Neuroprotective effects of magnesium sulphate evaluated by fluoride resistant acid phosphatase, inorganic phosphate, lactate dehydrogenase and nitric oxide in rats with ischemia

University essay from Uppsala universitet/Institutionen för kvinnors och barns hälsa

Abstract: Brain ischemia events are among the first three mortalities causes in the world associated with high treatments costs and in most cases some degree of permanent functional disability, thus it is necessary with new low cost and effective treatments. In the present study the potential neuroprotective effect of magnesium sulphate was evaluated by quantification of ischemic biomarkers: fluoride resistant acid phosphatase (FRAP), inorganic phosphate (Pi), lactate dehydrogenase (LDH) and nitric oxide (NO) in rats with global ischemia. Adult rats were anaesthetized (sodium thiopental and magnesium sulphate ( (9 animals) or saline solution (NaCl 0,9%) (11 animals) was infused via jugular vein. Cortical sample was extracted 30 minutes after infusion (normoxic condition), thereafter it was induced global ischemia via respiratory arrest caused by jugular administrated muscular relaxant (Flaxedil, 500μL), and 30 minutes after this state a cortical sample of contralateral hemisphere was taken (hypoxia condition). Samples were preserved with proteases inhibitors (PMFS y NaF) and homogenized. Biomarkers were quantified within 24h from the experiment by the following spectroscopic methods: Gomori (FRAP), Ammonium molybdate (Pi), Pyruvate to lactate reduction (LDH) and Griess (NO). FRAP activity was quantified as an inflammatory biomarker for the first time in the cerebral cortex. Global ischemia increased all biomarkers concentrations of the saline group. During normoxia condition magnesium sulphate reduced Pi (P=0,0002) and LDH activity (P=0,001), while during hypoxia it reduces Pi (P= 0,0002) and LDH activity (P=0,03) compared to saline values. These results strongly suggest the cortical neuroprotectiveeffects of magnesium sulphate in global ischemia induced by respiratory arrest, by reduction of cellular acidosis and energetic deficit.

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