ArticleBiology direct2026
Enhanced neuroprotection effects of transcranial direct current stimulation combined with 6-Gingerol in copper-overloaded traumatic brain injury via mGluR1.
Article in Biology direct, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo investigate the neuroprotective effects and underlying mechanisms of transcranial direct current stimulation (tDCS) combined with 6-Gingerol (6G) in a rat model of traumatic brain injury (TBI) complicated by copper overload, with particular emphasis on microglial polarization and mGluR1 signaling.
methodsA controlled cortical impact (CCI) was used to establish TBI in rats, followed by induction of copper overload via oral administration of copper sulfate. Animals were randomly assigned to sham, TBI, copper-overloaded TBI, and copper-overloaded TBI treated with 6G, tDCS, or their combination, with or without the mGluR1 inhibitor LY367385. Neurological function and cognition were evaluated using the modified neurological severity score (mNSS) and Morris water maze. Brain copper content, oxidative stress markers, and neuronal apoptosis were assessed by biochemical assays, Western blotting, and TUNEL staining. Microglial polarization was examined by immunofluorescence and qRT-PCR, and the involvement of mGluR1 signaling was verified pharmacologically.
resultsCombined tDCS and 6G treatment significantly improved neurological function and spatial learning compared with monotherapy or untreated copper-overloaded TBI. This combination reduced cerebral copper accumulation, attenuated oxidative stress, and decreased neuronal apoptosis. Furthermore, it promoted microglial polarization toward the anti-inflammatory M2 phenotype while suppressing M1-associated inflammatory markers. Inhibition of mGluR1 partially abolished these neuroprotective effects, indicating a critical role of mGluR1 signaling.
conclusiontDCS combined with 6G provides enhanced neuroprotection in copper-overloaded TBI by regulating copper homeostasis, suppressing oxidative stress, promoting microglial M2 polarization, and engaging mGluR1-dependent signaling pathways. These findings suggest a promising combinational therapeutic strategy for TBI complicated by metal dysregulation. CLINICAL TRIAL NUMBER: Not applicable.
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