The Effects of Carvacrol on Transient Receptor Potential (TRP) Channels in an Animal Model of Parkinson's Disease.

IF 2.9 3区 医学 Q2 NEUROSCIENCES
Neurotoxicity Research Pub Date : 2023-12-01 Epub Date: 2023-07-15 DOI:10.1007/s12640-023-00660-5
Tülay Akan, Yasemin Aydın, Orhan Tansel Korkmaz, Emel Ulupınar, Faruk Saydam
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Abstract

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.

Abstract Image

香芹酚对帕金森病动物模型瞬时受体电位通道的影响
在这项研究中,我们旨在研究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——香芹酚(CA)对帕金森病(PD)动物模型中瞬时受体电位(TRP)通道的影响。将64只成年雄性Spraque-Dawley大鼠分为4组:假手术组、PD动物模型组(单侧腔内注射6-羟多巴胺(6- ohda), 6µg/µl)、PD +载药组(二甲基亚砜(DMSO))、PD + CA组(10 mg/kg,每隔一天,共14 d)。取大鼠大脑致密质部(SNpc)和纹状体(CPu)各一半进行免疫组织化学分析,其余一半进行分子分析。CA处理显著增加PD动物SNpc中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。相比之下,CA处理后PD动物CPu中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细胞密度显著降低。RT-PCR和western blot分析显示,6-OHDA处理显著降低了SNpc和CPu中TRPA1和TPRPC1 mRNA的表达和蛋白水平。CA处理显著上调PD组TRPA1表达,而TRPC1水平未发生改变。由此可见,CA处理可能通过减少反应性星形胶质细胞形成和调节神经元和星形胶质细胞中TRP通道的表达来保护PD动物模型中多巴胺能神经元的数量。
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来源期刊
Neurotoxicity Research
Neurotoxicity Research 医学-神经科学
CiteScore
7.70
自引率
5.40%
发文量
164
审稿时长
6-12 weeks
期刊介绍: Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes. Published papers have focused on: NEURODEGENERATION and INJURY Neuropathologies Neuronal apoptosis Neuronal necrosis Neural death processes (anatomical, histochemical, neurochemical) Neurodegenerative Disorders Neural Effects of Substances of Abuse NERVE REGENERATION and RESPONSES TO INJURY Neural Adaptations Neurotrophin mechanisms and actions NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION Excitatory amino acids Neurotoxins, endogenous and synthetic Reactive oxygen (nitrogen) species Neuroprotection by endogenous and exogenous agents Papers on related themes are welcome.
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