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Background: The effect of soy products on the weight of overweight or obese people is controversial, so we aimed to conduct a systematic review and a meta-analysis of published randomized controlled trials to analyze whether supplementation with soy products can help them to lose weight. Methods: The relevant data before January 2019 in PubMed, Embase and Cochrane Library were searched. A random-effect model was adopted to calculate the weighted average difference of net changes of body weight, body mass index (BMI), body fat percentage, fat mass, waist circumference, etc. Results: A total of 22 trials (870 overweight or obese participants) were reflected in the present meta-analysis. Analysis showed that soy products significantly reduced body weight, BMI, body fat percent and waist circumference in overweight or obese Asian populations (−0.37 kg, P = 0.010; −0.27 kg/m2, P = 0.042; −0.36%, P = 0.032; −0.35 cm, P = 0.049) and more significant effects were observed in non-menopausal women reduced body weight (−0.59 kg, P = 0.041), BMI (−0.59, P = 0.041) and waist circumference (−0.59 cm, P = 0.041) in overweight or obese populations. Conclusion: This meta-analysis showed that soy products have weight loss effects, mainly due to soy protein, isoflavone and soy fiber.

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Inflammation is typically related to dysfunction of the blood-brain barrier (BBB) that leads to early brain injury (EBI) after subarachnoid hemorrhage (SAH). Resolvin D1 (RVD1), a lipid mediator derived from docosahexaenoic acid, possesses anti-inflammatory and neuroprotective properties. This study investigated the effects and mechanisms of RVD1 in SAH. A Sprague-Dawley rat model of SAH was established through endovascular perforation. RVD1was injected through the femoral vein at 1 and 12 h after SAH induction. To further explore the potential neuroprotective mechanism, a formyl peptide receptor two antagonist (WRW4) was intracerebroventricularly administered 1 h after SAH induction. The expression of endogenous RVD1 was decreased whereas A20 and NLRP3 levels were increased after SAH. An exogenous RVD1 administration increased RVD1 concentration in brain tissue, and improved neurological function, neuroinflammation, BBB disruption, and brain edema. RVD1 treatment upregulated the expression of A20, occludin, claudin-5, and zona occludens-1, as well as downregulated nuclear factor-κBp65, NLRP3, matrix metallopeptidase 9, and intercellular cell adhesion molecule-1 expression. Furthermore, RVD1 inhibited microglial activation and neutrophil infiltration and promoted neutrophil apoptosis. However, the neuroprotective effects of RVD1 were abolished by WRW4. In summary, our findings reveal that RVD1 provides beneficial effects against inflammation-triggered BBB dysfunction after SAH by modulating A20 and NLRP3 inflammasome.