The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury
Clinically, acute ischemic symptoms in the eyes are one of the main causes of vision loss, with the associated inflammatory response and oxidative stress being the key factors that cause injury. Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common type of ischemic optic neuropa...
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MDPI AG
2022-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/4/2095 |
| _version_ | 1797479380774027264 |
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| author | Yu-Yau Chou Jia-Ying Chien Jhih-Wei Ciou Shun-Ping Huang |
| author_facet | Yu-Yau Chou Jia-Ying Chien Jhih-Wei Ciou Shun-Ping Huang |
| author_sort | Yu-Yau Chou |
| collection | DOAJ |
| description | Clinically, acute ischemic symptoms in the eyes are one of the main causes of vision loss, with the associated inflammatory response and oxidative stress being the key factors that cause injury. Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common type of ischemic optic neuropathy (ION); however, there are still no effective or safe treatment options to date. In this study, we investigated the neuroprotective effects of n-butylidenephthalide (BP) treatment in an experimental NAION rodent model (rAION). BP (10 mg/kg) or PBS (control group) were administered on seven consecutive days in the rAION model. Rats were evaluated for visual function by flash visual evoked potentials (FVEPs) at 4 weeks after NAION induction. The retina and optic nerve were removed for histological examination after the rats were euthanized. The molecular machinery of BP treatment in the rAION model was analyzed using Western blotting. We discovered that BP effectively improves retinal ganglion cell survival rates by preventing apoptotic processes after AION induction and reducing the inflammatory response through which blood-borne macrophages infiltrate the optic nerve. In addition, BP significantly preserved the integrity of the myelin sheath in the rAION model, demonstrating that BP can prevent the development of demyelination. Our immunoblotting results revealed the molecular mechanism through which BP mitigates the neuroinflammatory response through inhibition of the NF-κB signaling pathway. Taken together, these results demonstrate that BP can be used as an exceptional neuroprotective agent for ischemic injury. |
| first_indexed | 2024-03-09T21:45:02Z |
| format | Article |
| id | doaj.art-7179bd7078c645e2913a835c8600ddfc |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T21:45:02Z |
| publishDate | 2022-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-7179bd7078c645e2913a835c8600ddfc2023-11-23T20:19:50ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-02-01234209510.3390/ijms23042095The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic InjuryYu-Yau Chou0Jia-Ying Chien1Jhih-Wei Ciou2Shun-Ping Huang3Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, TaiwanInstitute of Medical Sciences, Tzu Chi University, Hualien 970, TaiwanDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, TaiwanDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, TaiwanClinically, acute ischemic symptoms in the eyes are one of the main causes of vision loss, with the associated inflammatory response and oxidative stress being the key factors that cause injury. Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common type of ischemic optic neuropathy (ION); however, there are still no effective or safe treatment options to date. In this study, we investigated the neuroprotective effects of n-butylidenephthalide (BP) treatment in an experimental NAION rodent model (rAION). BP (10 mg/kg) or PBS (control group) were administered on seven consecutive days in the rAION model. Rats were evaluated for visual function by flash visual evoked potentials (FVEPs) at 4 weeks after NAION induction. The retina and optic nerve were removed for histological examination after the rats were euthanized. The molecular machinery of BP treatment in the rAION model was analyzed using Western blotting. We discovered that BP effectively improves retinal ganglion cell survival rates by preventing apoptotic processes after AION induction and reducing the inflammatory response through which blood-borne macrophages infiltrate the optic nerve. In addition, BP significantly preserved the integrity of the myelin sheath in the rAION model, demonstrating that BP can prevent the development of demyelination. Our immunoblotting results revealed the molecular mechanism through which BP mitigates the neuroinflammatory response through inhibition of the NF-κB signaling pathway. Taken together, these results demonstrate that BP can be used as an exceptional neuroprotective agent for ischemic injury.https://www.mdpi.com/1422-0067/23/4/2095ischemic optic neuropathyretinal ganglion cellapoptosisn-butylidenephthalideNF-kBneuroinflammation |
| spellingShingle | Yu-Yau Chou Jia-Ying Chien Jhih-Wei Ciou Shun-Ping Huang The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury International Journal of Molecular Sciences ischemic optic neuropathy retinal ganglion cell apoptosis n-butylidenephthalide NF-kB neuroinflammation |
| title | The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury |
| title_full | The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury |
| title_fullStr | The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury |
| title_full_unstemmed | The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury |
| title_short | The Protective Effects of n-Butylidenephthalide on Retinal Ganglion Cells during Ischemic Injury |
| title_sort | protective effects of n butylidenephthalide on retinal ganglion cells during ischemic injury |
| topic | ischemic optic neuropathy retinal ganglion cell apoptosis n-butylidenephthalide NF-kB neuroinflammation |
| url | https://www.mdpi.com/1422-0067/23/4/2095 |
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