Key result
Allopurinol treatment prevented oxidative stress, inflammation, and fibrosis in aged rats with isoproterenol-induced myocardial infarction.
Why the study?
Does allopurinol prevent oxidative stress, fibrosis, and myocardial damage in an isoproterenol-induced myocardial infarction aged rat model?
Does allopurinol prevent oxidative stress, fibrosis, and myocardial damage in an isoproterenol-induced myocardial infarction aged rat model?
Allopurinol demonstrates cardioprotective effects in an aged rat model of isoproterenol-induced myocardial infarction by reducing oxidative stress, inflammation, and fibrosis.
Should not yet change practice; leaves open translation of allopurinol cardioprotection from aged rats to humans.
We evaluated the preventive effect of allopurinol on isoproterenol (ISO) induced myocardial infarction in aged rats. Twelve- to fourteen-month-old male Long Evans rats were divided into three groups: control, ISO, and ISO + allopurinol. At the end of the study, all rats were sacrificed for blood and organ sample collection to evaluate biochemical parameters and oxidative stress markers analyses. Histopathological examinations were also conducted to assess inflammatory cell infiltration and fibrosis in heart and kidneys. Our investigation revealed that the levels of oxidative stress markers were significantly increased while the level of cellular antioxidants, catalase activity, and glutathione concentration in ISO induced rats decreased. Treatment with allopurinol to ISO induced rats prevented the elevated activities of AST, ALT, and ALP enzymes, and the levels of lipid peroxidation products and increased reduced glutathione concentration. ISO induced rats also showed massive inflammatory cells infiltration and fibrosis in heart and kidneys. Furthermore, allopurinol treatment prevented the inflammatory cells infiltration and fibrosis in ISO induced rats. In conclusion, the results of our study suggest that allopurinol treatment is capable of protecting heart of ISO induced myocardial infarction in rats probably by preventing oxidative stress, inflammation, and fibrosis.
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Sagor et al. (2015) studied Isoproterenol induced myocardial infarction. Allopurinol vs. Isoproterenol alone and control was evaluated on Oxidative stress markers, inflammatory cell infiltration, and fibrosis. Allopurinol treatment prevented oxidative stress, inflammation, and fibrosis in aged rats with isoproterenol-induced myocardial infarction.
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