Guzmán David Calderón, Herrera Maribel Ortiz, Brizuela Norma Osnaya, Mejía Gerardo Barragán, Olguín Hugo Juárez, Peraza Armando Valenzuela
Laboratorio de Neurociencias, Instituto Nacional de Pediatría (INP), Mexico.
Laboratorio de Bacteriología Experimental, INP, Mexico.
Auton Neurosci. 2017 Dec;208:113-116. doi: 10.1016/j.autneu.2017.11.001. Epub 2017 Nov 3.
Hypertension causes neuronal damage and apoptosis in the brain. Diazoxide is a drug used in the treatment of hypertension however, its effect on 5-hydroxyindole acetic acid (5-HIAA) and dopamine amines in adult animal models remains unclear. The purpose of this study was to determine the effect of oligoelements on 5-HIAA and dopamine in the brain of adult rats treated with diazoxide METHODS: Male Fisher rats (weight 250g) were treated as follows: Group I, NaCl 0.9% (control); group II, tracefusin® (1.5mL/rat); group III, diazoxide (20mg/rat) and group IV, tracefusin® (1.5mL/rat)+diazoxide (20mg/rat). All doses were intraperitoneally administered on daily basis for four consecutive days. After the last administration, the brain of the animals was obtained and dissected in cortex, hemispheres (striatum) and cerebellum/medulla oblongata to measure the levels of 5-HIAA, dopamine, lipid peroxidation and total ATPase activity through validated methods.
Dopamine and 5-HIAA levels decreased significantly in the group that received trace elements and diazoxide in the hemisphere regions, while in cerebellum/medulla oblongata, dopamine levels increased significantly in the groups that received diazoxide alone in. Lipid peroxidation in all brain regions increased significantly in the groups that received trace elements and diazoxide. ATPase dependent of calcium and magnesium decreased in the groups that received diazoxide alone or combined with trace elements in cerebellum/medulla oblongata regions.
The present results suggest that the use of trace elements and diazoxide alters metabolism of dopamine and 5-HIAA amines. Free radicals may be involved in this effect.
高血压会导致大脑中的神经元损伤和凋亡。二氮嗪是一种用于治疗高血压的药物，然而，其对成年动物模型中5-羟吲哚乙酸（5-HIAA）和多巴胺胺的影响仍不清楚。本研究的目的是确定微量元素对用二氮嗪治疗的成年大鼠大脑中5-HIAA和多巴胺的影响。方法：将雄性费希尔大鼠（体重250g）按以下方式处理：第一组，0.9%氯化钠（对照组）；第二组，Tracefusin®（1.5mL/只大鼠）；第三组，二氮嗪（20mg/只大鼠）；第四组，Tracefusin®（1.5mL/只大鼠）+二氮嗪（20mg/只大鼠）。所有剂量均连续四天每天腹腔注射。最后一次给药后，获取动物的大脑并在皮质、半球（纹状体）和小脑/延髓进行解剖，通过经过验证的方法测量5-HIAA、多巴胺、脂质过氧化和总ATP酶活性水平。
在半球区域接受微量元素和二氮嗪的组中，多巴胺和5-HIAA水平显著降低，而在小脑/延髓中，单独接受二氮嗪的组中多巴胺水平显著升高。在接受微量元素和二氮嗪的组中，所有脑区的脂质过氧化均显著增加。在小脑/延髓区域，单独接受二氮嗪或与微量元素联合使用的组中，钙和镁依赖性ATP酶降低。
目前的结果表明，微量元素和二氮嗪的使用会改变多巴胺和5-HIAA胺的代谢。自由基可能参与了这种作用。
