Lefter R, Balmus I M, Ciobica A, Antioch Iulia, Ababei D C, Bild W, Hritcu L D, Musteata M, Timofte D, Hogas S
Centre of Biomedical Research, Romanian Academy, Iasi, Romania.
"Alexandru Ioan Cuza" University of Iasi, Department of Exact Sciences and Natural Sciences, Institute of Interdisciplinary Research, Iasi, Romania.
Acta Endocrinol (Buchar). 2023 Jan-Mar;19(1):36-48. doi: 10.4183/aeb.2023.36. Epub 2023 Aug 14.
Recent studies suggested that MPTP could cause gastrointestinal motility deficits additionally to its nonconclusive and controverted effects on the CNS (behavior and brain oxidative stress) in rats. A possible interaction between MPTP typical impairments and magnesium modulatory potential was previously suggested, as magnesium role was described in neuroprotection, gastrointestinal function, and oxidative stress.
To investigate the possible modulatory effect of several magnesium intake formulations ( drinking water) in MPTP neurotoxicity and functional gastrointestinal impairment induction.
Adult male Wistar rats were subjected to 3-week magnesium intake-controlled diets (magnesium depleted food and magnesium enriched drinking water) previously to acute subcutaneous MPTP treatment (30 mg/ kg body weight). Gastrointestinal motility (one hour stool collection test), and behavioral patterns (Y maze task, elevated plus maze test, open field test, forced swim test) were evaluated. Followingly, brain and bowel samples were collected, and oxidative stress was evaluated (glutathione peroxidase activity, malondial-dehyde concentrations).
MPTP could lead to magnesium intake-dependent constipation-like gastrointestinal motility impairments, anxiety- and depressive-like affective behavior changes, and mild pain tolerance defects. Also, we found similar brain and intestinal patterns in magnesium-dependent oxidative stress.
While the MPTP effects in normal magnesium intake could be regarded as not fully relevant in rat models and limited to the current experimental conditions, the abnormalities observed in the affective behavior, gastrointestinal status, pain tolerance, peripheric and central oxidative status could be indicative of the extent of the systemic effects of MPTP that are not restricted to the CNS level, but also to gastro-intestinal system.
最近的研究表明，1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）除了对大鼠中枢神经系统（行为和脑氧化应激）有不确定且有争议的影响外，还可能导致胃肠动力障碍。此前曾提出MPTP典型损伤与镁调节潜力之间可能存在相互作用，因为镁在神经保护、胃肠功能和氧化应激方面的作用已被描述。
研究几种镁摄入配方（饮用水）对MPTP神经毒性和功能性胃肠损伤诱导的可能调节作用。
成年雄性Wistar大鼠在急性皮下注射MPTP（30mg/kg体重）之前，先进行为期3周的镁摄入控制饮食（低镁食物和富镁饮用水）。评估胃肠动力（1小时粪便收集试验）和行为模式（Y迷宫任务、高架十字迷宫试验、旷场试验、强迫游泳试验）。随后，采集脑和肠样本，并评估氧化应激（谷胱甘肽过氧化物酶活性、丙二醛浓度）。
MPTP可导致镁摄入依赖性便秘样胃肠动力障碍、焦虑样和抑郁样情感行为变化以及轻度疼痛耐受缺陷。此外，我们在镁依赖性氧化应激中发现了类似的脑和肠模式。
虽然在正常镁摄入情况下MPTP的作用在大鼠模型中可能被认为不完全相关且限于当前实验条件，但在情感行为、胃肠状态、疼痛耐受、外周和中枢氧化状态中观察到的异常可能表明MPTP的全身效应程度，这些效应不仅限于中枢神经系统水平，还涉及胃肠系统。
