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Fig. 7 | Journal of Inflammation

Fig. 7

From: Soluble epoxide hydrolase deficiency attenuates airway inflammation in COPD via IRE1α/JNK/AP-1 signaling pathway

Fig. 7

The interaction of sEH and ER stress in CSE-induced inflammatory factor secretion and macrophage migration in BEAS-2B cells. (A-E) Pretreatment with ERS inhibitor-TUDCA, IRE1 inhibitor- KIRA6, or JNK inhibitor-SP600125, the protein expression of IRE1α, p-IRE1α, sEH, JNK and p-JNK in BEAS-2B cells after stimulation with CSE. (F-H) qRT-PCR evaluating the effect of TUDCA, KIRA6, and SP600125 on the secretion of IL-6, IL-8, and TNF-α in BEAS-2B cells after stimulation with CSE. (I-K) ELISA analysis of the effect of TUDCA, KIRA6, and SP600125 on the secretion of IL-6, IL-8, and TNF-α in BEAS-2B cells after stimulation with CSE. (L) Transwell assay was performed to detect the migration ability of THP-1 in each group. (M) Statistical result of THP-1 cell migration. (N) Statistical result of cell morphological changes. Data represent the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001

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