Magnesium Gluconate Offers No More Protection than Magnesium Sulphate Following Diffuse Traumatic Brain Injury in Rats

Abstract

Objective: Previous studies have demonstrated that magnesium salts, including the sulphate and chloride forms, are neuroprotective following traumatic brain injury (TBI). Recently, studies in cardiac ischaemia/reperfusion injury have demonstrated that the gluconate salt of magnesium may provide superior protection against oxidative damage and postischaemic dysfunction than MgSO₄. We have therefore compared the efficacy of both MgSO₄ and magnesium gluconate (MgGl₂) on outcome following diffuse TBI in rats.

Methods: Adult male Sprague-Dawley rats were injured using the 2-metre impact acceleration model of diffuse TBI. At 30 min after injury, animals were administered with either 250μmoles/kg i.v. MgSO₄, MgGl₂, or equal volume saline vehicle. Thereafter, animals were assessed for motor and cognitive outcome using the rotarod and Barnes maze, respectively, or their brains removed at 3 days after TBI and used for histological examination.

Results: Treatment with either magnesium salt significantly improved functional outcome as compared to vehicle treated controls. Similarly, treatment with either magnesium salt attenuated the degree of histological dark cell change at 3 days after TBI relative to the vehicle treated animals. There were no significant differences between the magnesium treated groups.

Conclusions: We conclude that MgSO₄ and MgGl₂ are equally neuroprotective following TBI. Our results suggest that MgGl₂ may only be more effective in conditions that produce ischaemia, where high concentrations of reactive oxygen species are generated.

• magnesium salts
• neuroprotection
• traumatic brain injury
• ischaemia
• rat
• reactive oxygen species