Miao sour soup influences serum lipid via regulation of high-fat diet-induced intestinal flora in obese rats.

Obesity is associated with the gut microbiota and has been shown to cause gut microbiota disturbances. Our previous studies have demonstrated that Miao sour soup (SS) contains abundant short-chain fatty acids (SCFAs) which can be used as energy substrates of intestinal flora to selectively stimulate their growth and reproduction. Therefore, we explored whether the intestinal microbiota of rats with high-fat diet-induced obesity could be restored to normal by SS intervention. Male obese rats were divided into five groups randomly after successful modeling of obese rats: normal diet, high-fat diet (HDF), HFD + SS, HFD with antibiotic, and HFD with antibiotic + SS. After 12 weeks of intervention, the weight and serum lipid of obese rats decreased. Furthermore, 16S rRNA analysis showed an imbalance and a decrease in the abundance and diversity of intestinal flora in obese rats, which improved after SS intervention. At the phylum level, Firmicutes increased while Proteobacteria decreased. The composition of the intestinal flora recovered at the genus level, inhibiting the reproduction of pathogenic bacteria, while the levels of SCFA-producing bacteria such as Blautia and Lactococcus and the levels of SCFAs in cecal contents increased. In addition, SS reduced the levels of TNF-α and IL-6 in the intestinal mucosa of obese rats, increased the contents of PYY and GLP-1 in colon tissue, and increased the expression of tight junction protein Occludin and ZO-1 in the intestinal epithelium. Taken together, SS can regulate the intestinal flora of obese rats and improve the intestinal flora to facilitate weight loss and lipid reduction.

Integrative proteomics and metabolomics of Guizhou Miao Sour Soup affecting simple obese rats.

Miao Sour Soup (MSS) is a fermented product from the Qiandongnan region of Guizhou Province, which enrich many beneficial ingredients and is widely consumed in the whole China. Fermented food is beneficial to physical health with the potential positive regulating affection on simple obesity. In this study, we analyzed the mechanism of action of MSS to prevent simple obesity induced by high-fat diet by proteomics and metabolomics. Quantitative proteomics with tandem mass tagging labeling and liquid chromatography-mass spectrometry was used to analyze the changes of liver proteins and metabolites after the MSS intervention. MSS intervention upregulated 33 proteins and 9 metabolites and downregulated 19 proteins and 10 metabolites. Bioinformatics analysis showed that MSS could prevent simple obesity by acting on the PPAR signaling pathway, retinol metabolism, fatty acid ß-oxidation, fatty acid degradation, fatty acid biosynthesis, glycine, serine and threonine metabolism, pyruvate metabolism, citrate cycle (TCA cycle) and other signaling pathways. This study provides new insights into the use of MSS to prevent simple obesity caused by high-fat diets and the search for healthy eating patterns with MSS.

Multi-Scale Superpixel-Guided Structural Profiles for Hyperspectral Image Classification.

Hyperspectral image classification has received a lot of attention in the remote sensing field. However, most classification methods require a large number of training samples to obtain satisfactory performance. In real applications, it is difficult for users to label sufficient samples. To overcome this problem, in this work, a novel multi-scale superpixel-guided structural profile method is proposed for the classification of hyperspectral images. First, the spectral number (of the original image) is reduced with an averaging fusion method. Then, multi-scale structural profiles are extracted with the help of the superpixel segmentation method. Finally, the extracted multi-scale structural profiles are fused with an unsupervised feature selection method followed by a spectral classifier to obtain classification results. Experiments on several hyperspectral datasets verify that the proposed method can produce outstanding classification effects in the case of limited samples compared to other advanced classification methods. The classification accuracies obtained by the proposed method on the Salinas dataset are increased by 43.25%, 31.34%, and 46.82% in terms of overall accuracy (OA), average accuracy (AA), and Kappa coefficient compared to recently proposed deep learning methods.

Assessing the Potential Value and Mechanism of Kaji-Ichigoside F1 on Arsenite-Induced Skin Cell Senescence.

