The American journal of Chinese medicine
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Bladder cancer has a high recurrence rate and requires adjuvant intravesical management after surgery. The use of traditional agents for bladder cancer therapy is constrained by their toxicity and limited efficacy. This emphasizes the need for the development of safer, more effective compounds such as instillation agents. ⋯ Curcumin induces the downregulation of miR-7641 and subsequent upregulation of p16 which is a target of miR-7641 at the post-transcriptional level, which leads to the decreased invasion and increased apoptosis of bladder cancer cells. This is the first report to show a direct effect of curcumin on inducing changes in a miRNA suppressor with direct anticancer consequences in bladder cancer. Our study shows that curcumin may be a candidate agent for the clinical management of non-muscle-invasive bladder cancer.
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Hepatitis C virus (HCV) is recognized as a major causative agent of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Despite rapid progress in the development of direct-acting antivirals (DAA) against HCV infection in recent years, cost-effective antiviral drugs with more affordable prices still need to be developed. In this study, we screened a library of natural compounds to identify natural HCV inhibitors. ⋯ We identified the flavone or flavan-based compounds amentoflavone, 7,4[Formula: see text]-dihydroxyflavanone, and orobol with the inhibition of viral entry, replication, and translation of the HCV life cycle. Amentoflavone and orobol also showed inhibitory effects on resistant-associated variants to the NS5A inhibitor daclatasvir. The results of this study have the potential to benefit patients who are intolerant to the adverse effect of pegylated interferon or who harbor resistant strains refractory to treatment by current direct-acting antiviral agents.
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Na + /H + exchanger 1 (NHE1) plays a vital role in the oncogenesis and development of hepatocellular carcinoma (HCC) and has been regarded as a promising target for the treatment of HCC. Ginsenoside Rg3 (Rg3), a bioactive ginseng compound, is suggested to possess pleiotropic antitumor effects on HCC. However, the underlying mechanisms of Rg3 suppressing HCC remain unclear. ⋯ Moreover, results from in vivo and in vitro studies indicate that Rg3 treatment markedly decreased the expression of EGF, EGF receptor (EGFR), phosphorylated ERK1/2 and HIF-1 α. Conclusively, these findings suggested that NHE1 was stimulated by EGF, and Rg3 could decrease NHE1 expression by integrally inhibiting EGF-EGFR-ERK1/2-HIF- α signal axis in HCC. Together, our evidence indicated that Rg3 was an effective multi-targets antitumor agent for the treatment of HCC.
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[Formula: see text]-coumaric acid ([Formula: see text]-CA) is a common compound found in medicinal herbs, including Bambusae Caulis in Taeniam (BC). It has been used to treat various diseases in China and Korea. Our previous study demonstrated that BC inhibits pulmonary and intestinal inflammation. ⋯ Our results indicated that BC and [Formula: see text]-CA inhibited CS-induced lung inflammation by regulating pro-inflammatory productions such as cytokines, chemokine, protease and NF-[Formula: see text]B. Consequently, these data demonstrated that [Formula: see text]-CA inhibited pulmonary inflammation by suppressing NF-[Formula: see text]B activity, through which pro-inflammatory mediators were regulated. Therefore, [Formula: see text]-CA, which was shown to be a major component of BC, can be considered as a strong therapeutic candidate for treating pulmonary inflammatory diseases.
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Lilium bulbs have long been used as Chinese traditional medicines to alleviate the symptoms of various human inflammatory diseases. However, mechanisms of Lilium bulb-mediated anti-inflammatory activity and the bioactive components in Lilium bulbs remain unknown. In the present study, the anti-inflammatory activity of Lilium bulbs and the underlying mechanism of action were investigated in macrophages using Lilium bulb ethanol extracts (Lb-EE). ⋯ Mechanistic studies in LPS-stimulated RAW264.7 cells revealed that Lb-EE suppressed MyD88- and TRIF-induced NF-[Formula: see text]B transcriptional activation and the nuclear translocation of NF-[Formula: see text]B transcription factors. Moreover, Lb-EE inhibited IKK[Formula: see text]/[Formula: see text]-induced activation of the NF-[Formula: see text]B signaling pathway and IKK inhibition significantly reduced NO production in LPS-stimulated RAW264.7 cells. Taken together, these results suggest that Lb-EE plays an anti-inflammatory role by targeting IKK[Formula: see text]/[Formula: see text]-mediated activation of the NF-[Formula: see text]B signaling pathway during macrophage-mediated inflammatory responses.