LE3 .A278 2015

2015

Wilson, Brian

Acadia University

Bachelor of Science

Honours

Biology

Biology

Stroke is one of the leading causes of death and disability worldwide. Previous research suggests that relaxin peptide hormones protect the brain against ischemic and reperfusion-induced damage in a rat experimental model of stroke. Both nitric oxide (NO) levels and superoxide dismutase (SOD) enzyme activities were investigated in cultured rat brain slices to determine if NO signalling mediates the activity of relaxin-3, a form of relaxin expressed at high levels in the brain. It was hypothesized that treatment with H3 relaxin, the human version of relaxin-3, would decrease NO levels in rat brain tissue under oxygen- and glucose-deprived conditions by upregulating SOD enzyme activity. Brains from 10 day old rats were isolated, sliced coronally at the hypothalamic level and cultured for 2 weeks at 37ºC prior to treatment. Brain slices were subjected to one of the following treatments: oxygenated media with glucose (normoxic control), oxygen and glucose deprived (OGD) media (OGD control) and OGD media with either H3 relaxin, H3 relaxin with a RXFP3 receptor antagonist or a chimeric relaxin-3/insulin-5 peptide (R3/I5) for 1 hour and then returned to culture with fresh culture media for an hour. Subsequently, brain tissues were either stained with propidium iodide (PI) or used in a NO or SOD assay. PI positive cell counts suggest that OGD conditions resulted in greater cellular damage compared to normoxic controls. Treatments with both relaxin ligands and R3/I5 significantly reduced this damage. Tissue NO levels did not vary with treatment. However, SOD activity decreased in tissue treated with H3 relaxin or R3/I5. Perhaps relaxin-3 is initiating protective mechanisms in neural cells which indirectly reduce the formation of free radicals thus reducing SOD activity.

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https://scholar.acadiau.ca/islandora/object/theses:1211