Chronic exposure to inorganic arsenic is a major environmental public health issue worldwide affecting more than 220 million of people. Previous studies have shown the correlation between arsenic poisoning and cellular senescence; however, knowledge regarding the mechanism and effective prevention measures has not been fully studied. First, the associations among the ERK/CEBPB signaling pathway, oxidative stress, and arsenic-induced skin cell senescence were confirmed using the HaCaT cell model. In the arsenic-exposed group, the relative mRNA and protein expressions of ERK/CEBPB signaling pathway indicators (ERK1, ERK2, and CEBPB), cell cycle-related genes (p21, p16INK4a), and the secretion of SASP (IL-1α, IL-6, IL-8, TGF-ß1, MMP-1, MMP-3, EGF, and VEGF) and the lipid peroxidation product (MDA) were significantly increased in cells (P < 0.05), while the activity of antioxidant enzyme (SOD, GSH-Px, and CAT) was significantly decreased (P < 0.05), and an increased number of cells accumulated in the G1 phase (P < 0.05). Further Kaji-ichigoside F1 intervention experiments showed that compared to that in the arsenic-exposed group, the expression level of the activity of antioxidant enzyme was significantly increased in the Kaji-ichigoside F1 intervention group (P < 0.05), but the indicators of ERK/CEBPB signaling pathway, cell cycle-related genes, and SASP were significantly decreased (P < 0.05), and the cell cycle arrest relieved to a certain extent (P < 0.05). Our study provides some limited evidence that the ERK/CEBPB signaling pathway is involved in low-dose arsenic-induced skin cell senescence, through regulating oxidative stress. The second major finding was that Kaji-ichigoside F1 can downregulate the ERK/CEBPB signaling pathway and regulate the balance between oxidation and antioxidation, alleviating arsenic-induced skin cell senescence. This study provides experimental evidence for further understanding of Kaji-ichigoside F1, a natural medicinal plant that may be more effective in preventing and controlling arsenic poisoning.

Effects of Miao sour soup on hyperlipidemia in high-fat diet-induced obese rats via the AMPK signaling pathway.

Hyperlipidemia is a common characteristic of obese animals. Identifying the factors involved in the regulation of dietary lipid metabolism is the most beneficial way to improve health. Miao sour soup (MSS) is a fermented food made from tomato and red pepper that contains lycopene, capsaicin, and organic acids. We conducted this study to investigate the regulatory functions and mechanisms of MSS on the blood lipid levels of high-fat diet-induced obese rats. In our preventive study, rats were fed normal diet (ND1), high-fat diet (HFD1), HFD + 4 g/kg BW MSS (HFD + LS1), and HFD + 8 g/kg BW MSS (HFD + HS1). We found that MSS significantly reduced the body weight and fat accumulation and improved the blood lipid levels of rats. MSS significantly increased the expression of AMP-activated protein kinase-alpha (AMPKα), attenuated the expression of the adipogenic transcription factor sterol regulatory element-binding protein-1c (SREBP-1c), and suppressed the expression of fatty acid synthase (FAS) and acetyl-CoA carboxylase alpha (ACCα), the critical regulators of hepatic lipid metabolism. Additionally, we also conducted a treatment study, and we grouped rats to receive ND2, HFD2, PC2, HFD + LS2, and HFD + HS2 for another 10 weeks. MSS treatment reduced the body weight, fat deposition, and percentage of lipid droplets and regulated the plasma lipid content. MSS significantly increased the expression of AMPK and alleviated the expression of SREBP-1c, ACC, and FAS. Taken together, these findings suggest that MSS prevents and treats hyperlipidemia in obese rats by regulating the AMPK signaling pathway.

Oxymatrine attenuates arsenic-induced endoplasmic reticulum stress and calcium dyshomeostasis in hepatic stellate cells.

