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Phlorizin is a member of the chalcone class of organic compounds and was originally extracted from apples. Intensive studies about phlorizin have been conducted. The aim of this study was to determine the therapeutic effects of phlorizin on diet-induced obese mice and to investigate the underlying mechanism. The results show that phlorizin has a beneficial impact on body weight and fat mass, alleviates lipid metabolism and glucose homeostasis. Brown adipose tissue (BAT) temperature was increased and morphological abnormalities were improved in obese mice after phlorizin treatment. Phlorizin activates the Tyk2/STAT3 signalling pathway, up-regulates the protein expression of UCP1, PPARα, PPARγ, C/EBPβ and PRDM16, as well as increases BAT activity which contributes to antiobesity effects. This study suggests that phlorizin activates the Tyk2/STAT3 signalling pathway to induce thermogenesis in BAT and phlorizin has the therapeutic potential in treating obesity and comorbidity. [ABSTRACT FROM AUTHOR]

Background: Patients with inflammatory bowel disease are at increased risks of developing ulcerative colitis-associated colorectal cancer (CAC). Vitexin can suppress the proliferation of colorectal carcinoma cells in vitro orin vivo. However, different from colorectal carcinoma, CAC is more consistent with the transformation from inflammation to cancer in clinical chronic IBD patients. Therefore, we aim to investigated that vitexin whether possess benefic effects on CAC mice.Purpose: We aimed to determine the beneficial effects of vitexin on CAC mice and reveal its underlying mechanism.Methods: The mouse CAC model was induced by Azoxymethane and dextran sodium sulfate (AOM/DSS) and CAC mice were treated with vitexin. At the end of this study, inflammatory cytokines of IL-1β, IL-6, TNF-α, IL-10 as well as nitric oxide (NO) were detected by kits after long-term treatment of vitexin. Pathological changes and macrophage polarization were determined by H&E and immunofluorescence in adjacent noncancerous tissue and carcinomatous tissue respectively of CAC mice.Results: Our results showed that oral administration of vitexin could significantly improve the clinical signs and symptoms of chronic colitis, relieve colon damage, regulate colonic inflammatory cytokines, as well as suppress tumor incidence and tumor burden. Interesting, vitexin caused a significant increase in serum level of NO and a higher content of NO in tumor tissue. In addition, vitexin significantly decreased M1 phenotype macrophages in the adjacent noncancerous tissue, while markedly up-regulated M1 macrophage polarization in the tumor tissue in the colon of CAC mice.Conclusion: Vitexin can attenuate chronic colitis-associated carcinogenesis induced by AOM/DSS in mice and its protective effects are partly associated with its alternations in macrophage polarization in the inflammatory and tumor microenvironment . [ABSTRACT FROM AUTHOR]

Polysaccharide, as a promising candidate to meet the medication requirement of ulcerative colitis (UC), is increasingly attracting extensive interest. Dendrobium officinale has been widely used to treat gastrointestinal sickness in the clinical treatment of Traditional Chinese Medicine. However, it remains largely unknown whether polysaccharides (DOPS) from Dendrobium officinale can treat UC. The purpose of this paper is to confirm therapeutic action of DOPS to UC and explored its underlying mechanisms. We noted that DOPS could dramatically improve clinical signs and symptoms, decrease mortality, alleviate colonic pathological damage, and reestablish the balance of pro- and anti-inflammatory cytokines in DSS-induced acute UC mice. Moreover, DOPS treatment could also markedly suppress the activation of NLRP3 inflammasome and β-arrestin1 in vivo and in vitro . This study showed that DOPS possesses appreciable therapeutic effect to treat experimental acute UC mice. Its mechanism could be related to inhibition of NLRP3 inflammasome and β-arrestin1 signaling pathways. [ABSTRACT FROM AUTHOR]

Abstract: Aims: Multipotent mesenchymal stromal cells (MSC) have been reported to prevent the development of liver fibrosis and have emerged as a promising strategy for cell-based therapy. However, the underlying therapeutic mechanism remains unclear. Hepatic stellate cells (SC) activation is a pivotal event in the development of liver fibrosis. Main methods: We hypothesized that MSC play an important role in regulating SC proliferation and apoptosis through paracrine mechanisms. To investigate the paracrine interactions between MSC and SC, a co-culture experimental model was developed using human MSC (hMSC) and human SC (hSC). Key findings: We demonstrate that hMSC and hSC both express nerve growth factor (NGF) receptor p75. Results acquired from transwell co-culture experiments using hSC and hMSC showed that hMSC secrete NGF, which enhances hSC apoptosis. Transcription factor nuclear factor kappa B (NF-ΚB) and B cell leukemia-xl (Bcl-xl) take part in the process. Significance: These findings demonstrated that hMSC indirectly modulate activated hSC in vitro via NGF-mediated signaling cascades and provide a potential mechanism of how transplanted MSC are effective in treating liver fibrosis. [Copyright &y& Elsevier]

In the present study, we aimed to investigate the therapeutic effect of Vitexin on inhibiting ethanol-induced liver damage and explore the underling mechanism. In vitro , the injury was induced in LO2 cell by 100 mM ethanol. Cell viability, AST, oxidative stress, inflammation, apoptosis rate, and related gene and protein expressions were assessed. Alcoholic liver injury model was made by intragastric infusion of alcohol for 4 weeks on male KM mice. Liver index, AST, ALT, TC, TG, TP, TBIL in serum and liver pathology were evaluated. Meanwhile, the level of SOD, MDA and TNF-α also were detected by Kits. Quantitative RT-PCR and Western blotting analysis the Sirt1/p53 pathway related gene and protein expressions. In vitro , Vitexin restored cytoactive and inhibited the releasing of AST induced by ethanol in LO2 cell. Vitexin treatment significantly suppressed the elevation of aminotransferase, blood lipid, UA in mice. Vitexin ameliorated liver pathological changes induced by ethanol. Vitexin supplement restored the decrease of Sirt1/Bcl-2 expression, restrained the elevation of caspase3, cleaved caspse-3, p53 and ac-p53 expression in vivo and in vitro. Vitexin has a protective effect against ethanol-induced liver damage, and the underlying mechanism is probably through Sirt1/p53 mediated mitochondrial apoptotic pathway. Vitexin, a flavone C-glycoside in kinds of traditional medicinal plants which is commonly used in treatment of liver disorder, has extensive bioactivities, but the role of vitexin on alcoholic liver injury remains to be elucidated. Here we report that vitexin inhibits the enlargement of the liver, reverses related biochemical indicators, improves mortality and liver pathological changes induced by ethanol in mice. Besides, vitexin can also ameliorate LO2 cell viability and apoptosis rate induced by ethanol. The mechanism underlying vitexin's protective effect on alcoholic liver injury is related with its regulating on Sirt1/p53 mediated mitochondrial apoptotic pathway. Image 1 [ABSTRACT FROM AUTHOR]