Berberine (BBR) is an isoquinoline alkaloid isolated from various types of plants, including those from the Berberidaceae, Ranunculaceae, and Papaveraceae families. It has long been used in traditional Chinese medicine for treating diarrhea and gastrointestinal disorders. The medicinal properties of BBR include antimicrobial, anti-inflammatory, antioxidative, lipid-regulatory, and antidiabetic actions. Importantly, the efficacy of BBR against cancers has been assessed in several experimental studies and clinical trials. Gastrointestinal (GI) cancers are a group of the most prevalent cancers worldwide that are associated with high morbidity and mortality, and their associated mortality has been increasing over the years. Thus, GI cancers have become a burden to the patients and health care systems. This review summarizes the cellular and molecular mechanisms underlying the therapeutic effects of BBR and explores its potential preventive and therapeutic applications against GI cancers.

A folate-polyethylene glycol-chitosan derivative was synthesized and its structure was characterized. An optimal perfluorooctyl bromide nanocore template was obtained via utilizing the ultrasonic emulsification method combining with orthogonal design. The targeted nanoparticles containing targeted shell of folate-polyethylene glycol-chitosan derivative and perfluorooctyl bromide nanocore template of ultrasound imaging were prepared successfully by exploiting layer-by-layer self-assembly as contrast agent for ultrasound. Properties of the novel perfluorooctyl bromide nanoparticle were extensively studied by Dynamic Light Scattering and Transmission Electron Microscopy. The targeted nanoparticle diameter, polydispersity, and zeta potential are around 229.5 nm, 0.205, and44.7±0.6 mV, respectively. The study revealed that spherical core-shell morphology was preserved. Excellent stability of targeted nanoparticle is evidenced by two weeks of room temperature stability tests. The results of the cell viability assay and the hemolysis test confirmed that the targeted nanoparticle has an excellent biocompatibility for using in cell studies and ultrasound imaging in vivo. Most importantly, in vitro cell experiments demonstrated that an increased amount of targeted nanoparticles was accumulated in hepatocellular carcinoma cell line Bel7402 relative to hepatoma cell line L02. And targeted nanoparticles had also shown better ultrasound imaging abilities in vitro. The data suggest that the novel targeted nanoparticle may be applicable to ultrasonic molecular imaging of folate-receptor overexpressed tumor.

Objectives: Methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) plays an essential role in folate-mediated one-carbon metabolism which determines both homocysteine remethylation and de novo thymidylate biosynthesis. Hyperhomocysteinemia is positively associated with essential hypertension. This study aimed to investigate the association of MTHFD1 promoter methylation with essential hypertension. Methods: Using the quantitative methylation-specific polymerase chain reaction (qMSP), the levels of MTHFD1 promoter methylation in 243 essential hypertension patients, 218 age- and gender-matched healthy controls. The relative changes in serum MTHFD1 promoter methylation were analyzed using the 2^−ΔΔCt method. The percent of methylated reference (PMR) of MTHFD1 was used to evaluate the MTHFD1 promoter methylation levels. Results: In our current study, the MTHFD1 promoter methylation of hypertensive patients were both higher than the healthy control group (median PMR were 8.97% and 5.69%, respectively, all p < 0.001). Multivariable analysis showed MTHFD1 promoter hypermethylation increase the risk of essential hypertension (OR, 1.336; 95%CI, 1.235–1.446; p < 0.001). The area under the curve (AUC) of MTHFD1 promoter methylation was 0.739 in total patients with essential hypertension. Conclusions: MTHFD1 promoter hypermethylation was a potential biomarker for the diagnosis of essential hypertension.

The existence of cancer stem cells (CSCs) or cancer stem‑like cells (CSLCs) is regarded as the cause of tumor formation and recurrence. Matrine has been reported to exhibit antitumor effects in cancer cells. In the present study, a preliminary study was performed on the mechanisms of matrine on hepatocellular carcinoma (HCC) stem‑like cells. The HCC SMMC‑7721 cell line was cultured in tumor stem cell‑specific medium to form spheres, and different concentrations (1, 2 and 5 mg/kg) of cisplatin were then used in order to purify the most drug‑resistant cells, which were used as CSLCs. An MTT assay was performed to detect the inhibitory effects of matrine against CSLC proliferation. Quantitative polymerase chain reaction (qPCR) and western blot analysis were used to detect changes in cell adhesion regulating gene (CAR), E‑cadherin, laminin and fibronectin. As a result, using tryptose sulfite cycloserine medium culture and cisplatin‑resistance screening, CSLCs were successfully isolated from the SMMC‑7721 cell line. Matrine inhibited the proliferation of CSLCs in vitro. The results of qPCR and western blot analysis demonstrated that matrine upregulated the expression of CAR, E‑cadherin, laminin and fibronectin in CSLCs compared with the control treatment. A certain concentration of matrine exhibited antitumor effects on HCC stem like cells.