Ravisankar Periyasamy, Ravishankar Panneerselvam, Prithviraj Elumalai, Ravindran Rajan
Department of Anatomy, S.R.M. Dental College and Hospital, SRMIST, Ramapuram Campus, Pallikarani, India.
Department of Anatomy, Dr. A. L. Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani, Chennai, Tamil Nadu, India.
Int J Appl Basic Med Res. 2022 Apr-Jun;12(2):103-110. doi: 10.4103/ijabmr.ijabmr_692_21. Epub 2022 May 10.
Parkinson's disease (PD) a neurodegenerative disorder for which no preventive or long term effective treatment strategies are available. Epidemiological studies have failed to identify specific environmental, dietary or lifestyle factors for PD. However oxidative stress in the substantia nigra (SN) and Corpus striatum is the most broadly accepted hypothesis for the etiopathology of PD. Many experiments state the notion that augmentation of neurotrophic factors and glial cell-derived neurotrophic factors, could prevent or halt the progress of neurodegeneration in PD.
The present study was designed to assess the motor behaviour with apomorphine injection and level of enzymatic and non-enzymatic antioxidants after transplantation of Human Amniotic Epithelial (HAE) cells in 2,4,5 trihydroxyphenylethylamine (6-OHDA) lesioned striatum in rats.
Human Amniotic Epithelial (HAE) cells ameliorated 6-OHDA induced changes in rotational behaviour and modulated the antioxidants. 6-OHDA induced neurotoxicity by the generation of free radicals was pronounced by indication of increased Lipid peroxidation (LPO) levels and decrease in antioxidants level. The present result suggest that increased free radicals and the decrease in the antioxidant defence system possibly lead to structural and functional alterations in membrane-related events and play significant role of the 6-OHDA induced neurotoxicity. In HAE cells transplanted animals the level of LPO was significantly reduced in striatum (36%) and moderately reduced (20%) in midbrain of the 6-OHDA lesioned animals.
These alterations were found to be recovered after the HAE cells graft during long term. The 6-OHDA induced neurotoxicity by the generation of free radicals was pronounced by indication of the increased LPO level, decrease in antioxidants and alteration in the dopamine and its metabolites.
帕金森病(PD)是一种神经退行性疾病,目前尚无预防性或长期有效的治疗策略。流行病学研究未能确定PD的特定环境、饮食或生活方式因素。然而,黑质(SN)和纹状体中的氧化应激是PD病因学中最被广泛接受的假说。许多实验表明,增加神经营养因子和胶质细胞源性神经营养因子可以预防或阻止PD中神经退行性变的进展。
本研究旨在评估在大鼠2,4,5-三羟基苯乙胺(6-OHDA)损伤的纹状体中移植人羊膜上皮(HAE)细胞后,阿扑吗啡注射后的运动行为以及酶促和非酶促抗氧化剂的水平。
人羊膜上皮(HAE)细胞改善了6-OHDA诱导的旋转行为变化,并调节了抗氧化剂。6-OHDA通过产生自由基诱导神经毒性,表现为脂质过氧化(LPO)水平升高和抗氧化剂水平降低。目前的结果表明,自由基增加和抗氧化防御系统降低可能导致膜相关事件的结构和功能改变,并在6-OHDA诱导的神经毒性中起重要作用。在移植了HAE细胞的动物中,6-OHDA损伤动物的纹状体中LPO水平显著降低(36%),中脑中度降低(20%)。
长期观察发现,HAE细胞移植后这些改变得以恢复。通过LPO水平升高、抗氧化剂减少以及多巴胺及其代谢产物的改变表明,6-OHDA通过产生自由基诱导神经毒性。