Chaturvedi R K, Shukla S, Seth K, Chauhan S, Sinha C, Shukla Y, Agrawal A K
Developmental Toxicology Division, Industrial Toxicology Research Centre, Post Box-80, M.G. Marg Lucknow-226001, India.
Neurobiol Dis. 2006 May;22(2):421-34. doi: 10.1016/j.nbd.2005.12.008. Epub 2006 Feb 9.
In the present study, an attempt has been made to explore the neuroprotective and neuroreparative (neurorescue) effect of black tea extract (BTE) in 6-hydroxydopamine (6-OHDA)-lesioned rat model of Parkinson's disease (PD). In the neuroprotective (BTE + 6-OHDA) and neurorescue (6-OHDA + BTE) experiments, the rats were given 1.5% BTE orally prior to and after intrastriatal 6-OHDA lesion respectively. A significant recovery in d-amphetamine induced circling behavior (stereotypy), spontaneous locomotor activity, dopamine (DA)-D2 receptor binding, striatal DA and 3-4 dihydroxy phenyl acetic acid (DOPAC) level, nigral glutathione level, lipid peroxidation, striatal superoxide dismutase and catalase activity, antiapoptotic and proapoptotic protein level was evident in BTE + 6-OHDA and 6-OHDA + BTE groups, as compared to lesioned animals. BTE treatment, either before or after 6-OHDA administration protected the dopaminergic neurons, as evident by significantly higher number of surviving tyrosine hydroxylase immunoreactive (TH-ir) neurons, increased TH protein level and TH mRNA expression in substantia nigra. However, the degree of improvement in motor and neurochemical deficits was more prominent in rats receiving BTE before 6-OHDA. Results suggest that BTE exerts both neuroprotective and neurorescue effects against 6-OHDA-induced degeneration of the nigrostriatal dopaminergic system, suggesting that possibly daily intake of BTE may slow down the PD progression as well as delay the onset of neurodegenerative processes in PD.
在本研究中,已尝试探讨红茶提取物(BTE)对帕金森病(PD)6-羟基多巴胺(6-OHDA)损伤大鼠模型的神经保护和神经修复(神经挽救)作用。在神经保护(BTE + 6-OHDA)和神经挽救(6-OHDA + BTE)实验中,大鼠分别在纹状体内注射6-OHDA损伤前和损伤后口服1.5%的BTE。与损伤动物相比,BTE + 6-OHDA组和6-OHDA + BTE组在右旋苯丙胺诱导的转圈行为(刻板行为)、自发运动活性、多巴胺(DA)-D2受体结合、纹状体DA和3,4-二羟基苯乙酸(DOPAC)水平、黑质谷胱甘肽水平、脂质过氧化、纹状体超氧化物歧化酶和过氧化氢酶活性、抗凋亡和促凋亡蛋白水平方面均有显著恢复。6-OHDA给药前或给药后进行BTE治疗均可保护多巴胺能神经元,这可通过黑质中存活的酪氨酸羟化酶免疫反应性(TH-ir)神经元数量显著增加、TH蛋白水平升高和TH mRNA表达增加得以证明。然而,在6-OHDA给药前接受BTE的大鼠中,运动和神经化学缺陷的改善程度更为显著。结果表明,BTE对6-OHDA诱导的黑质纹状体多巴胺能系统变性具有神经保护和神经挽救作用,这表明每日摄入BTE可能会减缓PD的进展,并延缓PD神经退行性过程的发生。