Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro
AIM: To investigate the effect of skullcapflavone II (SCF-II) on the epithelial-mesenchymal transition (EMT) induced by transforming growth factor beta (TGF-β) in human corneal epithelial cells (HCECs), as well as to identify the signaling pathways that may be involved. METHODS: HCECs were cultured...
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Press of International Journal of Ophthalmology (IJO PRESS)
2025-02-01
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| Series: | International Journal of Ophthalmology |
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| Online Access: | http://ies.ijo.cn/en_publish/2025/2/20250202.pdf |
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| author | Meng-Xi Li Zhen Zhang Yue Zhang Fan-Ru Zhao Yu-Fan Li Yu-Fei Dang Yang-Yang Yue Li Li |
| author_facet | Meng-Xi Li Zhen Zhang Yue Zhang Fan-Ru Zhao Yu-Fan Li Yu-Fei Dang Yang-Yang Yue Li Li |
| author_sort | Meng-Xi Li |
| collection | DOAJ |
| description | AIM: To investigate the effect of skullcapflavone II (SCF-II) on the epithelial-mesenchymal transition (EMT) induced by transforming growth factor beta (TGF-β) in human corneal epithelial cells (HCECs), as well as to identify the signaling pathways that may be involved. METHODS: HCECs were cultured in vitro. At a SCF-II (5, 10 µmol/L) dose, cell viability was analysed with a cell counting kit-8 (CCK-8) assay, and cell migration was monitored with wound healing and Transwell migration assays. There were 4 groups: SCF-II, TGF-β, SCF-II+TGF-β and Control. Western blotting and immunofluorescence were performed to show the expression of EMT markers and the translocation of nuclear factor kappa-B (NF-κB) into the nucleus in the 4 groups. RESULTS: Treatment with SCF-II decreased HCEC viability in a dose-dependent manner. A concentration below 10 µmol/L did not present obvious cell toxicity, and survival rates were more than 70% at 48h. Treatment with SCF-II (5 and 10 µmol/L) significantly impeded migration in wound healing and Transwell migration assays (P<0.05), and EMT markers and NF-κB translocation into the nucleus were inhibited. After both TGF-β and SCF-II treatment, the migration of TGF-β-treated HCECs were suppressed by SCF-II (P<0.05). The expression levels of the mesenchymal markers N-cadherin (P<0.05), α-smooth muscle actin (α-SMA; P<0.05) and NF-κB (P<0.05) in both TGF-β- and SCF-II-treated HCECs were lower than those in the HCECs treated with TGF-β alone and higher than those in HCECs treated with SCF-II alone. Immunofluorescence showed that the entry of NF-κB into the nucleus in both TGF-β- and SCF-II-treated HCECs was less than that in the TGF-β-treated HCECs. CONCLUSION: SCF-II inhibit TGF-β-induced EMT in HCECs by potentially regulating the NF-κB signalling pathway. Thus, SCF-II represents a candidate putative therapeutic agent in corneal fibrotic diseases. |
| format | Article |
| id | doaj-art-a82cb6b1b1ef47e3ab344d1908c0b163 |
| institution | Kabale University |
| issn | 2222-3959 2227-4898 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Press of International Journal of Ophthalmology (IJO PRESS) |
| record_format | Article |
| series | International Journal of Ophthalmology |
| spelling | doaj-art-a82cb6b1b1ef47e3ab344d1908c0b1632025-01-16T07:54:35ZengPress of International Journal of Ophthalmology (IJO PRESS)International Journal of Ophthalmology2222-39592227-48982025-02-0118220921510.18240/ijo.2025.02.0220250202Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitroMeng-Xi Li0Zhen Zhang1Yue Zhang2Fan-Ru Zhao3Yu-Fan Li4Yu-Fei Dang5Yang-Yang Yue6Li Li7Yang-Yang Yue and Li Li. The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China. 18792890313@163.com; eyelili@126.comDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China; Xi'an People's Hospital (Xi'an Fourth Hospital), Shaanxi Eye Hospital, Affiliated Xi'an Fourth Hospital, Northwestern Polytechnical University, Xi'an 710000, Shaanxi Province, ChinaDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China; Xi'an People's Hospital (Xi'an Fourth Hospital), Shaanxi Eye Hospital, Affiliated Xi'an Fourth Hospital, Northwestern Polytechnical University, Xi'an 710000, Shaanxi Province, ChinaDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, ChinaDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, ChinaDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, ChinaDepartment of Vascular Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, ChinaDepartment of Ophthalmology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, ChinaAIM: To investigate the effect of skullcapflavone II (SCF-II) on the epithelial-mesenchymal transition (EMT) induced by transforming growth factor beta (TGF-β) in human corneal epithelial cells (HCECs), as well as to identify the signaling pathways that may be involved. METHODS: HCECs were cultured in vitro. At a SCF-II (5, 10 µmol/L) dose, cell viability was analysed with a cell counting kit-8 (CCK-8) assay, and cell migration was monitored with wound healing and Transwell migration assays. There were 4 groups: SCF-II, TGF-β, SCF-II+TGF-β and Control. Western blotting and immunofluorescence were performed to show the expression of EMT markers and the translocation of nuclear factor kappa-B (NF-κB) into the nucleus in the 4 groups. RESULTS: Treatment with SCF-II decreased HCEC viability in a dose-dependent manner. A concentration below 10 µmol/L did not present obvious cell toxicity, and survival rates were more than 70% at 48h. Treatment with SCF-II (5 and 10 µmol/L) significantly impeded migration in wound healing and Transwell migration assays (P<0.05), and EMT markers and NF-κB translocation into the nucleus were inhibited. After both TGF-β and SCF-II treatment, the migration of TGF-β-treated HCECs were suppressed by SCF-II (P<0.05). The expression levels of the mesenchymal markers N-cadherin (P<0.05), α-smooth muscle actin (α-SMA; P<0.05) and NF-κB (P<0.05) in both TGF-β- and SCF-II-treated HCECs were lower than those in the HCECs treated with TGF-β alone and higher than those in HCECs treated with SCF-II alone. Immunofluorescence showed that the entry of NF-κB into the nucleus in both TGF-β- and SCF-II-treated HCECs was less than that in the TGF-β-treated HCECs. CONCLUSION: SCF-II inhibit TGF-β-induced EMT in HCECs by potentially regulating the NF-κB signalling pathway. Thus, SCF-II represents a candidate putative therapeutic agent in corneal fibrotic diseases.http://ies.ijo.cn/en_publish/2025/2/20250202.pdfskullcapflavone iiepithelial-mesenchymal transitiontransforming growth factornuclear factor kappa-bhuman corneal epithelial cells |
| spellingShingle | Meng-Xi Li Zhen Zhang Yue Zhang Fan-Ru Zhao Yu-Fan Li Yu-Fei Dang Yang-Yang Yue Li Li Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro International Journal of Ophthalmology skullcapflavone ii epithelial-mesenchymal transition transforming growth factor nuclear factor kappa-b human corneal epithelial cells |
| title | Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro |
| title_full | Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro |
| title_fullStr | Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro |
| title_full_unstemmed | Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro |
| title_short | Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transition in vitro |
| title_sort | skullcapflavone ii suppresses tgf β induced corneal epithelial mesenchymal transition in vitro |
| topic | skullcapflavone ii epithelial-mesenchymal transition transforming growth factor nuclear factor kappa-b human corneal epithelial cells |
| url | http://ies.ijo.cn/en_publish/2025/2/20250202.pdf |
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