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Research Paper

Astragaloside IV suppresses histamine-induced inflammatory factors and mucin 5 subtype AC overproduction in nasal epithelial cells via regulation of inflammation-related genes

ORCID Icon &
Pages 6045-6056 | Received 06 Jul 2021, Accepted 04 Aug 2021, Published online: 05 Sep 2021

Figures & data

Table 1. Primer sequences for quantitative real-time RNA

Figure 1. Effect of histamine, and AS-IV on cell viability of nasal epithelial cells. Chemical structure of AS-IV (a). Effect of histamine on cell viability of nasal epithelial cells (b). Effect of AS-IV on cell viability of nasal epithelial cells (c). Effect of His + AS-IV on cell viability of nasal epithelial cells (d). The results were expressed as the mean ± SD of three independent experiments

Figure 1. Effect of histamine, and AS-IV on cell viability of nasal epithelial cells. Chemical structure of AS-IV (a). Effect of histamine on cell viability of nasal epithelial cells (b). Effect of AS-IV on cell viability of nasal epithelial cells (c). Effect of His + AS-IV on cell viability of nasal epithelial cells (d). The results were expressed as the mean ± SD of three independent experiments

Figure 2. AS-IV inhibited His-evoked inflammatory cytokine production in nasal epithelial cells. The levels of IL-6 (a), IL-8 (b), MCP-1 (c), IL-1β (d), GM-CSF (e), and eotaxin (f) were assayed by ELISA. The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 2. AS-IV inhibited His-evoked inflammatory cytokine production in nasal epithelial cells. The levels of IL-6 (a), IL-8 (b), MCP-1 (c), IL-1β (d), GM-CSF (e), and eotaxin (f) were assayed by ELISA. The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 3. AS-IV suppressed His-evoked MUC5AC overproduction in nasal epithelial cells. The contents of MUC5AC were assayed using ELISA. The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 3. AS-IV suppressed His-evoked MUC5AC overproduction in nasal epithelial cells. The contents of MUC5AC were assayed using ELISA. The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 4. Volcano plot showing DEGs between two groups (A, B, and C). Green, gray, and red dots in the Volcano plot showed significantly downregulated genes, insignificantly DEGs, upregulated genes, respectively. The DEGs with fold change ≥ 2.0 and p < 0.05 and are shown

Figure 4. Volcano plot showing DEGs between two groups (A, B, and C). Green, gray, and red dots in the Volcano plot showed significantly downregulated genes, insignificantly DEGs, upregulated genes, respectively. The DEGs with fold change ≥ 2.0 and p < 0.05 and are shown

Figure 5. Heatmap diagram indicating that the common DEGs in the three groups (a). Red and yellow squares in the heatmap showed mRNAs with up-regulated and down-regulated expression levels, respectively. KEGG pathway analyses of the overlapping genes (b)

Figure 5. Heatmap diagram indicating that the common DEGs in the three groups (a). Red and yellow squares in the heatmap showed mRNAs with up-regulated and down-regulated expression levels, respectively. KEGG pathway analyses of the overlapping genes (b)

Figure 6. Enrichment pathway of KEGG in NF-KAPPA B signaling pathway

Figure 6. Enrichment pathway of KEGG in NF-KAPPA B signaling pathway

Figure 7. Validation of RNA-SEQ results using quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 7. Validation of RNA-SEQ results using quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 8. Suppression of the NF-κB signaling pathway decreased His-evoked inflammatory cytokine response in nasal epithelial cells. The effect of NF-κB inhibitor (NF-κBi) on His-evoked secretion of IL-6, IL-8, MCP-1, IL-1β, GM-CSF, and eotaxin (a). The effect of NF-κBi on His-evoked mRNA expression of IL-6, IL-8, MCP-1, and IL-1β (b). The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Figure 8. Suppression of the NF-κB signaling pathway decreased His-evoked inflammatory cytokine response in nasal epithelial cells. The effect of NF-κB inhibitor (NF-κBi) on His-evoked secretion of IL-6, IL-8, MCP-1, IL-1β, GM-CSF, and eotaxin (a). The effect of NF-κBi on His-evoked mRNA expression of IL-6, IL-8, MCP-1, and IL-1β (b). The results were expressed as the mean ± SD of three independent experiments. #P < 0.01 vs. control group, *P < 0.01 vs. His group

Data Availability Statement

The datasets generated for this study are available on request to the corresponding author.