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Implantable Nanofiber Membranes with Synergistic Photothermal and autophagy inhibition Effects for Enhanced Tumor Therapy Efficacy

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Advanced Fiber Materials 2023年第5期5卷 1810-1825页

作者： Jiaxiang Mu Zhaoxu Meng Xinran Liu Ping Guan He Lian Wuya College of Innovation Shenyang Pharmaceutical UniversityShenyang 110016China Department of Biomedical Engineering School of Medical InstrumentationShenyang Pharmaceutical UniversityShenyang 110016China

Photothermal therapy(PTT)has been proposed as an advanced patient-centered strategy for tumor ***,the uncertain safety of conventional photothermal conversion agents and the presence of intracellular self-protective autophagy mechanisms pose obstacles to the clinical application and efficacy of *** we are deeply aware of the seriousness of these problems,we herein proposed an efficacy-enhancing strategy based on an implantable membrane platform(PPG@PB-HCQ)constructed from poly(lactic acid)(PLA),poly(ɛ-caprolactone)(PCL)and gelatin(Gel)electrospun nanofibers(PPG)and loaded with the biodegradable high-efficiency photothermal conversion agent Prussian blue(PB)and the autophagy inhibitor hydroxychloroquine sulfate(HCQ).Cellular experiments confirmed that the PPG@PB-HCQ nanofiber membrane exhibited a significantly stronger tumor cell-killing effect compared with the PTT *** enhancement features by of blocking the fusion of autophagosomes with *** intracellular overexpression of the proteins microtubule-associated protein 1 light chain 3(LC3)-II and p62 and the low expression of the proteins LC3-I and Rab7(members of the RAS oncogene family)further demonstrated autophagic flux ***,the potent antitumor effect of the PPG@PB-HCQ therapeutic platform in B16 tumor-bearing model mice verified the efficacy-enhancing strategy of synergistic PTT and protective autophagy *** present study provides a promising strategy for solving the difficulties of tumor treatment,as well as a new perspective for designing novel treatment platforms.

关键词： Photothermal therapy autophagy inhibition Nanofiber membrane Electrospinning Lysosomal alkalization

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autophagy Elicits Neuroprotection at the Subacute Phase of Transient Cerebral Ischaemia but Has Few Effects on Neurological Outcomes After Permanent Ischaemic Stroke in Rats

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Current Medical Science 2021年第4期41卷 803-814页

作者： Tao GUO Yi-hao DENG Ling-ling DONG Lu REN Hong-yun HE Department of Basic Medicine Medical SchoolKunming University of Science and TechnologyKunming 650500China

Objective autophagy was prominently activated by cerebral *** study was to investigate the exact role of autophagy in ischaemic *** Two rat models of transient middle cerebral artery occlusion(tMCAO)and permanent MCAO(pMCAO)were *** brain tissues in the penumbra were obtained to observe the dynamic variations of autophagy activity with Beclin1 and LC3 antibodies by Western *** the characteristic time points,when autophagy activity was markedly elevated or reduced,the autophagy activation signaling was intervened with rapamycin and 3-methyladenine,***,key proteins in the autopahgic/lysosomal pathway were detected with the antibodies of LC3,p62,ubiquitin,LAMP-1 and cathepsin ***,TTC staining,neurological score and immunofluorescence were performed to evaluate brain infarct volume,neurological deficit and neuron survival,*** Both Beclin1 and LC3 expression levels were remarkably altered at 6 h,12 h,2 days and 7 days after ***,the dynamic changes of autophagy activity following pMCAO were identical to those after *** autophagy induction nor autophagy inhibition was able to ameliorate the pMCAO-induced neurological injury due to lysosomal dysfunction,as indicated by low levels of LAMP-1 and cathepsin B,accompanied with the accumulation of LC3-II,ubiquitin and insoluble ***,autophagy induction elicited overt neuroprotection at 2 and 7 days after tMCAO,and this neuroprotection might be elicited by the enhancement of autophagy *** Our study suggests that autophagy confers neuroprotection at the subacute phase of tMCAO but has few effects on neurological outcomes after pMCAO.

关键词： permanent cerebral stroke transient cerebral ischaemia autophagy induction autophagy inhibition neuroprotection

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