Shinan Zhou, Lu Liang, Wenyan Zhong, Jingjing Chen, Li Xiao
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引用次数: 0
Abstract
Introduction: Excessive neuroinflammation resulting from chronic alcohol intake is an important risk factor for central nervous system injury. The aim of this study was to investigate the effect of kaempferol (KAE) on alcohol-induced neural injury and its underlying mechanism.
Methods: C57BL/6 N mice were employed to develop a binge-on-chronic alcohol exposure model, with different doses of KAE as an interventional drug for 6 weeks. Neuronal damage and microglial activation in the brain, as well as colonic tissue damage and serum lipopolysaccharide (LPS) concentrations, were systematically assessed. Additionally, Caco-2 cells were exposed to alcohol to induce intestinal epithelial injury in vitro.
Results: Chronic alcohol exposure let to significant neuronal damage in the cortex and hippocampus of mice. KAE treatment effectively attenuated microglial activation and reduced neuronal damage in the brains of alcohol-exposed mice. Analysis of colonic tissues revealed that KAE administration inhibited miRNA-122a expression, alleviated pathological damage, and enhanced occludin expression, thereby significantly lowing serum LPS concentrations in alcohol-fed mice. In vitro, KAE markedly decreased miRNA-122a expression and enhanced occludin levels in Caco-2 cells treated with alcohol. Furthermore, overexpression of miRNA-122a was found to diminish occludin protein production in Caco-2 cells, which was significantly counteracted by KAE treatment.
Conclusion: KAE treatment enhanced intestinal barrier function to alleviate neuronal damage caused by microglial activation mediated by gut-derived LPS under alcohol expose. This effect of KAE was involved in the enhance of intestinal occludin expression by inhibiting the expression of miRNA-122a. This suggested that KAE had the potential to prevent alcohol-induced neurological damage.
期刊介绍：
NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool.
The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works.
We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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