Black chokeberry (Aronia melanocarpa L.) polyphenols attenuate obesity-induced colonic inflammation by regulating gut microbiota and the TLR4/NF-κB signaling pathway in high fat diet-fed rats.

This study investigated the potential benefits of black chokeberry polyphenol (BCP) supplementation on lipopolysaccharide (LPS)-stimulated inflammatory response in RAW264.7 cells and obesity-induced colonic inflammation in a high fat diet (HFD)-fed rat model. Our findings demonstrated that BCP treatment effectively reduced the production of nitric oxide (NO) and pro-inflammatory cytokines (TNF-α, IL-1ß, IL-6, and MCP-1) in LPS-induced RAW264.7 cells and concurrently mitigated oxidative stress by modulating the levels of malondialdehyde (MDA), catalase (CAT), and glutathione peroxidase (GSH-Px) in a dose-dependent manner. Furthermore, BCP supplementation significantly ameliorated HFD-induced obesity, improved glucose tolerance, and reduced systemic inflammation in HFD-fed rats. Notably, BCP treatment suppressed the mRNA expression of pro-inflammatory cytokines and alleviated intestinal barrier dysfunction by regulating the mRNA and protein expression of key tight junction proteins (ZO-1, occludin, and claudin-1), thereby inhibiting colonic inflammation caused by the TLR4/NF-κB signaling pathway. Additionally, BCP treatment altered the composition and function of the gut microbiota, leading to an increase in the total content of short-chain fatty acids (SCFAs), particularly acetic acid, propionic acid, isobutyric acid, and butyric acid. Collectively, our results highlighted the potential of BCP supplementation as a promising prebiotic strategy for treating obesity-induced colonic inflammation.

Modulation of the gut microbiota and lipidomic profiles by black chokeberry (Aronia melanocarpa L.) polyphenols via the glycerophospholipid metabolism signaling pathway.

Black chokeberry (Aronia melanocarpa L.) is rich in polyphenols with various physiological and pharmacological activities. However, the relationship between the modulation effect of black chokeberry polyphenols on obesity and the alteration of lipid metabolism is not clearly understood. This study aimed to investigate the beneficial effects of the black chokeberry polyphenols (BCPs) treatment on the structure of gut microbiota, lipid metabolism, and associated mechanisms in high-fat diet (HFD)-induced obese rats. Here, we found that a high-fat diet promoted body weight gain and lipid accumulation in rats, while oral BCPs supplementation reduced body weight, liver, and white adipose tissue weight and alleviated dyslipidemia and hepatic steatosis in HFD-induced obese rats. In addition, BCPs supplementation prevented gut microbiota dysbiosis by increasing the relative abundance of Bacteroides, Prevotella, Romboutsia, and Akkermansia and decreasing the relative abundance of Desulfovibrio and Clostridium. Furthermore, 64 lipids were identified as potential lipid biomarkers through lipidomics analysis after BCPs supplementation, especially PE (16:0/22:6), PE (18:0/22:6), PC (20:3/19:0), LysoPE (24:0), LysoPE (24:1), and LysoPC (20:0). Moreover, our studies provided new evidence that composition of gut microbiota was closely related to the alteration of lipid profiles after BCPs supplementation. Additionally, BCPs treatment could ameliorate the disorder of lipid metabolism by regulating the mRNA and protein expression of genes related to the glycerophospholipid metabolism signaling pathway in HFD-induced obese rats. The mRNA and protein expression of PPARα, CPT1α, EPT1, and LCAT were significantly altered after BCPs treatment. In conclusion, the results of this study indicated that BCPs treatment alleviated HFD-induced obesity by modulating the composition and function of gut microbiota and improving the lipid metabolism disorder via the glycerophospholipid metabolism signaling pathway.

Protective effect of Pai-Nong-San against AOM/DSS-induced CAC in mice through inhibiting the Wnt signaling pathway / 中国天然药物

Pai-Nong-San (PNS), a prescription of traditional Chinese medicine, has been used for years to treat abscessation-induced diseases including colitis and colorectal cancer. This study was aimed to investigate the preventive effects and possible protective mechanism of PNS on a colitis-associated colorectal cancer (CAC) mouse model induced by azoxymethane (AOM)/dextran sodium sulfate (DSS). The macroscopic and histopathologic examinations of colon injury and DAI score were observed. The inflammatory indicators of intestinal immunity were determined by immunohistochemistry and immunofluorescence. The high throughput 16S rRNA sequence of gut microbiota in the feces of mice was performed. Western blot was used to investigate the protein expression of the Wnt signaling pathway in colon tissues. PNS improved colon injury, as manifested by the alleviation of hematochezia, decreased DAI score, increased colon length, and reversal of pathological changes. PNS treatment protected against AOM/DSS-induced colon inflammation by regulating the expression of CD4

Generation and characterization of dipeptidyl peptidase-IV inhibitory peptides from trypsin-hydrolyzed α-lactalbumin-rich whey proteins.

