Combination of vitamin E and Lactobacillius plantarum reverses mercuric chloride-induced neurotoxicity: Implication of BDNF, CREB and MAPK proteins expressions

Abstract

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.