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- 저자 : Bailong Li (검색결과 2 건)
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Bailong Tao,Chuanchuan Lin,Ai Guo,Yonglin Yu,Xian Qin,Kai Li,Hongchuan Tian,Weiwei Yi,Dengliang Lei,Lixue Chen 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.104 No.-
Infected wound healing remains a critical threat, which frequently delays the healing process and evenleads to severe life-threatening complications. Herein, we reported an effective anti-infection approach,which was based on copper ions-releasing hydroxyapatite/polydopamine (HA-Cu/PDA) nanocompositeswith photothermal effect. The HA-Cu/PDA nanocomposites was fabricated through a co-precipitationreaction between polydopamine (PDA)-coated hydroxyapatite nanoparticles (HA)-loaded Cu2+ (HA-Cu). Through a synergistic effect of released Cu2+ and photothermal efficiency of PDA coating, and the HACu/PDA nanocomposites exhibited extraordinary antibacterial capacities against Escherichia coli (E. coli)and Staphylococcus aureus (S. aureus). The nanocomposites presented good biocompatibility for mouseembryonic fibroblast (NIH-3T3) cells and promoted NIH3T3 cells to migrate toward wound sites. Additionally, this nanocomposite could stimulate the tissue remodeling-related gene expression toinduce the blood vessels formation, granulation tissues and collagen deposition, and eventually enhancewound healing. In vivo study further verified that HA-Cu/PDA nanocomposites with NIR irradiation couldsignificantly improve bacterial infected wound healing through the prominent antibacterial property,reduced inflammatory response, the formation of granulation tissue, collagen deposition, and angiogenesisability. Thus, this study develops a versatile strategy for a broad range of wound healing and skinreconstruction caused by bacterial infection.
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Hongjin Qu,Lei Liu,Zhe Liu,Hongran Qin,Zebin Liao,Penglin Xia,Yanyong Yang,Bailong Li,Fu Gao,Jianming Cai 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
As a common serious complication of thoracic radiotherapy, radiation-induced pulmonary fibrosis (RIPF) severely limits radiation therapy approaches. Epithelial–mesenchymal transition (EMT) is a direct contributor to the fibroblast pool during fibrogenesis, and prevention of EMT is considered an effective strategy to inhibit tissue fibrosis. Our previous study revealed that TANK-binding kinase 1 (TBK1) regulates EMT in lung cancer cells. In the present study, we aimed to investigate the therapeutic potential of targeting TBK1 to prevent RIPF and EMT progression. We found radiationinduced EMT and pulmonary fibrosis in normal alveolar epithelial cells and lung tissues. TBK1 knockdown or inhibition significantly reversed EMT in vivo and in vitro and attenuated pulmonary fibrosis and collagen deposition. Moreover, we observed that TBK1 was elevated in a time- and dose-dependent manner by radiation. Meanwhile, radiation also induced time- and dose-dependent activation of AKT and ERK, each of whose inhibitors suppressed radiation-induced EMT. Intriguingly, silencing of TBK1 with shRNA also blocked the radiation-induced activation of AKT and ERK signaling. The ERK inhibitor did not obviously affect the expression of TBK1 or phosphorylated AKT, while AKT inhibition suppressed activation of ERK without changing the expression of TBK1. Finally, we found that a TBK1 inhibitor inhibited inflammatory cytokine expression in a RIPF model and Amlexanox protected normal cells and mice from ionizing radiation. In conclusion, our results indicate that the TBK1–AKT–ERK signaling pathway regulates radiation-induced EMT in normal alveolar epithelial cells, suggesting that TBK1 is a potential target for pulmonary fibrosis prevention during cancer radiotherapy
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