Kaempferol attenuates retinal ganglion cell death by suppressing NLRP1/NLRP3 inflammasomes and caspase-8 via JNK and NF-κB pathways in acute glaucoma
Autor: | Xiaomin Wu, Tongmei Zheng, Xiuchun Wang, Yiwei Chen, Chao-bin Lin, Fujin Wu |
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Rok vydání: | 2018 |
Předmět: |
Retinal Ganglion Cells
0301 basic medicine genetic structures Cell Survival Inflammasomes Blotting Western Inflammation Pharmacology Real-Time Polymerase Chain Reaction Caspase 8 Antioxidants Article 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine NLR Family Pyrin Domain-Containing 3 Protein medicine Animals Kaempferols Intraocular Pressure Adaptor Proteins Signal Transducing Retina business.industry NLRP1 JNK Mitogen-Activated Protein Kinases NF-kappa B p50 Subunit Glaucoma NF-κB eye diseases Mice Inbred C57BL Disease Models Animal Ophthalmology 030104 developmental biology medicine.anatomical_structure Microscopy Fluorescence Retinal ganglion cell chemistry Reperfusion Injury sense organs Signal transduction medicine.symptom Apoptosis Regulatory Proteins Kaempferol business 030217 neurology & neurosurgery |
Zdroj: | Eye (Lond) |
ISSN: | 1476-5454 0950-222X |
DOI: | 10.1038/s41433-018-0318-6 |
Popis: | Aims or purpose Glaucoma is the leading cause of vision loss and blindness in the world. Elucidating the pathogenesis of glaucoma and developing effective treatment should be the priority. Inflammation and oxidative stress play essential roles in glaucoma pathogeneisis. Kaempferol is a natural flavonol and has anti-inflammatory and anti-oxidative activities. In this study, we explored the potential effects of kaempferol on acute glaucoma. Methods We established the retinal ischemia-reperfusion (I/R) mice model and administrated kaempferol to I/R mice. We monitored the retina thickness change, retinal ganglion cell (RGC) death, caspase-8 and caspase-3 activation, NLRP1/NLRP3 inflammasomes activation, pro-inflammatory cytokines production, and activations of NF-κB and MAPKs signaling pathways. Results Kaempferol prevented retina thickness change and RGC death in I/R mice. The activations of caspase-8, caspase-3, and NLRP1/NLRP3 inflammasome activation were inhibited by kaempferol. Kaempferol prevented pro-inflammatory cytokines productions in I/R mice. The activation of NF-κB and JNK signaling pathways was also inhibited by Kaempferol in I/R mice. Conclusion Kaempferol attenuated retinal ganglion cell death by suppressing NLRP1/NLRP3 inflammasomes and caspase-8 via inhibiting NF-κB and JNK pathways in acute glaucoma. |
Databáze: | OpenAIRE |
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