{'fraction_non_alphanumeric': 0.034129692832764506, 'fraction_numerical': 0.017064846416382253, 'mean_word_length': 6.04, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Myeloid differentiation factor 2 inhibitor, 2i‐10, alleviates dendritic spine loss in rats with cardiac ischemia‐reperfusion injury via decreasing brain inflammation

Previous studies have been reported that cardiac ischemia/reperfusion (I/R) injury, which is a life‐threatening cardiovascular event, caused brain damage by provoked brain inflammation. 2i‐10, a cinnamamide derivative, is able to inhibit inflammatory cytokines production through a direct inhibition of myeloid differentiation factor 2 (MD2). However, the effects of 2i‐10 on brain pathologies during cardiac I/R injury have not been investigated. We hypothesized that treatment with 2i‐10 at the onset of reperfusion ameliorates brain damage via reducing brain mitochondrial dysfunction, dendritic spine loss, beta‐amyloid (Aβ) aggregations and inflammatory cytokine levels in the setting of cardiac I/R injury.