L-Selenocysteine induced HepG-2 cells apoptosis through reactive oxygen species-mediated signaling pathway.

BACKGROUND: Currently, Liver cancer is the fifth most common tumor and the second most important reason for cancer-related death in the world. However, there are still many limitations of the clinical treatment of liver cancer, and new treatment options are clearly needed. Fortunately, studies have shown that L-Selenocysteine has a certain effect on cancer. This study was to investigate the effects of L-Selenocysteine on the inhibition of cell proliferation and the promotion of apoptosis of HepG-2 cells through ROS mediated fine signaling pathway. MATERIALS AND METHODS: CCK-8 assay was applied to evaluating the cytotoxic effect of L-Selenocysteine on HepG-2 cells. Electron microscopy, flow cytometry and Western Blot was utilization in further researching cells signaling pathways. RESULTS: The growth of HepG-2 cells was inhibited by L-selenocysteine ​​treatment in a dose-dependent manner. The cell viability decreased to 52.20%, 43.20% and 30.83% under the treatment of 4, 8, 16 µM L-selenocysteine, respectively. L-Selenocysteine had higher cytotoxicity towards HepG-2 cells than normal cells. L-Selenocysteine can induce the apoptosis of HepG-2 cells by increasing the DNA fragmentation, and activating the Caspase-3. In addition, it was found that the mechanism of the induction to HepG-2 cell apoptosis by L-Selenocysteine was closely related to the overproduction of ROS and promoted apoptosis through the Bcl-2 signaling pathway. CONCLUSIONS: Our data suggest that L-selenocysteine ​​may cause mitochondrial damage and subsequently stimulate ROS production. ROS can damage cellular DNA and mediate the production of Casapase-8, Bid, Bcl-2 and other proteins, affecting downstream signaling pathways, and ultimately induced apoptosis.

Infant friendly adhesive film containing glucose for neonatal hypoglycemia.

Neonatal hypoglycemia is a common disease in newborns, which can precipitate energy shortage and follow by irreversible brain and neurological injury. Herein, we present a novel approach for treating neonatal hypoglycemia involving an adhesive polyvinylpyrrolidone/gallic acid (PVP/GA) film loading glucose. The PVP/GA film with loose cross-linking can be obtained by mixing their ethanol solution and drying complex. When depositing this soft film onto wet tissue, it can absorb interfacial water to form a hydrogel with a rough surface, which facilitates tight contact between the hydrogel and tissue. Meanwhile, the functional groups in the hydrogels and tissues establish both covalent and non-covalent bonds, leading to robust bioadhesion. Moreover, the adhered PVP/GA hydrogel can be detached without damaging tissue as needed. Furthermore, the PVP/GA films exhibit excellent antibacterial properties and biocompatibility. Notably, these films effectively load glucose and deliver it to the sublingual tissue of newborn rabbits, showcasing a compelling therapeutic effect against neonatal hypoglycemia. The strengths of the PVP/GA film encompass excellent wet adhesion in the wet and highly dynamic environment of the oral cavity, on-demand detachment, antibacterial efficacy, biocompatibility, and straightforward preparation. Consequently, this innovative film holds promise for diverse biomedical applications, including but not limited to wearable devices, sealants, and drug delivery systems.

Vitamin E in paediatric non-alcoholic fatty liver disease: a meta-analysis.

AIMS: There is currently no specific treatment for non-alcoholic fatty liver disease (NAFLD) in children, but recent studies have shown that vitamin E may be effective. Therefore, we conducted a meta-analysis of trials in which vitamin E was used to treat paediatric NAFLD. METHODS: We searched the PubMed, Embase, Scopus and Cochrane Library databases to identify related articles published prior to March 2020 that examined the effect of vitamin E for the treatment of paediatric NAFLD. RESULTS: The results showed that vitamin E significantly decreased low-density lipoprotein (LDL) and total cholesterol (TCHO) levels. However, no significant changes were found in other indicators, including body mass index (BMI), triglyceride (TG) levels, high-density lipoprotein (HLD) levels, fasting insulin levels, homeostatic model assessment (HOMA-IR), alanine transaminase (ALT) levels, aspartate aminotransferase (AST) levels, glutamate transpeptidase (GGT) levels, ballooning degeneration and fibrosis (P > 0.05). Although the P value of NAS was less than 0.05, the evidence was not strong enough. We also found that treatment with vitamin E significantly increased fasting glucose (FSG) levels if the intervention time was ≤12 months. CONCLUSIONS: Vitamin E therapy can improve blood lipids to some extent, but its effect on children's liver function and liver tissue is not apparent, and the finding that this therapy increases FSG levels still needs more research. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42020177663.