Background and Aims Probiotics was considered as a potential therapy for nonalcoholic fatty liver disease (NAFLD) without approval and comprehensive assessment in recent years, which call for a meta-analysis. Methods We performed electronic and manual searches including English and Chinese databases published before April 2019, with the use of mesh term and free text of “nonalcoholic fatty liver disease” and “probiotics.” Clinical trials evaluating the efficacy of probiotic therapy in NAFLD patients were included according to the eligibility criteria. With the use of random effects models, clinical outcomes were presented as weighted mean difference (WMD) with 95% confidence interval (CI), while heterogeneity and meta-regression were also assessed. Results 28 clinical trials enrolling 1555 criterion proven NAFLD patients with the use of probiotics from 4 to 28 weeks were included. Overall, probiotic therapy had beneficial effects on body mass index (WMD: -1.46, 95% CI: [-2.44, -0.48]), alanine aminotransferase (WMD: -13.40, 95% CI: [-17.03, -9.77]), aspartate transaminase (WMD: -13.54, 95% CI: [-17.86, -9.22]), gamma-glutamyl transpeptidase (WMD: -9.88, 95% CI: [-17.77, -1.99]), insulin (WMD: -1.32, 95% CI: [-2.43, -0.21]), homeostasis model assessment-insulin resistance (WMD: -0.42, 95% CI: [-0.73, -0.12]), and total cholesterol (WMD: -15.38, 95% CI: [-26.50, -4.25]), but not in fasting blood sugar, lipid profiles, or tumor necrosis factor-alpha. Conclusion The systematic review and meta-analysis support that probiotics are superior to placebo in NAFLD patients and could be utilized as a common complementary therapeutic approach.

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The bones and connective tissues of the murine jaws and skull are partly derived from cephalic neural crest cells (CNCCs). Here, we report that mice deficient of protogenin (Prtg) protein, an immunoglobulin domain-containing receptor expressed in the developing nervous system, have impairments of the palatine and skull. Data from lineage tracing experiments, expression patterns of neural crest cell (NCC) marker genes and detection of apoptotic cells indicate that the malformation of bones in Prtg-deficient mice is due to increased apoptosis of rostral CNCCs (R-CNCCs). Using a yeast two-hybrid screening, we found that Prtg interacts with Radil, a protein previously shown to affect the migration and survival of NCCs in zebrafish with unknown mechanism. Overexpression of Prtg induces translocation of Radil from cytoplasm to cell membrane in cultured AD293 cells. In addition, overexpression of Prtg and Radil activates α5β1-integrins to high-affinity conformational forms, which is further enhanced by the addition of Prtg ligand ERdj3 into cultured cells. Blockage of Radil by RNA interference abolishes the effect of ERdj3 and Prtg on the α5β1-integrin, suggesting that Radil acts downstream of Prtg. Prtg-deficient R-CNCCs display fewer activated α5β1-integrins in embryos, and these cells show reduced migratory ability in in vitro transwell assay. These results suggest that the inside-out activation of the α5β1-integrin mediated by ERdj3/Prtg/Radil signaling is crucial for proper functions of R-CNCCs, and the deficiency of this pathway causes premature apoptosis of a subset of R-CNCCs and malformation of craniofacial structures.

Objective Ovarian cancer is one of three malignant tumors of the female reproductive system. Our previous studies showed that the traditional Chinese medicine naringin significantly inhibited the proliferation of platinum-resistant ovarian cancer cells in vitro, and that the mechanism may be related to the NF-κB pathway. Methods The MTT assay was used to detect the sensitivity of SKOV3 and SKOV3/CDDP cells to cisplatin, the effect of different naringin concentrations on the proliferation of SKOV3/CDDP cells, and the reversal of cisplatin resistance in naringin-treated SKOV3/CDDP cells. Western blotting was used to detect β-catenin, c-Myc, and cyclin D1 protein levels in the different cell lines. Results MTT results showed that different concentrations of naringin inhibited the proliferation of SKOV3 and SKOV3/CDDP cells, and that the inhibition increased with increasing concentrations and prolonged incubation times. Western blotting revealed that compared with controls (SKOV3/CDDP-0), β-catenin, c-Myc and cyclin D1 proteins levels were significantly decreased in SKOV3/CDDP-C, SKOV3/CDDP-N 20, and SKOV3/CDDP-CN 20 cells, suggesting that naringin inhibited the proliferation of SKOV3/CDDP cells in a concentration and time dependent manner. Conclusions Non-cytotoxic naringin reduced the expression of β-catenin, c-Myc, and cyclin D1 in SKOV3/CDDP cells and partially reversed cisplatin resistance in SKOV3/CDDP CN 20 cells.