The immune enhancing effect of antimicrobial peptide LLv on broilers chickens.

To evaluate the effect and its mechanism of heat-resistant antimicrobial peptide LLv on broilers, three hundred 1-day-old healthy AA+ female broilers were allocated into 5 groups with 6 replicates in each group and 10 birds in each replicate. Birds were given a basal diet, an antibiotic diet (10.2 mg/kg chlortetracycline hydrochloride), and the basal diet supplemented with 10, 50, and 100 mg/kg LLv for 42 d, respectively. Compared with the group which birds were fed an antibiotic-free basal diet (control group), supplementing 100 mg/kg LLv increased 21-day IgA, IgM, IL-4, AIV-Ab, IFN-γ levels and 42-day IgA, IgM, IL-4, AIV-Ab levels and reduced 42-day IL-1 levels in serum (P < 0.05). Compared with antibiotic group, the 10 and 50 mg/kg LLv decreased 42-day IgM levels in serum (P < 0.05). The 100 mg/kg LLv increased 21-day AIV-Ab levels and 42-day IL-4, AIV-Ab levels and reduced 42-day IL-1 levels in serum (P < 0.05). Compared with control group, the 100 mg/kg LLv increased the expression rate of sIgA secretory cells and sIgA content in jejunal mucosa at 21 d and 42 d (P < 0.05), which did not differ from antibiotic group (P > 0.05). Compared with antibiotic group, the 10 mg/kg LLv reduced 21-day sIgA content and the 50 mg/kg LLv reduced 42-d the expression rate of sIgA secretory cells in jejunal mucosa (P < 0.05). Compared with control group, the 100 mg/kg LLv increased the expression of TCR, IL-15, CD28, BAFF, CD86, CD83, MHC-II, and CD40 genes in jejunal mucosa at 21 d and 42 d (P < 0.05). Compared with antibiotic group, the 100 mg/kg LLv increased the expression of 21-day BAFF, CD40, MHC-II, CD83 genes and the expression of 42-day BAFF, TCR, IL-15, CD40, CD83 genes in jejunal mucosa (P < 0.05). The results showed that the addition of LLv to the ration had a promotional effect on the immune function of broiler chickens.

Naringin Inhibits the Proliferation, Migration, Invasion and Epithelial-to-Mesenchymal Transition of Gastric Cancer Cells via the PI3K/AKT Signaling Pathway.

Background: Gastric cancer is a common malignant tumor of the human digestive system. Currently, the treatment of gastric cancer is still dominated by radiotherapy, chemotherapy and surgery. Although the treatment is very effective, we are also trying to find new treatment methods. Traditional Chinese Medicine (TCM) may play an important role in the treatment of gastric cancer. Study Objective: The aim of this study is to explore the effects of naringin on the proliferation, migration, invasion and apoptosis of gastric cancer and its potential mechanisms. Methods: MGC803 and MKN45 viability were detected by MTT assay. The effects of naringin on cell cloning, migration and invasion were determined by colony formation assay, cell scratch test and transwell assay (ThermoFisher Scientific™, Waltham, Massachusetts USA), respectively. Cell cycle and apoptosis were assayed by flow cytometry. Associated proteins were measured using Western blot and immunohistochemistry (IHC). The experimental results were further verified in nude mice. Setting: This study was carried out in Department of Experimental Animal Center of Xi'an Jiaotong University and the Translation Medicine Center of the First Affiliated Hospital of Xi'an Jiaotong University in China. Results: Cells remained mainly in G0/G1 phase and apoptosis was increased. The nude mouse model showed that naringin treatment could inhibit the growth of tumors in nude mice. Cell scratch tests and transwell assay showed that the invasion and migration abilities of the gastric cancer cell line were significantly reduced after naringin treatment. Western blot showed that the expression of Vimentin, Zeb1 and P-AKT was downregulated and that E-cadherin was upregulated after naringin treatment. Conclusion: Naringin can block the cell-cycle, induce cancer cell apoptosis, and inhibit the epithelial mesenchymal transition (EMT) process by inhibiting the PI3K-AKT/Zeb1 pathway in gastric cancer cells. Therefore, naringin can inhibit the development of gastric cancer.

Porous Se@SiO2 nanosphere-coated catheter accelerates prostatic urethra wound healing by modulating macrophage polarization through reactive oxygen species-NF-κB pathway inhibition.

