L-Theanine: Neuroprotective against Trichloroethylene-induced Parkinsons disease hallmarks

Justin Z Y Shen
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Abstract

Trichloroethylene (TCE), a common water pollutant linked to Parkinson’s Disease (PD), induces dopaminergic neurodegeneration. L-Theanine (L-Th) was explored as a potential treatment for TCE-induced PD due to its previously elucidated neuroprotective properties. Cell viability, cytotoxicity, and cell density were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell viability assay (n=8), lactate dehydrogenase (LDH) assay (n=4), and cell image analysis (n=6), respectively. GT1-7 and SK-N-SH cells served as dopaminergic and neuronal cell models, respectively. In GT1-7 cells, L-Th 600 μM diminished TCE 1000 μM-induced cell death and TCE 1000 μM-induced LDH release by 81% (p<0.001) and 38% (p<0.001), respectively, after 48 h. L-Th also did not significantly impact LDH leakage in healthy GT1-7 cells. In SK-N-SH cells, L-Th 600 μM attenuated TCE 100 μM’s neurodegenerative effects by increasing cellular density and cellular area by 118% (p<0.01) and 170% (p<0.001), respectively, after 24 h. L-Th’s mitigation of TCE’s neurotoxic and neurodegenerative effects in dopaminergic neurons can prevent dopaminergic neurodegeneration: linked to PD onset. L-Th’s ability to preserve healthy GT1-7 cells indicates that L-Th not neurotoxic in vitro. This research marks the identification of the first potential treatment for TCE-induced PD. Future investigations should explore the mechanism of L-Th and TCE’s interactions. Keywords: Trichloroethylene, environmental toxin, L-Theanine, Parkinson’s disease, neurodegeneration.
l -茶氨酸:对三氯乙烯诱导的帕金森病特征的神经保护作用
三氯乙烯(TCE)是一种与帕金森病(PD)有关的常见水污染物,可诱导多巴胺能神经变性。l -茶氨酸(L-Th)由于其先前阐明的神经保护特性而被探索作为tce诱导的PD的潜在治疗方法。分别采用3-(4,5-二甲基噻唑-2-酰基)-2,5-二苯基溴化四唑(MTT)细胞活力测定(n=8)、乳酸脱氢酶(n=4)测定(n=4)和细胞图像分析(n=6)评估细胞活力、细胞毒性和细胞密度。GT1-7和SK-N-SH细胞分别作为多巴胺能和神经元细胞模型。在GT1-7细胞中,L-Th 600 μM作用48 h后,TCE 1000 μM诱导的细胞死亡和LDH释放分别减少81% (p<0.001)和38% (p<0.001), L-Th对健康GT1-7细胞LDH泄漏也无显著影响。在SK-N-SH细胞中,L-Th 600 μM在24 h后通过增加细胞密度和细胞面积分别增加118% (p<0.01)和170% (p<0.001)来减弱TCE 100 μM的神经退行性作用。L-Th减轻TCE对多巴胺能神经元的神经毒性和神经退行性作用,可以预防与PD发病相关的多巴胺能神经退行性作用。L-Th保存健康GT1-7细胞的能力表明L-Th在体外无神经毒性。这项研究标志着tce诱导的PD的第一个潜在治疗方法的确定。今后的研究应进一步探讨L-Th和TCE相互作用的机制。关键词:三氯乙烯,环境毒素,l -茶氨酸,帕金森病,神经变性
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