Long Nie

With the UC incidence increasing worldwide, it is of great importance to prevent and treat UC. However, efficient treatment options for UC are relatively limited. Due to the potentially serious adverse effects of existing drugs, there is an increasing demand for alternative candidate resources from natural and functional foods. Astragalin (AG) is a type of anti-inflammatory flavonoid, with Moringa oleifera and Cassia alata being its main source. In this study, we investigated the therapeutic effects of AG in mice with dextran sulfate sodium (DSS)-induced colitis. Our results suggested that AG treatment reduced the weight loss and disease activity index (DAI), prevented colon shortening and alleviated colonic tissue damage. AG treatment reduced the expression of proinflammatory cytokines and related mRNAs (such as TNF-α, IL-6 and IL-1β), inhibited the colonic infiltration of macrophages and neutrophils, ameliorated metabolic endotoxemia, and improved intestinal mucosal barrier function (expression levels of mRNAs such as ZO-1, occludin and Muc2 were increased). Western blotting analysis revealed that AG downregulated the NF-κB signaling pathway. Moreover, AG treatment partially reversed the alteration of gut microbiota in the colitic mice mainly by increasing the abundance of potentially beneficial bacteria (such as Ruminococcaceae) and decreasing the abundance of potentially harmful bacteria (such as Escherichia-Shigella). Ruminococcaceae and Enterobacteriaceae (Escherichia-Shigella) were thought to be the key groups for AG to improve UC. Therefore, AG might exert a good anti-UC effect through Microbiota/LPS/TLR4/NF-kB-related pathways in mice. The results of this study revealed the anti-inflammatory effect and mechanism of AG and provide an important reference for studying the mechanism of natural flavonoids in preventing inflammation-driven diseases.

Moringa oleifera Lam. is an essential herb used for the treatment of inflammation, diabetes, high blood pressure, and other diseases. In this study, phenolic extracts of M. oleifera leaves were obtained and analyzed. The results showed that the main identifiable phenols were astragalin, chlorogenic acid, isoquercitrin, kaempferitrin, luteolin, quercetin, and rutin. The effects of M. oleifera polyphenol extract (MOPE) on experimental colitis induced by 3% dextran sulfate sodium (DSS) were investigated. The results showed that oral administration of MOPE significantly alleviated the symptoms of DSS‐induced colitis. MOPE significantly reduced weight loss, the disease activity index, colon shortening, and mucosal damage. In addition, MOPE attenuated the infiltration of CD3 + T cells, CD177 + neutrophils, and F4/80 + macrophages and significantly inhibited the secretion of IL‐6 and TNF‐ α . After the MOPE administration, the expression of proteins associated with the NF‐ κ B signaling pathway changed. Specifically, compared with that of the DSS group, the protein expression of NF‐ κ B p65 and p‐I κ B α was downregulated, and the expression of I κ B α was upregulated. This study revealed the anti‐inflammatory effects and mechanisms of MOPE in the colon, indicating its potential use in preventing inflammation‐driven diseases.

Lung cancer is one of the most common types of malignancy in humans and is a leading cause of cancer-related deaths among men and women worldwide. Aberrantly expressed microRNAs in non-small cell lung cancer (NSCLC) contribute to tumor occurrence and development as either tumor suppressors or promoters. MicroRNA-379 (miR‑379) is dysregulated in several types of human cancer. However, its expression pattern, role and underlying mechanism in NSCLC progression and metastasis are poorly understood. In this study, assay of reverse transcription-quantitative polymerase chain reaction showed that miR‑379 was downregulated in both NSCLC tissue and cell lines. Low miR‑379 expression in NSCLC tissues was significantly correlated with TNM stage and lymph node metastasis. In addition, functional experiments revealed that restoring the expression of miR‑379 inhibited cell proliferation, migration and invasion of NSCLC. The insulin-like growth factor receptor-1 (IGF‑1R) was identified as a direct target of miR‑379 in NSCLC. IGF‑1R was highly expressed in NSCLC tissues and inversely correlated with miR‑379 expression. Downregulation of IGF‑1R had tumor suppressive roles similar to that of miR‑379 overexpression on NSCLC cell proliferation, migration and invasion. Moreover, the upregulation of IGF‑1R effectively rescued the tumor suppressive roles induced by miR‑379 overexpression in NSCLC. The resumption of the expression of miR‑379 inhibited the activation of AKT and ERK signaling pathways in NSCLC. These findings suggested that miR‑379 acts as a tumor suppressor in NSCLC by directly targeting IGF‑1R and indirectly regulating AKT and ERK signaling pathways. miR‑379 provides novel therapeutic targets for the treatment of patients with this disease.

BACKGROUND: The aim of this study was to test the effect of TNF484 on cell proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells. MATERIALS AND METHODS: Various doses (0, 1, 10, 50, and 100 nM) of TNF484 were applied to the HepG2 and Bel7402 cells, and cell proliferation was measured by using 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide assay after 72 h. Cell migration rate was measured using the xCELLigence system, and the cell invasion ability was examined by the three-dimensional spheroid BME cell invasion assay. The expression level of ADAM17 was also measured with RT-PCR. RESULTS: With the treatment of TNF484, the cell proliferation of HepG2 and Bel7402 cells was inhibited in a dose-dependent manner. Moreover, under TNF484 treatment, the cell migration rate as well as cell invasion ability of the HepG2 and Bel7402 cells were suppressed. CONCLUSION: TNF484 could inhibit the cell proliferation, migration, and invasion of some HCC cell lines, making it a potential therapeutic option for liver cancer treatment.