Green Tea Catechin Prevents Hypoxia/Reperfusion-Evoked Oxidative Stress-Regulated Autophagy-Activated Apoptosis and Cell Death in Microglial Cells

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molecular levels influencing a large number of metabolic pathways.

Acute cerebral ischemia/reperfusion injury (ACIR) rat model was used to investigate the effect of spermine on oxidative stress and apoptosis. Sixty healthy and clean male Sprague-Dawley rats were randomly divided into 3 groups: The sham-operated group (n=12), the model group (n=12) and the experiment group (n=36). The experiment group was further divided into 3 subgroups: The SPE-10 group (n=12), the SPE-25 group (n=12) and the SPE-50 group (n=12). Rats in the experimental sub-groups SPE-10, SPE-25 and SPE-50 were injected with 10, 25 and 50 mg/kg of spermine, respectively, one week before the establishment of rat models. Rats in the sham-operated and model groups were injected with 0.9% NaCl solution. We evaluated the effect of spermine on malondialdehyde (MDA) level and superoxide dismutase (SOD) activity using ELISA kits. Bax and Bcl-2 levels were measured using western blot analysis. Our results showed that after spermine injection, MDA levels markedly decreased, while SOD activity increased significantly. The variations in MDA levels and SOD activity were dose (spermine)-dependent. Bax protein levels increased significantly, while Bcl-2 levels decreased significantly after the onset of ACIR injuries. After spermine injection, there was a significant decrease in Bax levels. Bcl-2 levels in these rats markedly increased. The observed decline in Bax levels and the increase in Bcl-2 levels in the experimental groups were dose-dependent. We concluded that spermine protected nerve tissues in rats with ACIR by decreasing the MDA level, increasing SOD activity and modifying the balance between Bax and Bcl-2 proteins.