Benign prostatic hyperplasia (BPH) patients experience complications after surgery. We studied oxidative stress scavenging by porous Se@SiO2 nanospheres in prostatic urethra wound healing after transurethral resection of the prostate (TURP). Beagle dogs were randomly distributed into two groups after establishing TURP models. Wound recovery and oxidative stress levels were evaluated. Re-epithelialization and the macrophage distribution at the wound site were assessed by histology. The mechanism by which porous Se@SiO2 nanospheres regulated macrophage polarization was investigated by qRT-PCR, western blotting, flow cytometry, immunofluorescence and dual luciferase reporter gene assays. Our results demonstrated that Porous Se@SiO2 nanosphere-coated catheters advance re-epithelization of the prostatic urethra, accelerating wound healing in beagle dogs after TURP, and improve the antioxidant capacity to inhibit oxidative stress and induced an M2 phenotype transition of macrophages at the wound. By restraining the function of reactive oxygen species (ROS), porous Se@SiO2 nanospheres downregulated Ikk, IκB and p65 phosphorylation to block the downstream NF-κB pathway in macrophages in vitro. Since activation of NF-κB signaling cascades drives macrophage polarization, porous Se@SiO2 nanospheres promoted macrophage phenotype conversion from M1 to M2. Our findings suggest that porous Se@SiO2 nanosphere-coated catheters promote postoperative wound recovery in the prostatic urethra by promoting macrophage polarization toward the M2 phenotype through suppression of the ROS-NF-κB pathway, attenuating the inflammatory response. STATEMENT OF SIGNIFICANCE: The inability to effectively control post-operative inflammatory responses after surgical treatment of benign prostatic hyperplasia (BPH) remains a challenge to researchers and surgeons, as it can lead to indirect cell death and ultimately delay wound healing. Macrophages at the wound site work as pivotal regulators of local inflammatory response. Here, we designed and produced a new type of catheter with a coating of porous Se@SiO2 nanosphere and demonstrated its role in promoting prostatic urethra wound repair by shifting macrophage polarization toward the anti-inflammatory M2 phenotype via suppressing ROS-NF-κB pathway. These results indicate that the use of porous Se@SiO2 nanosphere-coated catheter may provide a therapeutic strategy for postoperative complications during prostatic urethra wound healing to improve patient quality of life.

Finasteride accelerates prostate wound healing after thulium laser resection through DHT and AR signalling.

OBJECTIVES: Urinary tract infection, urinary frequency, urgency, urodynia and haemorrhage are common post-operative complications of thulium laser resection of the prostate (TmLRP). Our study mainly focuses on the role of finasteride in prostate wound healing through AR signalling. MATERIALS AND METHODS: TmLRP beagles were randomly distributed into different treatment groups. Serum and intra-prostatic testosterone and DHT level were determined. Histological analysis was conducted to study the re-epithelialization and inflammatory response of the prostatic urethra in each group. We investigated the role of androgen in proliferation and inflammatory response in prostate. In addition, the effects of TNF-α on prostate epithelium and stromal cells were also investigated. RESULTS: Testosterone and DHT level increased in testosterone group and DHT decreased in finasteride group. Accelerated wound healing of prostatic urethra was observed in the finasteride group. DHT suppressed proliferation of prostate epithelium and enhanced inflammatory response in prostate. We confirmed that DHT enhanced macrophages TNF-α secretion through AR signalling. TNF-α suppressed proliferation of prostate epithelial cells and retarded cell migration. TNF-α also played a pivotal role in suppressing fibroblasts activation and contraction. CONCLUSION: Testosterone treatment repressed re-epithelialization and wound healing of prostatic urethra. Finasteride treatment may be an effective way to promote prostate re-epithelialization.

Androgen Deprivation Accelerates the Prostatic Urethra Wound Healing After Thulium Laser Resection of the Prostate by Promoting Re-Epithelialization and Regulating the Macrophage Polarization.

BACKGROUND: Complications after a thulium laser resection of the prostate (TmLRP) are related to re-epithelialization of the prostatic urethra. Since prostate growth and development are induced by androgen, the aim of this study was to determine the role and explore the mechanism of androgen in wound healing of the prostatic urethra. METHODS: Beagles that received TmLRPs were randomly distributed into a castration group, a testosterone undecanoate (TU) group, and a control group. The prostate wound was assessed once a week using a cystoscope. Histological analysis was then carried out to study the re-epithelialization of the prostatic urethra in each group. The inflammatory response in the wound tissue and urine was also investigated. RESULTS: The healing of the prostatic urethra after a TmLRP was more rapid in the castration group and slower in the TU group than that in the control group. Castration accelerated re-epithelialization by promoting basal cell proliferation in the wound surface and beneath the wound and by accelerating the differentiation of basal cells into urothelial cells. Castration reduced the duration of the inflammatory phase and induced the conversion of M1 macrophages to M2 macrophages, thus accelerating the maturation of the wound. By contrast, androgen supplementation enhanced the inflammatory response and prolonged the inflammatory phase. Moreover, the anti-inflammatory phase was delayed and weakened. CONCLUSION: Androgen deprivation promotes re-epithelialization of the wound, regulates the inflammatory response, and accelerates wound healing of the prostatic urethra after a TmLRP. Prostate 77:708-717, 2017. © 2017 Wiley Periodicals, Inc.