Dipeptidyl peptidase-IV (DPP-IV) is an enzyme that break down the antidiabetic hormone glucagon-like peptide-1. Therefore, inhibition of DPP-IV could be an effective strategy to treat Type 2 diabetes (T2D). The α-lactalbumin-rich whey protein concentrate was hydrolyzed by trypsin, and the hydrolysates were then fractionated at a semi-preparative scale using a Superdex Gel filtration Chromatography. The peptides were analyzed by using HPLC coupled with tandem mass spectrometry (RP-HPLC-MS/MS), and their Dipeptidyl peptidase-IV inhibitory activity was determined by the enzymatic assay. Among tested fragments, a potent fragment (LDQWLCEKL), with the half-maximal inhibitory concentration (IC50) of 131 µM was obtained. Further analysis shows that the LDQWLCEKL peptide corresponds to the amino acid sequence of f(115-123) in α-lactalbumin. Furthermore, LDQWLCEKL exhibited a typical non-competitive mode of inhibition. The results indicate that α-lactalbumin contains active peptides with DPP-IV inhibitory activity that may be used to prevent and treat T2D.

Study on the molecular mechanism of osteoporosis treated by Epimedium based on network pharmacology / 中国药理学通报

Aim To investigate the potential molecular basis of Epimedium and to clarify the molecular mechanism of Epimedium in the treatment of osteoporosis.Methods The method of network pharmacology was used to determine and screen the known compounds corresponding to Epimedium,and predict the drug-related gene/protein targets,and combined with bioinformatics,the specific target of osteoporosis prevention and treatment of Epimedium was determined,and then the signal pathway enrichment was analysed,the molecular mechanism of Epimedium in treatment of osteoporosis was further explored.Results A total of 130 corresponding compounds were retrieved in the TCMID database from Epimedium.According to the values of OB and DL,23 blood transfusion components were screened,in which 101 targets were obtained using the related target prediction technique.Through the secondary mining of the gene chip of GEO chip database,we obtained a total of 124 significantly different genes.And a total of 355 known target genes closely related to the development of osteoporosis were retrieved in the disease-related database.Using the cytoscape to construct and synthesize the protein-protein interaction network of active ingredients and diseases,221 key genes were screened out by network topological analysis.Using ClueGO analysis,it was shown that Epimedium was directly engaged in the signal pathways involved in the key nodes of osteoporosis,which were mainly related to the direct regulation of bone metabolism,such as Wnt signaling pathway,TGF-β signaling pathway and Notch signaling pathway,and that Epimedium regulated other signal pathways,such as PI3K-Akt signaling pathway,VEGF signaling pathway and thyroid hormone signaling pathway.Conclusions Epimedium has the characteristics of multiple targets and multicomponent in the treatment of osteoporosis,which could not only be directly involved in bone cell differentiation and regulation of the balance of osteogenesis and osteoclasts,but also affect and interfere with the bone microenvironment through other systemic systems,such as circulatory system,nervous system,which is consistent with the current mechanism of treatment of osteoporosis.

Supercritical CO2 fluid extraction of Rosmarinus officinalis and capability of extracts eliminate OH radical / 中国中药杂志

<p><b>OBJECTIVE</b>Supercritical CO2 fluid extraction process of antioxidation active components from Rosmarinus officinalis was studied.</p><p><b>METHOD</b>A new extraction process of components extracted from R. officinalis by supercritical CO2 fluid extraction (SFE-CO2 ) was studied in detail. The capability of that the extract eliminate *OH radical was tested by electron paramagnetic resonance (EPR) technique and spin catch technique.</p><p><b>RESULT AND CONCLUSION</b>With free radical clearance as index, by range and variance analysis, the optimum extraction process conditions were: keeping pressure at 30 MPa and temperature at 75 degrees C for 1 h, in the same time adding alcohol 0.30 mL x g(-1).</p>