Abstract
Accumulating evidence points to a critical role of the brain gut axis as an important paradigm for many central nervous system diseases. Recent studies suggest that propolis has obvious neuroprotective properties and functionality in regulating intestinal bacteria flora, hinting at a potential key effect at both terminals of this axis regulation. However, currently no clear evidence confirms the effects of propolis on alcohol-induced depression. Here, we establish an alcoholic depression model with C57BL/6J mice and demonstrate that treatment with propolis protects against alcohol-induced depressive symptoms by behavioral tests. In addition, propolis attenuates the injury of nerve cells in the hippocampal region and restores the serum levels of brain-derived neurotrophic factor (BDNF) and dopamine (DA) in mice with alcohol-induced depression. Pathology and biotin tracer assays show that propolis repairs the intestinal leakage caused by alcohol. Additionally, propolis treatment increases the expression levels of intestinal intercellular tight junctions’ (TJs’) structural proteins Claudin-1, Occludin and zona occludens-1 (ZO-1), as well as the activation state of the liver kinase B1/AMP-activated protein kinase (LKB1/AMPK) signaling pathway, which is closely related to the intestinal permeability. Furthermore, propolis can reduce the levels of pro-inflammatory, lipopolysaccharide (LPS) and fatty-acid-binding protein 2 (FABP2), suggesting the significance of the inflammatory response in alcoholic depression. Collectively, our findings indicate that propolis exerted an improving effect on alcohol-induced depressive symptoms by ameliorating brain gut dysfunction.
Highlights
Depression, characterized by disrupted mood, along with an array of symptoms of the emotional, motivational, cognitive and physiological domains, is the leading cause of psychiatric disability around the world [1,2]
We aimed to investigate the protective effects of propolis on alcoholinduced depressive symptoms in C57BL/6J mice
Mice in each group were periodically fed on diets, and the body weight and food consumption were monitored for 10 weeks
Summary
Depression, characterized by disrupted mood, along with an array of symptoms of the emotional, motivational, cognitive and physiological domains, is the leading cause of psychiatric disability around the world [1,2]. Organization (WHO), it is estimated that more than 300 million people of all ages suffer from depression, resulting in significant economic and emotional strain on society [3]. Over the past 40 years of research, numerous risk causes for depression have been identified, including both genetic and environmental factors [4,5]. Alcohol abuse is frequently linked to depression and even serves as a serious risk factor for the development of despondent mental diseases [6]. Increasing amounts of evidences show that comorbid depression and problematic alcohol use often co-occur and tremendously enhance suicide-related events [7–11]. Many hypotheses have been proposed to explain the biological mechanism of alcoholic depression, such as short-chain fatty acids [12], intestinal microbiota [13,14] and neuropeptide systems [15], key information about its regulation remains ambiguous [16]
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