Synergistic Inhibitory Effect of Honey and Lactobacillus plantarum on Pathogenic Bacteria and Their Promotion of Healing in Infected Wounds.

Prevention and control of infections have become a formidable challenge due to the increasing resistance of pathogens to antibiotics. Probiotics have been discovered to have positive effects on the host, and it is well-known that some Lactobacilli are effective in treating and preventing inflammatory and infectious diseases. In this study, we developed an antibacterial formulation consisting of honey and Lactobacillus plantarum (honey-L. plantarum). The optimal formulation of honey (10%) and L. plantarum (1 × 109 CFU/mL) was used to investigate its antimicrobial effect and mechanism in vitro, and its healing effect on wound healing of whole skin infections in rats. Biofilm crystalline violet staining and fluorescent staining results indicated that the honey-L. plantarum formulation prevented the biofilm formation in Staphylococcus aureus and Pseudomonas aeruginosa and increased the number of dead bacteria in the biofilms. Further mechanism studies revealed that the honey-L. plantarum formulation may inhibit biofilm formation by upregulating biofilm-related genes (icaA, icaR, sigB, sarA, and agrA) and downregulating quorum sensing (QS) associated genes (lasI, lasR, rhlI, rhlR, and pqsR). Furthermore, the honey-L. plantarum formulation decreased the number of bacteria in the infected wounds of rats and accelerated the formation of new connective tissue to promote wound healing. Our study suggests that the honey-L. plantarum formulation provides a promising option for the treatment of pathogenic infections and wound healing.

Strictosamide alleviates the inflammation in an acute ulcerative colitis (UC) model.

The ulcerative colitis (UC) is a typical inflammatory bowel disease (IBD) causing great damages, while strictosamide (STR) is a natural alkaloid that possesses strong anti-inflammatory property in infection and inflammation-related diseases. Our study is aimed at evaluating the anti-inflammatory activity of STR in the course of UC. Briefly, male Balb/c mice were treated with 3.5% dextran sulfate sodium (DSS) for 6 consecutive days to establish an acute model of UC, and the administration of gradient concentrations of STR was subsequently performed. Accordingly, colonic pathological alterations including the reduced ratio of colon weight/length, decreased disease activity index (DAI), and attenuated H&E damage were found in UC mice after STR treatment. Based on the analyses of real-time PCR and western blot, downregulation of pro-inflammatory cytokines (TNF-α, IL-1ß, and IL-6) was also determined in the colonic tissue of UC mice after the treatment of STR. ELISA and immunohistochemical staining further suggest the relief of inflammation in UC mice with decreased expressions of MPO and iNOS after STR treatment. In addition, STR was also validated to significantly inhibit NF-κB signaling in UC mice by western blot and Electrophoretic Mobility Shift Assay (EMSA). Meanwhile, restricted inflammation was also determined in STR-treated IEC6 and HT-29 cells. The utilization of PDTC, an inhibitor of NF-κB, further demonstrated that STR ameliorated the inflammation by inhibiting the NF-κB signaling in vitro. In summary, our study suggests that STR could be a potential candidate for IBD therapy.

Ginsenoside Rb1 promotes the growth of mink hair follicle via PI3K/AKT/GSK-3ß signaling pathway.

AIMS: Hair follicles play a critical role in the process of hair growth. The dermal papilla cells (DPCs) are an important component in the hair follicle regeneration and growth. This study investigated the effects of ginsenoside Rb1 on the growth of cultured mink hair follicles and DPCs. MAIN METHODS: The mink hair follicles were treated with ginsenoside Rb1 for 9 days and their lengths were measured every three days. Real-time PCR was used to determine the mRNA expression of vascularization endothelial growth factor A (VEGF-A), VEGF receptor 2 (VEGF-R2) and TGF-ß1. In addition, the levels of proteins were detected by western blot. Cell proliferation was determined by immunofluorescence staining of proliferation marker Ki-67 and cell cycle analysis was performed on flow cytometry. Moreover, cell migration was evaluated by wound healing assay. KEY FINDINGS: Ginsenoside Rb1 promoted the growth of hair follicles, and proliferation and migration of DPCs. Ginsenoside Rb1 improved the expression levels of VEGFA and VEGF-R2, while attenuated the TGF-ß1 expression both in hair follicles and DPCs. Furthermore, ginsenoside Rb1 facilitated the activation of PI3K/AKT/GSK-3ß signaling pathway in hair follicles and DPCs. SIGNIFICANCE: The results reveals a crucial role of PI3K/AKT/GSK-3ß signaling pathway in ginsenoside Rb1-induced growth of hair follicles and DPCs.

Optimal Control Model of Tumor Treatment with Oncolytic Virus and MEK Inhibitor.

Tumors are a serious threat to human health. The oncolytic virus is a kind of tumor killer virus which can infect and lyse cancer cells and spread through the tumor, while leaving normal cells largely unharmed. Mathematical models can help us to understand the tumor-virus dynamics and find better treatment strategies. This paper gives a new mathematical model of tumor therapy with oncolytic virus and MEK inhibitor. Stable analysis was given. Because mitogen-activated protein kinase (MEK) can not only lead to greater oncolytic virus infection into cancer cells, but also limit the replication of the virus, in order to provide the best dosage of MEK inhibitors and balance the positive and negative effect of the inhibitors, we put forward an optimal control problem of the inhibitor. The optimal strategies are given by theory and simulation.

Analysis and simulation of an Adefovir anti-hepatitis B virus infection therapy immune model with alanine aminotransferase.

Hepatitis B virus (HBV) infection models and anti-HBV infection therapy models have been set up to understand and explain clinical phenomena. Many of these models have been proposed based on Zeuzem et al. and Nowak et al.'s basic virus infection model (BVIM). Some references have pointed out that the basic infection reproductive number of the BVIM is biologically questionable and gave the modified models with standard mass action incidences. This study describes one anti-HBV therapy immune model with alanine aminotransferase (ALT) based on standard mass action incidences. There are two basic infection reproductive numbers R0 and R1 in the model. It is proved that if R0 < 1 and R1 < 1, the disease free equilibrium is locally and globally asymptotically stable, respectively. For the endemic equilibrium, simulation shows that if R1 > 1, it may be also globally asymptotically stable. Simulations based on clinical data of HBV DNA and ALT can explain some clinical phenomena. Simulations of the correlation between liver cells, HBV DNA, cytotoxic T lymphocytes and ALT are also given.

[Research progress on anti-tumor mechanism of Trichinella spiralis].

Trichinella spiralis has restrain effect on tumors. Different amount of T. spiralis can emerge different tumor inhibition effect T. spiralis infection can reduce tumor growth to various extents in mice bearing tumor cells at different times post infection. Each developmental stage of T. spiralis in the host may have anti-tumor effect T. spiralis may play anti-tumor roles by stimulating cell-mediated immune response, and/or possessing tumor-associated antigen and anti-tumor active substances of the parasite.