Folic acid, as a key source of methyl donor in DNA methylation, has been proved to play a beneficial role in inflammation modulation, usually impaired in alcoholic liver disease (ALD)....

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.

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Garlic oil (GO) is a kind of natural extract extracted from garlic, which has strong antioxidant activity. This study elucidates the protective mechanism of GO against alcohol‐induced high triglyceride levels. Sixty male Sprague Dawley rats were assigned to five groups, including a control group (CON), a model group (MOD) treated with alcohol 56% v/v at 8 ml kg −1 day −1 for 2 weeks then 10 ml kg −1 day −1 for 8 weeks, a low‐dose GO group (GO‐L) given GO at 20 mg kg −1 day −1 , a high‐dose GO group (GO‐H) given GO at 40 mg kg −1 day −1 , and a positive group (POS) given diammonium glycyrrhizinate at 200 mg kg −1 day −1 . The results showed that GO could significantly reduce the serum and liver triglyceride levels caused by alcohol exposure ( p < .05). The GO‐H group significantly reduced MDA level, increased SOD and GSH‐Px levels in serum, liver, and colon ( p < .05), significantly increased the levels of Sirt1 and PGC‐1α proteins and reduced FoxO1 protein level in liver ( p < .05), and significantly increased the levels of ZO‐1 and Claudin1 proteins in the colon compared to the MOD group ( p < .05). The 16S rRNA sequencing showed that the intestinal flora of the GO‐H group was significantly changed compared with the MOD group. In summary, GO has the potential to improve high triglyceride levels in serum and liver induced by alcohol exposure, which may be related to the inhibition of oxidative stress regulation of Sirt1 and its downstream proteins, and to the restoration of the intestinal barrier and intestinal flora.