Mesencephalic cell cultures are a good model to study the vulnerability of dopaminergic neurons and reproduce, in vitro, experimental models of Parkinson's disease. Rotenone associated as an environmental neurotoxin related to PD, is able to provoke dopaminergic neuron degeneration by inhibiting complex I of the mitochondrial respiratory chain and by inducing accumulation of α-synuclein. Recently, rotenone has been described to activate RhoA, a GTPase protein. In the present study we evaluated a possible neuroprotective effect of Rho-inhibitor molecules on rotenone-damaged dopaminergic (DA) neurons obtained from mouse primary mesencephalic cell culture. Our results showed that Clostridium Botulinum C3 toxin (C3) and simvastatin, as RhoA inhibitors, were able to protect DA neurons from rotenone damages. In fact, pretreatment with C3 or simvastatin significantly prevented the reduction of [3H]dopamine uptake, neurites injury and the expression patterns of proteins like α-syn, actin and connexin 43.

中文翻译：

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体外对鱼藤酮治疗的多巴胺能神经元的Rho抑制和神经保护作用。

中脑细胞培养是研究多巴胺能神经元脆弱性并在体外复制帕金森氏病实验模型的良好模型。鱼藤酮是与PD相关的环境神经毒素，它能够通过抑制线粒体呼吸链的复合物I并诱导α-突触核蛋白积聚，从而引起多巴胺能神经元变性。最近，已经描述鱼藤酮激活RhoA，一种GTPase蛋白。在本研究中，我们评估了Rho抑制剂分子对从小鼠原代中脑细胞培养物中获得的鱼藤酮损伤的多巴胺能（DA）神经元的可能的神经保护作用。我们的结果表明，肉毒梭菌C3毒素（C3）和辛伐他汀作为RhoA抑制剂能够保护DA神经元免受鱼藤酮的损害。实际上，