Mercury is the third most hazardous heavy metal and its toxicity causes a severe health risk through unfavorable detrimental pathological and biochemical effects. Mercury is widely found in many ecological and certain occupational settings.

Objectives

The aim of this study is to elucidate the neuroprotective role of vitamin E (VE) and Lactobacillus plantarum (LTB) either alone or in combination against a toxic sublethal dose of Mercuric chloride (MC).

Methods

First group served as a normal control group; rats from the second group were intoxicated with (5 mg/kg MC once daily); the third group was treated with VE; the fourth group was treated with LTB; and the fifth group was treated with VE and LTB. All treatments were given daily along with MC for fourteen days.

Results

The results of the current study confirmed that MC prompted an elevation in serum TNF-α, IL-6 and brain lipid peroxides, protein expression of mitogen-activated protein kinase (MAPK) and mRNA expression of Bax and caspase-3 level as well as DNA degradation. However, Brain-derived neurotrophic factor (BDNF) and cAMP response element-binding (CREB) protein expressions, GSH level and SOD activity were down-regulated. The intake of LTB and/or VE along with MC intoxication significantly mitigated the alteration in all the previous parameters. Moreover, histopathological analysis of brain sections confirmed that MC-induced brain injury and LTB or VE alone or together were capable of ameliorating brain artitechture.

Conclusions

The combination of LTB and VE was an effective therapy in the management of MC-induced neuroioxicity and this combination can be considered a useful therapeutic candidate against brain injury induced by MC. BDNF, MAPK and CREB protein expressions are implicated in MC -induced brain injury and its treatment.

中文翻译：

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维生素E和植物乳杆菌的组合可逆转氯化汞诱导的神经毒性：BDNF，CREB和MAPK蛋白表达的意义

汞是第三大危险重金属，其毒性通过不利的有害病理和生化作用导致严重的健康风险。在许多生态和某些职业环境中广泛发现汞。

目标

这项研究的目的是阐明维生素E（VE）和植物乳杆菌（LTB）单独或组合使用对有毒的亚致死剂量氯化汞（MC）的神经保护作用。

方法

第一组作为正常对照组。第二组大鼠中毒（每天一次，每次5 mg / kg MC）；第三组接受VE治疗；第四组接受LTB治疗；第五组接受VE和LTB治疗。每天与MC一起接受所有治疗，持续14天。

结果

本研究的结果证实，MC促使血清TNF-α，IL-6和脑脂质过氧化物，丝裂原激活蛋白激酶（MAPK）的蛋白表达以及Bax和caspase-3水平的mRNA表达升高。 DNA降解。然而，脑源性神经营养因子（BDNF）和cAMP反应元件结合（CREB）蛋白表达，谷胱甘肽水平和SOD活性被下调。LTB和/或VE的摄入以及MC中毒显着减轻了所有先前参数的改变。此外，对脑切片的组织病理学分析证实，MC诱发的脑损伤以及单独或一起使用LTB或VE能够改善脑动脉。

结论

LTB和VE的组合是一种有效的治疗MC引起的神经毒性的方法，该组合可被视为对抗MC诱导的脑损伤的有效治疗候选物。BDNF，MAPK和CREB蛋白表达与MC诱发的脑损伤及其治疗有关。