In this study, we aimed to investigate the effects of carvacrol (CA), a widely used phytochemical having anti-oxidant and neuroprotective effects, on transient receptor potential (TRP) channels in an animal model of Parkinson’s disease (PD). A total of 64 adult male Spraque-Dawley rats were divided into four groups: sham-operated, PD animal model (unilateral intrastriatal injections of 6-hydroxydopamine (6-OHDA), 6 µg/µl), PD + vehicle (dimethyl sulfoxide (DMSO)) treatment, and PD + CA treatment (10 mg/kg, every other day, for 14 days). Half of the brain samples of substantia nigra pars compacta (SNpc) and striatum (CPu) were collected for immunohistochemistry and the remaining half were used for molecular analyses. CA treatment significantly increased the density of dopaminergic neurons immunolabeled with tyrosine hydroxylase and transient receptor potential canonical 1 (TRPC1) channel in the SNpc of PD animals. In contrast, the density of astrocytes immunolabeled with glial fibrillary acetic acid and transient receptor potential ankyrin 1 (TRPA1) channel significantly decreased following CA treatment in the CPu of PD animals. RT-PCR and western blot analyses showed that 6-OHDA administration significantly reduced TRPA1 and TPRPC1 mRNA expression and protein levels in both SNpc and CPu. CA treatment significantly upregulated TRPA1 expression in PD group, while TRPC1 levels did not display an alteration. Based on this data it was concluded that CA treatment might protect the number of dopaminergic neurons by reducing the reactive astrogliosis and modulating the expression of TRP channels in both neurons and astrocytes in an animal model of PD.

在本研究中，我们旨在研究香芹酚 (CA)（一种广泛使用的具有抗氧化和神经保护作用的植物化学物质）对帕金森病 (PD) 动物模型中瞬时受体电位 (TRP) 通道的影响。总共 64 只成年雄性 Spraque-Dawley 大鼠分为四组：假手术组、PD 动物模型（单侧纹状体内注射 6-羟基多巴胺 (6-OHDA)，6 µg/µl）、PD + 载体（二甲基亚砜DMSO)) 治疗，以及 PD + CA 治疗（10 mg/kg，每隔一天，持续 14 天）。收集一半的黑质致密部（SNpc）和纹状体（CPu）脑样本用于免疫组织化学，其余一半用于分子分析。CA 治疗显着增加了 PD 动物 SNpc 中用酪氨酸羟化酶和瞬时受体电位规范 1 (TRPC1) 通道免疫标记的多巴胺能神经元的密度。相反，在PD动物的CPu中进行CA治疗后，用神经胶质原纤维乙酸和瞬时受体电位锚蛋白1（TRPA1）通道免疫标记的星形胶质细胞的密度显着降低。RT-PCR 和蛋白质印迹分析表明，6-OHDA 给药显着降低 SNpc 和 Cpu 中 TRPA1 和 TPRPC1 mRNA 表达和蛋白水平。CA治疗显着上调PD组中TRPA1的表达，而TRPC1水平没有显示出变化。基于这些数据得出的结论是，在PD动物模型中，CA治疗可能通过减少反应性星形胶质细胞增生和调节神经元和星形胶质细胞中TRP通道的表达来保护多巴胺能神经元的数量。