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The effects of retinol oral supplementation in 6-hydroxydopamine dopaminergic denervation model in Wistar rats.
Neurochemistry international ( IF 4.4 ) Pub Date : 2019-02-07 , DOI: 10.1016/j.neuint.2019.02.002 Alice Kunzler 1 , Camila Tiefensee Ribeiro 1 , Juciano Gasparotto 1 , Lyvia Lintzmaier Petiz 2 , Helen Thais da Rosa Silva 1 , Jeferson Delgado da Silva 1 , Rafael Bortolin 3 , Priscila Oliveira de Souza 1 , Fabiano Barreto 4 , Pedro Espitia-Perez 5 , Carlos Eduardo Schnorr 3 , Nauana Somensi 1 , José Cláudio Fonseca Moreira 1 , Daniel Pens Gelain 1
Neurochemistry international ( IF 4.4 ) Pub Date : 2019-02-07 , DOI: 10.1016/j.neuint.2019.02.002 Alice Kunzler 1 , Camila Tiefensee Ribeiro 1 , Juciano Gasparotto 1 , Lyvia Lintzmaier Petiz 2 , Helen Thais da Rosa Silva 1 , Jeferson Delgado da Silva 1 , Rafael Bortolin 3 , Priscila Oliveira de Souza 1 , Fabiano Barreto 4 , Pedro Espitia-Perez 5 , Carlos Eduardo Schnorr 3 , Nauana Somensi 1 , José Cláudio Fonseca Moreira 1 , Daniel Pens Gelain 1
Affiliation
Vitamin A (retinol) is involved in signaling pathways regulating gene expression and was postulated to be a major antioxidant and anti-inflammatory compound of the diet. Parkinson's disease (PD) is a progressive neurodegenerative disorder, characterized by loss of nigral dopaminergic neurons, involving oxidative stress and pro-inflammatory activation. The aim of the present study was to evaluate the neuroprotective effects of retinol oral supplementation against 6-hydroxydopamine (6-OHDA, 12 μg per rat) nigrostriatal dopaminergic denervation in Wistar rats. Animals supplemented with retinol (retinyl palmitate, 3000 IU/kg/day) during 28 days exhibited increased retinol content in liver, although circulating retinol levels (serum) were unaltered. Retinol supplementation did not protect against the loss of dopaminergic neurons (assessed through tyrosine hydroxylase immunofluorescence and Western blot). Retinol supplementation prevented the effect of 6-OHDA on Iba-1 levels but had no effect on 6-OHDA-induced GFAP increase. Moreover, GFAP levels were increased by retinol supplementation alone. Rats pre-treated with retinol did not present oxidative damage or thiol redox modifications in liver, and the circulating levels of TNF-α, IL-1β, IL-6 and IL-10 were unaltered by retinol supplementation, demonstrating that the protocol used here did not cause systemic toxicity to animals. Our results indicate that oral retinol supplementation is not able to protect against 6-OHDA-induced dopaminergic denervation, and it may actually stimulate astrocyte reactivity without altering parameters of systemic toxicity.
中文翻译：
视黄醇口服补充剂对Wistar大鼠6-羟基多巴胺多巴胺能神经支配模型的影响。
维生素A（视黄醇）参与调节基因表达的信号传导途径，并被认为是饮食中的主要抗氧化剂和抗炎化合物。帕金森氏病（PD）是一种进行性神经退行性疾病，其特征是失去了黑色素多巴胺能神经元，涉及氧化应激和促炎性激活。本研究的目的是评估Wistar大鼠视黄醇口服补充剂对6-羟基多巴胺（6-OHDA，每只大鼠12μg）黑质纹状体多巴胺能神经支配的神经保护作用。尽管循环视黄醇水平（血清）未改变，但在28天内补充视黄醇（棕榈酸视黄酯，3000 IU / kg /天）的动物肝脏中的视黄醇含量增加。视黄醇补充不能防止多巴胺能神经元的丢失（通过酪氨酸羟化酶免疫荧光和蛋白质印迹评估）。视黄醇的补充阻止了6-OHDA对Iba-1水平的影响，但对6-OHDA诱导的GFAP增加没有影响。此外，仅通过补充视黄醇可以增加GFAP水平。视黄醇预处理的大鼠在肝脏中未表现出氧化损伤或巯基氧化还原修饰，并且补充视黄醇不会改变TNF-α，IL-1β，IL-6和IL-10的循环水平，表明此处使用的方案不会对动物造成全身毒性。我们的结果表明，口服视黄醇补充剂无法预防6-OHDA诱导的多巴胺能神经支配，
更新日期：2019-02-07
中文翻译：
视黄醇口服补充剂对Wistar大鼠6-羟基多巴胺多巴胺能神经支配模型的影响。
维生素A（视黄醇）参与调节基因表达的信号传导途径，并被认为是饮食中的主要抗氧化剂和抗炎化合物。帕金森氏病（PD）是一种进行性神经退行性疾病，其特征是失去了黑色素多巴胺能神经元，涉及氧化应激和促炎性激活。本研究的目的是评估Wistar大鼠视黄醇口服补充剂对6-羟基多巴胺（6-OHDA，每只大鼠12μg）黑质纹状体多巴胺能神经支配的神经保护作用。尽管循环视黄醇水平（血清）未改变，但在28天内补充视黄醇（棕榈酸视黄酯，3000 IU / kg /天）的动物肝脏中的视黄醇含量增加。视黄醇补充不能防止多巴胺能神经元的丢失（通过酪氨酸羟化酶免疫荧光和蛋白质印迹评估）。视黄醇的补充阻止了6-OHDA对Iba-1水平的影响，但对6-OHDA诱导的GFAP增加没有影响。此外，仅通过补充视黄醇可以增加GFAP水平。视黄醇预处理的大鼠在肝脏中未表现出氧化损伤或巯基氧化还原修饰，并且补充视黄醇不会改变TNF-α，IL-1β，IL-6和IL-10的循环水平，表明此处使用的方案不会对动物造成全身毒性。我们的结果表明，口服视黄醇补充剂无法预防6-OHDA诱导的多巴胺能神经支配，
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