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Wogonin Attenuates Nasal Polyp Formation by Inducing Eosinophil Apoptosis Through HIF-1α and Survivin Suppression
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A5823 - Wogonin Attenuates Nasal Polyp Formation by Inducing Eosinophil Apoptosis Through HIF-1α and Survivin Suppression
Author Block: R. Khalmuratova1, J. Mo2, H. Shin3; 1Seoul National University, Seoul, Korea, Republic of, 2Dept of Otorhinolaryngology, Chonan, Korea, Republic of, 3Department of Pharmacology, Seoul National University, Seoul, Korea, Republic of.
Abstract
Rationale: Chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is an inflammatory sinonasal disorder characterized by eosinophilic inflammation and T-helper 2 skewing. Eosinophil accumulation in sinonasal mucosa comprises a major feature of CRSwNP. Persistent eosinophilic inflammation is related to prolonged eosinophil survival as well as their accumulation in tissues.
Objective: The current study aimed to investigate the effect of the flavone wogonin in nasal polyposis by assessing its ability to induce eosinophil apoptosis in vitro and attenuate eosinophilic CRSwNP in mice.
Methods: Double immunofluorescence, immunohistochemistry, flow cytometry, and immunoblotting were performed to evaluate hypoxia-inducible factor (HIF)-1α, survivin, and apoptotic markers in the human eosinophilic EoL-1 cell line or sinonasal tissues from patients with CRS with or without NPs. Wogonin effects on nasal polypogenesis were investigated in previously developed murine models.
Results: In sinonasal specimens from patients with CRS, HIF-1α and survivin were up-regulated in eosinophils from patients with polyps compared with levels in patients without polyps. Under hypoxia, HIF-1α and survivin expression was up-regulated in EoL-1 cells. Wogonin down-regulated both HIF-1α and survivin in EoL-1 cells. Moreover, overexpression of survivin protected EoL-1 cells against caspase-dependent apoptosis in response to wogonin. In contrast, wogonin did not induce apoptosis in THP-1, RPMI 2650, and HMC-1 cells. Thus, wogonin could induce eosinophil apoptosis in a cell type-specific manner. Moreover, wogonin attenuated nasal polyp formation in a murine model.
Conclusion: Our findings suggest that wogonin could induce caspase-3 activation by suppressing HIF-1α and survivin expression in EoL-1 cells. Further studies regarding novel therapeutic options for CRSwNP targeting eosinophil apoptosis are needed.
Author Block: R. Khalmuratova1, J. Mo2, H. Shin3; 1Seoul National University, Seoul, Korea, Republic of, 2Dept of Otorhinolaryngology, Chonan, Korea, Republic of, 3Department of Pharmacology, Seoul National University, Seoul, Korea, Republic of.
Abstract
Rationale: Chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) is an inflammatory sinonasal disorder characterized by eosinophilic inflammation and T-helper 2 skewing. Eosinophil accumulation in sinonasal mucosa comprises a major feature of CRSwNP. Persistent eosinophilic inflammation is related to prolonged eosinophil survival as well as their accumulation in tissues.
Objective: The current study aimed to investigate the effect of the flavone wogonin in nasal polyposis by assessing its ability to induce eosinophil apoptosis in vitro and attenuate eosinophilic CRSwNP in mice.
Methods: Double immunofluorescence, immunohistochemistry, flow cytometry, and immunoblotting were performed to evaluate hypoxia-inducible factor (HIF)-1α, survivin, and apoptotic markers in the human eosinophilic EoL-1 cell line or sinonasal tissues from patients with CRS with or without NPs. Wogonin effects on nasal polypogenesis were investigated in previously developed murine models.
Results: In sinonasal specimens from patients with CRS, HIF-1α and survivin were up-regulated in eosinophils from patients with polyps compared with levels in patients without polyps. Under hypoxia, HIF-1α and survivin expression was up-regulated in EoL-1 cells. Wogonin down-regulated both HIF-1α and survivin in EoL-1 cells. Moreover, overexpression of survivin protected EoL-1 cells against caspase-dependent apoptosis in response to wogonin. In contrast, wogonin did not induce apoptosis in THP-1, RPMI 2650, and HMC-1 cells. Thus, wogonin could induce eosinophil apoptosis in a cell type-specific manner. Moreover, wogonin attenuated nasal polyp formation in a murine model.
Conclusion: Our findings suggest that wogonin could induce caspase-3 activation by suppressing HIF-1α and survivin expression in EoL-1 cells. Further studies regarding novel therapeutic options for CRSwNP targeting eosinophil apoptosis are needed.
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