infection did not alter AIM2 mRNA levels in HBEpiCs but markedly increased AIM2 mRNA levels in THP-1 cells. (B) LDH release assay indicated that H1N1 infection did not affect LDH release in HBEpiCs but markedly increased LDH-1 release in THP-1 cells. (C) Dual-immunofluorescence staining demonstrated the formation of ASC-AIM2 complexes in THP-1 cells post-H1N1 infection (scale bar, 10 μ m). (D) Western blot analysis revealed no significant changes in AIM2, caspase-1, or GSDMD protein levels in HBEpiCs following H1N1 infection but increased expression of AIM2, caspase-1 and GSDMD in THP-1 cells following H1N1 infection (E). (F) Flow cytometry analysis revealed no significant cell death in HBEpiCs following infection, (G) whereas THP-1 cells treated with the supernatant from H1N1-infected HBEpiC cultures presented markedly increased cell death compared with the control. The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. control. AIM2, absent in melanoma 2; HBEpiCs, human bronchial epithelial cells; H1N1, influenza A; RT-qPCR, reverse transcription-quantitative PCR; GSDMD, gasdermin D; Con, control; MOI, multiplicity of infection.
Techniques Used: Activation Assay, Infection, Quantitative RT-PCR, Lactate Dehydrogenase Assay, Immunofluorescence, Staining, Western Blot, Expressing, Flow Cytometry, Control, Standard Deviation, Reverse Transcription, Real-time Polymerase Chain Reaction
Figure Legend Snippet: TP modulates the inflammatory response and immune cell activity in H1N1-infected HBEpiCs and THP-1 cells. (A) No significant changes were observed in HBEpiCs treated with various concentrations of TP (5, 10 and 20 nM) following H1N1 infection compared with the control. (B) After TP treatment, the levels of the inflammatory cytokines IL-1β, IL-6, TNF-α and IL-8 in HBEpiCs were markedly lower than those in the untreated group. (C) The viability of THP-1 cells pretreated with H1N1-infected HBEpiC culture supernatant decreased after TP treatment. (D) The levels of IL-1β, IL-6, TNF-α, and IL-8 in THP-1 cells were markedly lower after TP treatment. (E) The adhesion of THP-1 cells to HBEpiCs induced by H1N1 infection decreased in a dose-dependent manner with increasing TP concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) The migration capacity of THP-1 cells was markedly reduced when the supernatant from H1N1-infected HBEpiC cultures was treated with TP (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. control. TP, triptolide; H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control.
Techniques Used: Activity Assay, Infection, Control, Concentration Assay, Migration, Standard Deviation
Figure Legend Snippet: Effects of TP on AIM2 signaling, LDH leakage, and pyroptosis in HBEpiCs and THP-1 cells. (A) RT-qPCR analysis revealed that TP treatment did not alter AIM2 mRNA expression in HBEpiCs but markedly reduced AIM2 mRNA levels in THP-1 cells. (B) TP did not affect the LDH leakage rate in HBEpiCs but markedly reduced LDH leakage in THP-1 cells. (C) Dual-fluorescence staining revealed that TP treatment decreased the formation of ASC-AIM2 complexes in THP-1 cells (scale bar, 10 μ m). (D) Western blot analysis indicated that TP treatment did not markedly affect the expression of these proteins in HBEpiCs. (E) TP treatment reduced the protein expression of AIM2, caspase-1, and GSDMD in THP-1 cells. (F) Flow cytometry revealed no difference in cell death between HBEpiCs treated with 20 nM TP and the control. (G) In THP-1 cells infected with H1N1 and treated with 20 nM TP, a significant reduction in cell death was identified compared with that in the H1N1 infection group. The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. control. TP, triptolide; AIM2, absent in melanoma 2; LDH, lactate dehydrogenase; HBEpiCs, human bronchial epithelial cells; RT-qPCR, reverse transcription-quantitative PCR; H1N1, influenza A; GSDMD, gasdermin D; Con, control.
Techniques Used: Quantitative RT-PCR, Expressing, Fluorescence, Staining, Western Blot, Flow Cytometry, Control, Infection, Standard Deviation, Reverse Transcription, Real-time Polymerase Chain Reaction
Figure Legend Snippet: AIM2 overexpression reverses the immunosuppressive effects of TP in THP-1 cells. (A) Transfection with Ad-AIM2 upregulated the expression of AIM2 compared with that of Ad-NC in THP-1 cells. (B) AIM2 protein levels were elevated in THP-1 cells overexpressing AIM2 compared with control THP-1 cells. (C) In THP-1 cells, AIM2 overexpression increased the LDH leakage rate. (D) AIM2 overexpression reversed the TP-induced reduction in adhesion between THP-1 cells and HBEpiCs (scale bar, 10 μ m). (E) AIM2 overexpression enhanced the migration ability of THP-1 cells compared with that of H1N1-treated control cells and reversed the TP-induced decrease in THP-1 cell migration (scale bar, 50 μ m). (F) AIM2 overexpression reversed the TP-induced reduction in inflammatory cytokine levels. The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. Con; # P<0.05, ## P<0.01, ### P<0.001 vs. Ad-AIM2. AIM2, absent in melanoma 2; TP, triptolide; LDH, lactate dehydrogenase; HBEpiCs, human bronchial epithelial cells; H1N1, influenza A; GSDMD, gasdermin D; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control.
Techniques Used: Over Expression, Transfection, Expressing, Control, Migration, Standard Deviation


