Mulberry (Morus multicaulis) branch bark powder have showed effective hypoglycemic activity in our previous research. This study aims to explore the mechanism of protect effect on diabetes mice of mulberry branch bark as food supplement based on non-targeted GC-MS metabolomics’ platform. Animal model of double diabetes was established with high fat diet and Streptozotocin injection. Mice were fed with mulberry branch bark powder (MBBP) for five weeks to study its therapeutic effect. The metabolite feature of diabetes model and treatment group mice were characterized using a gas chromatography-mass spectrometry-based metabolomics, complemented with the biochemical evaluation, histological inspection, immunohistochemistry observations and enzyme protein detection. A panel of endogenous metabolites were revealed that are relevant to disturbed metabolic processes among groups. The serum metabolic profiles were significantly different between the model group and treatment group. The manner of MBBP treatment showed to be significantly dose dependent and 20% MBBP treatment gain a relatively greater benefit than others. The metabolic disorders in model group include enhanced activation of the sorbitol pathway and galactose metabolite, increased activities of gluconeogenesis, fatty acid oxidation, proteins catabolism and attenuated activities of pentose phosphate pathway, glycolysis and aerobic oxidation pathways, internal synthesis of cholesterol, inositol production. MBBP treatment ameliorate these abnormal metabolize as revealed by differential metabolites comparing with that of model mice, such as decreasing the accumulation of ketone body, enhancing NADPH biosynthesis, partially reversing oxidative stress and energy metabolism disturbance. Mulberry branch bark had a re-balancing effect on the disturbed metabolic pathways in the diabetic mice. Based on the metabolic pathways network, oral administration of MBBP could ameliorate the hyperglycemia and hyperlipidemia symptoms in a global scale and restore the abnormal metabolic state to a near normal level in a dose dependent pattern.

Acinetobacter baumannii is an emerging human pathogen that causes hospital-acquired infections. The trend in increased antimicrobial resistance limits the choice of effective antimicrobial agents. The present study reports the resistance to Acinetobacter baumannii and analyzes the associations between antibiotic use and resistance rates at a general hospital between 2010 and 2014. A total of 1,861 isolates were obtained from clinical cultures, accounting for 10.33% of all detected bacteria (1,861/18,016). The strains were mainly from respiratory samples (1,628 isolates, 87.5%) and the intensive care unit (696 isolates, 37.4%). The resistance rates of Acinetobacter baumannii to the majority of antibiotics were >50%, particularly the resistance rate to cefoperazone/sulbactam increased from 47.37 in 2011 to 89.25% in 2014. However, the rates of imipenem and cilastatin sodium decreased from 81.03 to 69.44% due to the antibiotic policy. There were Pearson significant associations between the use of three antibiotics and resistance in Acinetobacter baumannii to this drug, piperacillin/tazobactam (r=0.976, P<0.01), gentamicin (r=0.870, P<0.01) and cefoxitin (r=0.741, P<0.05). Therefore, a combination of drugs should be adopted to treat Acinetobacter baumannii infections. Microbiology laboratory support and surveillance policies are essential to control the emergence of multidrug-resistance Acinetobacter baumannii.

Diabetes mellitus (DM) is an endocrine-metabolic disorder that has limited approaches to treat effectively. Morus alba L., also known as mulberry, is a well-known medicinal plant, and its branch bark has shown hypoglycemic activity. It is rich in antioxidant and anti-inflammatory ingredients. In this study, we used metabolomics combined with network pharmacology to investigate the molecular mechanism and potential key targets of mulberry branch bark powder (MBBP) for treating DM. Serum metabolomics was performed to analyze the differences in metabolites and enrich metabolic pathways. Network pharmacology, based on systems biology tools, was applied to generate the pathway-target-compound network. Integrated analyses were then used to screen for key targets. To verify the obtained key targets, we used a molecular docking method and experimental validation. Our findings revealed that thirty-five endogenous metabolites contributed to the therapeutic impact of MBBP against DM. The analysis of 10 hub genes in the compound-target network partially supported the enrichment of metabolic pathways. Further analysis focused on two compounds (eugenol and mulberrofuran A) and three key targets (NOS2, MAOA, and CYP1A1). This study explores the active compounds of MBBP against DM and provides a novel perspective for improving DM treatment based on key targets.

Mulberrofuran A (MFA), a natural product originally isolated from the root bark of Morus alba L. (Sang-Bai-Pi), is a structurally distinctive mulberry-derived 2-arylbenzofuran bearing a prenyl-related side chain. Although MFA has attracted attention because of its phytochemical uniqueness and reported biological relevance, the available evidence specific to MFA remains limited and fragmented. In addition, pharmacological interpretations are often complicated by the frequent use of indirect evidence derived from structurally related mulberrofuran analogues, other arylbenzofurans, or complex Morus extracts. This review critically summarizes current knowledge on the chemistry, occurrence, and biological relevance of MFA, while explicitly distinguishing direct MFA-specific evidence from indirect and contextual evidence. Available studies suggest that MFA may be associated with antimicrobial activity and modulation of arachidonic acid-related inflammatory pathways, whereas its putative roles in metabolic regulation, cardiovascular protection, antiviral activity, antioxidant effects, and anticancer relevance are currently supported mainly by structurally related compounds or broader mulberry literature rather than robust MFA-specific validation. We further discuss the limitations of the current evidence base, including methodological heterogeneity, incomplete statistical reporting, the lack of pharmacokinetic and toxicity data, and the absence of clinical validation. Rather than establishing MFA as a confirmed therapeutic agent, the available literature supports its consideration as an emerging natural product candidate that warrants rigorous chemical, pharmacological, and translational investigation.