“…Consistent with many previous studies, taurine exerted a benificial effect on the viability and proliferation of NSCs [22][23][24][25][26]. Our results clearly demonstrated that taurine treatment (5-20 mM) significantly promoted cell viability by MTT assay (Fig.…”
Section: Discussionsupporting
confidence: 94%
“…2). Of note, NSCs grew normally in culture without taurine, and it was reported that taurine treatment during the first 1.5 h in culture was not sufficient to sustain its effect on increasing BrdU incorporation [12,25,27,28]. This observation suggests that the action of taurine requires a prolonged incubation with cells therefore is not the result of shortterm effects, such as membrane stabilization or activation of membrane-located proliferation receptors [12,29].…”
Cell transplantation of neural stem cells (NSCs) is a promising approach for neurological recovery both structurally and functionally. However, one big obstacle is to promote differentiation of NSCs into neurons and the followed maturation. In the present study, we aimed to investigate the protective effect of taurine on the differentiation of NSCs and subsequent maturation of their neuronal lineage, when exposed to oxygen-glucose deprivation (OGD). The results suggested that taurine (5-20 mM) promoted the viability and proliferation of NSCs, and it protected against 8 h of OGD induced impairments. Furthermore, 20 mM taurine promoted NSCs to differentiate into neurons after 7 days of culture, and it also protected against the suppressive impairments of 8 h of OGD. Consistently, taurine (20 mM) promoted the neurite sprouting and outgrowth of the NSC differentiated neurons after 14 days of differentiation, which were significantly inhibited by OGD (8 h). At D21, the mushroom spines and spine density were promoted or restored by 20 mM taurine. Taken together, the enhanced viability and proliferation of NSCs, more differentiated neurons and the promoted maturation of neurons by 20 mM taurine support its therapeutic application during stem cell therapy to enhance neurological recovery. Moreover, it protected against the impairments induced by OGD, which may highlight its role for a more direct therapeutic application especially in an ischemic stroke environment.
“…Consistent with many previous studies, taurine exerted a benificial effect on the viability and proliferation of NSCs [22][23][24][25][26]. Our results clearly demonstrated that taurine treatment (5-20 mM) significantly promoted cell viability by MTT assay (Fig.…”
Section: Discussionsupporting
confidence: 94%
“…2). Of note, NSCs grew normally in culture without taurine, and it was reported that taurine treatment during the first 1.5 h in culture was not sufficient to sustain its effect on increasing BrdU incorporation [12,25,27,28]. This observation suggests that the action of taurine requires a prolonged incubation with cells therefore is not the result of shortterm effects, such as membrane stabilization or activation of membrane-located proliferation receptors [12,29].…”
Cell transplantation of neural stem cells (NSCs) is a promising approach for neurological recovery both structurally and functionally. However, one big obstacle is to promote differentiation of NSCs into neurons and the followed maturation. In the present study, we aimed to investigate the protective effect of taurine on the differentiation of NSCs and subsequent maturation of their neuronal lineage, when exposed to oxygen-glucose deprivation (OGD). The results suggested that taurine (5-20 mM) promoted the viability and proliferation of NSCs, and it protected against 8 h of OGD induced impairments. Furthermore, 20 mM taurine promoted NSCs to differentiate into neurons after 7 days of culture, and it also protected against the suppressive impairments of 8 h of OGD. Consistently, taurine (20 mM) promoted the neurite sprouting and outgrowth of the NSC differentiated neurons after 14 days of differentiation, which were significantly inhibited by OGD (8 h). At D21, the mushroom spines and spine density were promoted or restored by 20 mM taurine. Taken together, the enhanced viability and proliferation of NSCs, more differentiated neurons and the promoted maturation of neurons by 20 mM taurine support its therapeutic application during stem cell therapy to enhance neurological recovery. Moreover, it protected against the impairments induced by OGD, which may highlight its role for a more direct therapeutic application especially in an ischemic stroke environment.
“…The high glutamate concentration is necessary, because we used the RGC-5 cell line and not primary RGCs. 15 RGC-5 cells are much more insensitive than primary RGCs, and therefore the concentrations of different drugs found (like in our study 9 mg/mL CSA) cannot be translated to primary cells or in-vivo situations. Therefore, also no conclusions about a possible immunosuppressant or toxic effect of CSA for the found CSA concentration in an in-vivo situation can be drawn.…”
Section: Discussionmentioning
confidence: 75%
“…15,36 However, a comparison between the results has to be interpreted with caution, because the experimental settings were different in each study.…”
Section: Discussionmentioning
confidence: 99%
“…16,[21][22][23] Furthermore, many neuroprotective substances that showed a neuroprotective effect on RGC-5 cells were also neuroprotective on primary RGCs. 15,17,19,[24][25][26][27][28] Therefore, and because of the lack of other cell lines that might better suit to analyze the potential neuroprotective properties of CSA against excitotoxicity in the RGCs, we chose this cell line. Furthermore, we just recently published two papers that focused on the redifferentiation of RGC-5 cells using Staurosporine and Trichostatin-A (TSA) and the induction of apoptosis.…”
CSA can effectively protect RGC-5 cells against glutamate-induced excitotoxicity. Therefore, CSA should be tested in further experiments to evaluate its potential as a neuroprotective substance against RGC disorders.
After introduction of vitreoretinal surgery more than 40 years ago, further development of the procedure involved a continuous reduction of potential toxic effects by irrigating solutions, endoillumination or mechanical manipulation. Recently, additional efforts were made to prevent neurodegeneration via pharmacological intervention. Taurine as additive for irrigating solutions can be considered as an example for neuroprotectants in vitreoretinal surgery. Approval of neuroprotective agents demands an increased effort for preclinical and clinical evaluation. To date, only few neuroprotective substances are used in clinical routine in the context of vitreoretinal surgery, however, experimental data suggest a high potential of various neuroprotective agents. The following article gives an overview of current neuroprotective approaches feasible for vitreoretinal surgery and a critical analysis of their clinical relevance.
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