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Neuroprotective Effects of Thymoquinone in Acrylamide-Induced Peripheral Nervous System Toxicity Through MAPKinase and Apoptosis Pathways in Rat
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Neuroprotective Effects of Thymoquinone in Acrylamide-Induced Peripheral Nervous System Toxicity Through MAPKinase and Apoptosis Pathways in Rat
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Neuroprotective Effects of Thymoquinone in Acrylamide-Induced Peripheral Nervous System Toxicity Through MAPKinase and Apoptosis Pathways in Rat
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Journal Article
Neuroprotective Effects of Thymoquinone in Acrylamide-Induced Peripheral Nervous System Toxicity Through MAPKinase and Apoptosis Pathways in Rat
2019
Overview
Acrylamide (ACR) is extensively used in industrial areas and has been demonstrated to induce neurotoxicity via oxidative stress and apoptosis. In this study, we assessed the probable protective effects of thymoquinone (TQ), an active constituent of Nigella sativa, against ACR-induced neurotoxicity. ACR (50 mg/kg, i.p., for 11 days) and TQ (2.5, 5 and 10 mg/kg, i.p., for 11 days) were administered to rats. On 12th day, gait score was examined and rats were sacrificed. Malondialdehyde (MDA) and reduced glutathione (GSH) contents were determined in sciatic nerve. Furthermore, western blotting was conducted. The exposure of rats to ACR caused severe gait disabilities. The MDA and GSH contents were increased and decreased, respectively. ACR decreased P-ERK/ERK ratio and myelin basic protein (MBP) content, but significantly increased P-JNK/JNK, P-P38/P38, Bax/Bcl-2 ratios and caspase 3 and 9 levels. Concurrently administration of TQ (5 and 10 mg/kg) with ACR, prevented gait abnormalities and meaningfully reduced MDA and elevated the GSH contents. Furthermore, TQ (5 mg/kg) elevated the P-ERK/ERK ratio and MBP content while reduced the P-JNK/JNK, P-P38/P38 ratios and apoptotic markers. MAP kinase and apoptosis signaling pathways were involved in ACR-induced neurotoxicity in rat sciatic nerve and TQ significantly reduced ACR neurotoxicity. TQ afforded neuroprotection, in part, due to its anti-oxidative stress and anti-apoptotic mechanisms.