BACKGROUND: Oxymatrine is the main bioactive component of Sophora flavescens. It exhibits various biological activities and has been used in various liver diseases, including hepatic fibrosis (HF). Hepatic stellate cells (HSCs) are the primary cell type involved during HF progression. Oxymatrine treatment could suppress the proliferation of HSCs and degrade the extracellular cell matrix (ECM), presumed to be associated with HF. However, the mechanism is still unknown. METHODS: NaAsO2 induces HF in LX2 cells. Oxymatrine was used to treat NaAsO2- induced LX2 cells. Then, the LX2 cell proliferation, apoptosis, ECM secretion protein, oxidative stress index, and intracellular calcium concentration were respectively measured. Furthermore, after knocking down GRP78 [endoplasmic reticulum (ER) chaperone BiP] or overexpressing of SERCA2 (ATPase sarcoplasmic/ER Ca2+ transporting 2) in NaAsO2-induced LX2 cells, we detected the changes in ER stress and calcium homeostasis in LX2 cells. RESULTS: NaAsO2 exposure promoted apoptosis, increased ECM secretion, produced ER stress, and disrupted calcium homeostasis, which could be attenuated by oxymatrine treatment. Furthermore, knockdown of GRP78 to alleviate ER stress, or overexpression of SERCA2 to restore intracellular calcium homeostasis can inhibit the NaAsO2 effect. CONCLUSIONS: Oxymatrine treatment could improve calcium homeostasis and attenuate ER stress to reverse NaAsO2-induced HSC activation and ECM secretion, which are the significant phenotypes of HF. The ER stress and calcium homeostasis may be the therapeutic targets for HF.

Comparative proteomic analysis of fluoride treated rat bone provides new insights into the molecular mechanisms of fluoride toxicity.

Long-term excessive intake of fluoride (F) could lead to chronic fluorosis. To explore the underlying molecular mechanisms, present study is designed to elucidate the effect of fluoride on proteome expression of bone in sodium fluoride (NaF)-treated SD rats. Hematoxylin and eosin (H&E) staining was used to determine the severity of osteofluorosis, and bone samples were submitted for iTRAQ analysis. The results showed that the cortical thickness and trabecular area of femur bone in medium- and high-dose groups were higher than in control group. Contrary to this, trabecular area was reduced in the low-dose group, indicating that the bone mass was increased in medium- and high-dose groups, and decreased in the low-dose group. Thirteen (13), 35, and 34 differentially expressed proteins were identified in low-, medium-, and high-dose group, respectively. The medium- and high-dose groups shared a more similar protein expression pattern. These proteins were mainly associated with collagen metabolism, proteoglycans (PGs), matrix metalloproteinases (MMPs), etc. The results suggested that the effect of NaF on SD rats is in a dose-dependent manner. Some key proteins found here may be involved in affecting the bone tissues and bone marrow or muscle, and account for the complex pathology and clinical symptoms of fluorosis.

iTRAQ-Based Proteomics Analysis of Serum Proteins in Wistar Rats Treated with Sodium Fluoride: Insight into the Potential Mechanism and Candidate Biomarkers of Fluorosis.

Fluorosis induced by exposure to high level fluoride is quite widespread in the world. The manifestations of fluorosis include dental mottling, bone damage, and impaired malfunction of soft tissues. However, the molecular mechanism of fluorosis has not been clarified until now. To explore the underlying mechanisms of fluorosis and screen out serum biomarkers, we carried out a quantitative proteomics study to identify differentially expressed serum proteins in Wistar rats treated with sodium fluoride (NaF) by using a proteomics approach of isobaric tagging for relative and absolute quantitation (iTRAQ). We fed Wistar rats drinking water that had 50, 150, and 250 mg/L of dissolved NaF for 24 weeks. For the experimental duration, each rat was given an examination of the lower incisors to check for the condition of dental fluorosis (DF). By the end of the treatment, fluoride ion concentration in serum and lower incisors were detected. The results showed that NaF treatment can induce rat fluorosis. By iTRAQ analysis, a total of 37 differentially expressed serum proteins were identified between NaF-treated and control rats. These proteins were further analyzed by bioinformatics, out of which two proteins were validated by enzyme-linked immunoadsorbent assays (ELISA). The major proteins were involved in complement and coagulation cascade, inflammatory response, complement activation, defense response, and wound response, suggesting that inflammation and immune reactions may play a key role in fluorosis pathogenesis. These proteins may contribute to the understanding of the mechanism of fluoride toxicity, and may serve as potential biomarkers for fluorosis.