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Background/Aim. Macroangiopathy is the major cause of death and disability in type 2 diabetic patients. Studies have shown that liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, can protect cardiovascular system by inhibiting chronic inflammation of diabetes. However, a study about the effects of liraglutide on peripheral blood vessels and peripheral blood leukocytes has not been reported yet. The aim of this study was to determine vasculoprotective effect, vascular protection and mechanism of action of liraglutide in addition to its hypoglycemic effect. Methods. A total of 60 hospitalized patients with type 2 diabetes were recruited from December 2013 to December 2014 at the First Affiliated Hospital of Dalian Medical University, PR China. Before the treatment with liraglutide, height and weight were measured to calculate body mass index (BMI). Blood urea nitrogen (BUN) and so on were detected. Homeostasis model assessment of insulin resistance (HOMA-IR) and islet β cell function (HOMA-β) were computed. After applying liraglutide for three months, all indexes were measured again. The effects of liraglutide on these indexes were analyzed by paired sample t-test. Results. After the treatment with liraglutide, values of glycosylated hemoglobin ‒ HbA1c (8.46 ± 1.62 vs. 7.26 ± 1.40%) and 2h postprandial blood glucose ‒ 2hPBG (11.95 vs. 9.6 mmol/L) decreased significantly (p < 0.05). Body weight (87.3 vs. 82.5 kg) and BMI (30.37 vs. 28.63 kg/m2) decreased by 5.5% and 5.7%, respectively (p < 0.05). Also, levels of triglycerides (TG) (2.57 ± 1.54 vs. 1.81 ± 0.70 mmol/L) and LDL-cholesterol (2.92 ± 0.78 vs. 1.89 ± 0.66 mmol/L) reduced significantly (p < 0.05). Ankle-brachial index (ABI) decreased from 1.24 ± 0.10 to 1.14 ± 0.06 cm/s by 8%, while brachial-ankle pulse wave velocity (ba-PWV) decreased from 1,442.15 ± 196.26 to 1,316.85 ± 146.63 cm/s by 8.7%, and both differences were statistically significant (p < 0.001). Conclusion. Liraglutide, with a good hypoglycemic effect, can significantly reduce postprandial blood glucose and HbA1c, but cannot significantly improve fasting plasma glucose, insulin resistance and islet β cell function. It also considerably decreased body weight, BMI and TG. Liraglutide can significantly lower ba-PWV and ABI to protect peripheral blood vessels.

Development of new effective antimicrobial drugs is still a big challenge to date due to microbial infection remains an inevitable problem against human health. In this study, fatty acids extract of Lucilia sericata larvae (LFAs) was obtained and evaluated by gas chromatograph-mass spectrometry (GC-MS), and its antibacterial activity against Staphylococcus aureus (S. aureus) and Streptococcus pneumoniae (S. pneumoniae) was investigated. We found that LFAs exhibited effective antibacterial activity against S. aureus and S. pneumoniae with minimal inhibitory concentrations (MICs) of 125 μg/mL and 100 μg/mL, respectively. The bacterial wall and membrane were the main targets, which was confirmed by fluorescence microscopy, scanning electron microscopy and transmission electron microscopy. Furthermore, a notable anti-biofilm activity against S. aureus and S. pneumoniae was also observed, which was able to both prevent biofilm formation and eradicate mature biofilms of these bacteria. As a promising antibacterial agent, LFAs showed good application prospects in clinical practice. [ABSTRACT FROM AUTHOR]

Fatty acids (FAs) are potential therapeutic agents for cutaneous wound healing; however, the mechanisms underlying this effect have not been clearly defined. In this study, we extracted and characterized FAs from dried Lucilia sericata larvae and investigated the molecular basis by which FAs promote cutaneous wound healing. We first confirmed that FA sodium salts (FASSs) stimulated proliferation, migration, and tube formation of cultured human umbilical vein endothelial cells (HUVECs) in a dose-dependent manner. We then showed that FASSs promoted endothelial-to-mesenchymal transition (EndMT), which plays an important role in stabilizing the neovasculature during angiogenesis. Mechanistically, FASSs up-regulated the expression of angiogenesis-related growth factors, platelet-derived growth factor (PDGF), transforming growth factor-β1 (TGF-β1), and vascular endothelial growth factor A (VEGFA), and activated angiogenesis-related signaling pathways, AKT, ERK, and TGF-β/Smad3. In a rat acute cutaneous-wound model, FAs promoted wound healing. Following treatment, we further found that expression of anti-apoptosis-related factors (c-Myc and Bcl-2) was up-regulated and expression of apoptosis-related factors (p53 and Bad) was down-regulated. Our findings suggest that FAs can promote cutaneous wound healing by inducing angiogenesis, partly by activating AKT, ERK, and TGF-β/Smad3 signaling., Competing Interests: None., (AJTR Copyright © 2020.)