Abstract
•It down-regulated BDNF protein expression, GSH level, and SOD activity.•Vitamin E and Lactobacillius plantarum ameliorated the previous signs.
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.
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).
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 withLTB; and the fifth group was treated with VE and LTB. All treatments were given daily along with MC for fourteen days.
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.
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.