The present study was designed to determine the antihyperglycemic function of ginsenoside Rh2 (GS-Rh2) by the regeneration of β-cells in mice that underwent 70% partial pancreatectomy (PPx), and to explore the mechanisms of GS-Rh2-induced β-cell proliferation. Adult C57BL/6J mice were subjected to PPx or a sham operation. Within 14 days post-PPx, mice that underwent PPx received GS-Rh2 (1 mg/kg body weight) or saline injection. GS-Rh2-treated mice exhibited an improved glycemia and glucose tolerance, an increased serum insulin levels, and β-cell hyperplasia. Meanwhile, increased β-cell proliferation percentages and decreased β-cell apoptosis percentages were also observed in GS-Rh2-treated mice. Further studies on the Akt/Foxo1/PDX-1 signaling pathway revealed that GS-Rh2 probably induced β-cell proliferation via activation of Akt and PDX-1 and inactivation of Foxo1. Studies on the abundance and activity of cell cycle proteins suggested that GS-Rh2-induced β-cell proliferation may ultimately be achieved through the regulation of cell cycle proteins. These findings demonstrate that GS-Rh2 administration could inhibit the tendency of apoptosis, and reverse the impaired β-cell growth potential by modulating Akt/Foxo1/PDX-1 signaling pathway and regulating cell cycle proteins. Induction of islet β-cell proliferation by GS-Rh2 suggests its therapeutic potential in the treatment of diabetes.

No abstract

Aim The objectives of this laboratory‐based study were to investigate the effects of GH12 on Enterococcus faecalis biofilm and virulence. Methodology Minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of GH12 against E. faecalis were first determined. A time‐kill assay was further conducted. The effects of GH12 on the expression of virulence and stress genes in E. faecalis were evaluated by RT‐qPCR. Crystal violet stain was used to investigate the effects of GH12 on E. faecalis biofilm formation and 1‐day‐old biofilm. Finally, an ex vivo tooth model contaminated with E. faecalis was used to evaluate the antimicrobial activity of GH12 as an irrigant by CFU counting, SEM and CLSM. One‐way anova and Tukey’s multiple comparisons test were used to compare the differences amongst groups (α = 0.05). Results The MICs and MBCs of GH12 against E. faecalis were 8.0 ± 0.0 and 16.0 ± 0.0 mg L−1, respectively, and GH12 at 32.0 mg L−1 reduced the bacterial numbers by more than 99.9% within 1 min. Various virulence genes (efaA, esp and gelE) and stress genes (dnaK, groEL, ctsR and clpPBCEX) in E. faecalis were significantly downregulated by GH12 at sub‐MIC levels (P < 0.05). Additionally, both E. faecalis biofilm formation and the biomass of 1‐day‐old E. faecalis biofilm were significantly reduced by GH12 (P < 0.05). Elimination of E. faecalis in biofilms from root canal walls was achieved through irrigation with 64.0 mg L−1 GH12 for 30 min. CLSM analysis revealed that GH12 at 64.0 mg L−1 was most effective in eliminating bacteria within dentinal tubules (P < 0.05). Conclusion In a laboratory setting, and when used as an irrigant, GH12 suppressed E. faecalis, downregulated specific virulence and stress‐associated genes, eliminated intracanal E. faecalis protected by biofilms and killed bacteria in dentinal tubules. These results emphasize the need for preclinical and clinical studies to explore the potential of GH12 as an antimicrobial agent during root canal treatment.

Aims:  To identify the presence of mouse β‐defensin 3 (Mbd3) (the human homologue of β‐defensin 2) in different tissues and to define the antimicrobial properties of recombinant MBD3 (rMBD3) against a panel of human pathogens. Methods and Results:  Mbd3 gene expression in different mouse tissues before or after lipopolysaccharide (LPS) injection was compared by semi‐quantitative RT‐PCR. This analysis demonstrated that epithelial and mucosal tissues expressed Mbd3 independent of LPS stimulation. Evaluation of the antimicrobial properties of recombinant rMBD3 was determined by assessing the median inhibition concentration (IC50), minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC)/minimal fungicidal concentration (MFC) against various human pathogens. Conclusion:  Mbd3 gene expression by epithelial and mucosal tissues suggested that MBD3 likely plays an early defensive role against microbial infections. This activity was most significant against filamentous fungi. Significance and Impact of the Study:  The data presented in this report suggested that formulations containing rMBD3 and related molecules could serve to treat fungal and bacterial infections.