Valproic acid attenuates inflammation of optic nerve and apoptosis of retinal ganglion cells in a rat model of optic neuritis

2017 ◽  
Vol 96 ◽  
pp. 1363-1370 ◽  
Author(s):  
Qiang Liu ◽  
Haining Li ◽  
Juan Yang ◽  
Xiaoyan Niu ◽  
Chunmei Zhao ◽  
...  
Neuroscience ◽  
2012 ◽  
Vol 224 ◽  
pp. 282-293 ◽  
Author(s):  
Z.Z. Zhang ◽  
Y.Y. Gong ◽  
Y.H. Shi ◽  
W. Zhang ◽  
X.H. Qin ◽  
...  

2020 ◽  
Author(s):  
Jian Kang ◽  
Shu-Qing Liu ◽  
Yi-Fan Song ◽  
Meng-Ru Wang ◽  
Yao-Juan Chu ◽  
...  

Abstract Background: Inflammatory demyelination and axonal injury of the optic nerve are hallmarks of optic neuritis (ON), which often occurs in multiple sclerosis and is a major cause of visual disturbance in young adults. Although a high dose of corticosteroids can promote visual recovery, it cannot prevent permanent neuronal damage. Novel and effective therapies are thus required. Given the recently defined capacity of matrine (MAT), a quinolizidine alkaloid derived from the herb Radix Sophorae flavescens, in immunomodulation and neuroprotection, we tested in this study the effect of matrine on rats with experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Results: MAT administration, started at disease onset, significantly suppressed optic nerve infiltration and demyelination, with reduced numbers of Iba1 + macrophages/microglia and CD4 + T cells, compared to those from vehicle-treated rats. Increased expression of neurofilaments, an axon marker, reduced numbers of apoptosis in retinal ganglion cells (RGCs), and reduced numbers of Iba1 + macrophages/microglia and CD4 + T cells were also observed in the retina after MAT treatment. Conclusions: Taken as a whole, our results demonstrate that MAT attenuated inflammation, demyelination and axonal loss in the optic nerve, and protected RGCs from inflammation-induced cell death. MAT may therefore have potential as a novel treatment for this disease that may result in blindness.


2019 ◽  
Author(s):  
Jian Kang ◽  
Shu-Qing Liu ◽  
Yi-Fan Song ◽  
Meng-Ru Wang ◽  
Yao-Juan Chu ◽  
...  

Abstract Background: Inflammatory demyelination and axonal injury of the optic nerve are hallmarks of optic neuritis (ON), which often occurs in multiple sclerosis and is a major cause of blindness in young adults. Although a high dose of corticosteroids can promote visual recovery, it cannot prevent permanent neuronal damage. Novel and effective therapies are thus required. Given the recently defined capacity of matrine (MAT), a quinolizidine alkaloid derived from the herb Radix Sophorae flavescens, in immunomodulation and neuroprotection, we tested in this study the effect of matrine on ON in rats with experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Results: MAT administration, started at disease onset, significantly suppressed optic nerve infiltration and demyelination, with reduced numbers of Iba1+ macrophages/microglia and CD4+ T cells, compared to those from vehicle-treated rats. Increased expression of neurofilaments, an axon marker, and decreased apoptosis in retinal ganglion cells (RGCs) were also observed after MAT treatment. Conclusions: Taken as a whole, our results demonstrate that MAT attenuated inflammation, demyelination and axonal loss in the optic nerve, and protected RGCs from inflammation-induced cell death. MAT may therefore have potential as a novel treatment for this disease that causes blindness.


2020 ◽  
Author(s):  
Jian Kang ◽  
Shu-Qing Liu ◽  
Yi-Fan Song ◽  
Meng-Ru Wang ◽  
Yao-Juan Chu ◽  
...  

Abstract Background: Inflammatory demyelination and axonal injury of the optic nerve are hallmarks of optic neuritis (ON), which often occurs in multiple sclerosis and is a major cause of blindness in young adults. Although a high dose of corticosteroids can promote visual recovery, it cannot prevent permanent neuronal damage. Novel and effective therapies are thus required. Given the recently defined capacity of matrine (MAT), a quinolizidine alkaloid derived from the herb Radix Sophorae flavescens, in immunomodulation and neuroprotection, we tested in this study the effect of matrine on ON in rats with experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Results: MAT administration, started at disease onset, significantly suppressed optic nerve infiltration and demyelination, with reduced numbers of Iba1+ macrophages/microglia and CD4+ T cells, compared to those from vehicle-treated rats. Increased expression of neurofilaments, an axon marker, and decreased apoptosis in retinal ganglion cells (RGCs) were also observed after MAT treatment. Conclusions: Taken as a whole, our results demonstrate that MAT attenuated inflammation, demyelination and axonal loss in the optic nerve, and protected RGCs from inflammation-induced cell death. MAT may therefore have potential as a novel treatment for this disease that causes blindness.


2010 ◽  
Vol 90 (2) ◽  
pp. 254-260 ◽  
Author(s):  
Sebastian Thaler ◽  
Michal Fiedorowicz ◽  
Robert Rejdak ◽  
Tomasz J. Choragiewicz ◽  
Dorota Sulejczak ◽  
...  

2009 ◽  
Vol 29 (4) ◽  
pp. 275-280 ◽  
Author(s):  
Nils-Claudius Gellrich ◽  
Constantin Stuehmer ◽  
Kai-Hendrik Bormann ◽  
Isabella Mücke ◽  
Alexander Schramm ◽  
...  

2019 ◽  
Vol 96 ◽  
pp. 134-139 ◽  
Author(s):  
Dongyan Pan ◽  
Xin Chang ◽  
Mengqiao Xu ◽  
Mingke Zhang ◽  
Shoumei Zhang ◽  
...  

2005 ◽  
Vol 193 (1) ◽  
pp. 163-171 ◽  
Author(s):  
Muriel B. Sättler ◽  
Ricarda Diem ◽  
Doron Merkler ◽  
Iris Demmer ◽  
Ina Boger ◽  
...  

2020 ◽  
pp. 112067212097428
Author(s):  
Lu Li ◽  
Yu Su ◽  
Juejun Liu ◽  
Changzheng Chen

Non-arteritic anterior ischemic optic neuropathy (NAION) is characterized by the progressive and irreversible death of retinal ganglion cells (RGCs) which is caused by the insufficient blood supply to the optic nerve (ON) head. At present, hormone therapy is used to reduce optic edema, followed by nerve nutrition therapy to protect the ON. However, no surgical or medical therapy has proven to be beneficial consistently in treating NAION. Vincamine is an alkaloid extracted from the Apocynaceae Vinca plant. Vincamine and its derivatives acting as cerebral vasodilators can easily cross the blood-brain barrier, improve the metabolism of ischemic tissue and protect the neuron. In this study, we aimed to investigate the potential neuroprotection of Vincamine in the photodynamic induced rat model of NAION (rAION), to evaluate its effects and possible mechanisms. We found that Vincamine can rescue RGC death and reduce the number of apoptotic cells. The protection of Vincamine might play through the PI3K/Akt/eNOS signaling pathway. Therefore, Vincamine can be an effective therapy method for NAION.


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