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      저자 : Jiancheng Tu (검색결과 2 건)
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        ZL-2, a cathelicidin-derived antimicrobial peptide, has a broad antimicrobial activity against gram-positive bacteria and gram-negative bacteria in vitro and in vivo

        Jiancheng Tu,Shusheng Wang,Geping Wu,Yun Zuo,Lei Zhao 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.10

        Alloferons are a group of naturally occurringpeptides primarily isolated from insects that are capable ofstimulating mouse and human NK cell cytotoxicity towardcancer cells. In this study, we found that a modified antibacterialpeptide had a broad range of action against bothgram-positive and gram-negative bacteria. A time-courseexperiment showed that CFU counts rapidly decreasedafter ZL-2 treatment, with the bacteria nearly eliminatedwithin 4 h. We also examined the synergy between thepeptide and antibiotics. The peptide ZL-2 resulted in asignificant synergistic improvement in the potencies ofampicillin, erythromycin and ceftazidime against methicillin-resistant bacteria. In addition, ZL-2 had no detectablecytotoxicity in mouse spleen cells or a mouse animalmodel. In the mouse model by i.p. inoculation with Escherichiacoli, timely treatment of i.p. injection with ZL-2resulted in 100-fold reduction in bacteria load in blood aswell as 80 % protection from death in the inoculated animals. In conclusion, we successfully identified a modifiedpeptide with maximal bactericidal activity. This study alsoprovides a potential therapeutic for the treatment of E. colisepticemia by increasing the activity of antimicrobials.

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        The effect of Lfcin-B on non-small cell lung cancer H460 cells is mediated by inhibiting VEGF expression and inducing apoptosis

        Shusheng Wang,Jiancheng Tu,Cuijie Zhou,Jianwei Li,Long Huang,Lei Tao,Lei Zhao 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.2

        Lfcin-B, an antimicrobial peptide found invarious exocrine secretions of mammals, showed antitumoreffects. However, the effect and relative mechanism ofLfcin-B on non-small cell lung cancer is unclear. In thisstudy, assay of cell viability, quantitative real-time PCR,Western blot, annexin V/propidium iodide assay, flowcytometry and tumor-xenograft model were applied toelucidate the mechanism of Lfcin-B on non-small cell lungcancer NCI-H460 (H460) cells. Lfcin-B significantly suppressedthe proliferation of H460 cells in vitro. Additionally,the transcription and translation of the VEGF gene inH460 cells were restrained after exposure to Lfcin-B. Moreover, the apoptosis of H460 cells was induced byLfcin-B through stimulating caspase-3, caspase-9 andpreventing survivin expression on both the transcriptionand translation level. Meanwhile, Lfcin-B increased theproduction of reactive oxygen species and suppressed theRNA of antioxidant enzymes (GPX1, GPX2, SOD3 andcatalase) in H460 cells. Finally, Lfcin-B significantly preventedthe tumor growth in the H460-bearing mice model. These results indicated that Lfcin-B could be a potentialcandidate for the treatment of lung cancer.

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