Datasets of Figure 1-4 and 16S rRNA sequencing raw data

Published: 11 April 2020| Version 1 | DOI: 10.17632/b75k6sxknr.1
Contributor:
Hao Wang

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Datasets for our study: Metformin inhibits pro-inflammatory macrophages in atherosclerotic apolipoprotein E-/- mice by suppressing microbial LPS/TLR4/NF-κB axis via restoring gut microbiota. Atherosclerosis (AS) is closely associated with chronic low-grade inflammation and gut dysbiosis. Metformin (MET) presents pleiotropic benefits for the control of chronic metabolic diseases. However, the exact impact and associated mechanism of MET intervention on gut bacteria and inflammation of atherosclerosis remains largely unknown. In the present study, ApoE deficient (ApoE-/-) mice were randomly allocated into atherosclerosis model group (AS) and AS+MET group. After 11 weeks of intervention, mice were euthanized and associated microbial community and inflammation indications were respectively investigated. Results showed that pathological plague lesion in aorta was attenuated after MET administration using oil red O staining, Masson’s trichrome staining and hematoxylin and eosin (HE) staining. Moreover, MET intervention rectified gut dysbiosis by reducing the relative abundance of Firmicutes, the ratio of Firmicutes to Bacteroidetes, Proteobacteria, Romboutsia, as well as elevating Bacteroidetes, Akkermansia and Bifidobacterium levels. Subsequently, microbial plasma lipopolysaccharide (LPS) level was lower in AS+MET group. Pro-inflammatory tumor necrosis factor (TNF)-α and interleukin (IL)-6 were decreased, while IL-1β and anti-inflammatory IL-10 showed no significant difference. Moreover, MET treatment suppressed F4/80+ infiltrated macrophages and lowered associated TLR-4, NF-κB and TNF-α expression in aorta. 1. Datasets of Figure 1-4. Fig. 1. Metformin ameliorated pathological lesion in atherosclerotic ApoE-/- mice. (A) The schematic diagram of the study. (B) Representative sections of the valve area of the aortic root of the heart were stained with Oil Red O, Masson’s trichrome and Hematoxylin and Eosin; quantitative analysis as lesion area/total area (%) shown in Oil red O staining. Fig. 2. Metformin rectified gut dysbiosis and improved associated plasma LPS level. (A) Observed-species index and PCoA analysis showing difference in terms of species in fecal samples. (B) Relative abundance of microbial species at the phylum and genus levels. (C) Determination of plasma lipopolysaccharide (LPS) levels. Fig. 3. Metformin reduced plasma pro-inflammatory cytokines. Plasma of mice from two groups were collected respectively for detection of TNF-α (A), IL-1β (B), IL-6 (C) and IL-10 (D) concentrations using flow CBA kit. Fig. 4. Metfomin inhibited inflammatory macrophages in atherosclerosis. (A) After obtaining cell suspensions from aorta root of atheroclerotic ApoE-/- mice, F4/80+ macrophages were detected by flow cytometry. (B) After isolation of macrophages, TNF-ɑ, NF-κB and TLR-4 expression were determined by western blot. **P<0.001, ***P<0.0001. 2. 16S rRNA sequencing raw data: 5 samples in AS group and 5 samples in AS+MET group

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