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Harnessing antimicrobial peptide-coupled photosensitizer to combat drug-resistant biofilm infections through enhanced photodynamic therapy

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Acta Pharmaceutica Sinica B 2024年第4期14卷 1759-1771页

作者： Duoyang Fan Xiaohui Liu Yueming Ren Ziheng luo Yanbing Li Jie Dong Seraphine VWegner Fei Chen Wenbin Zeng xiangya School of Pharmaceutical Sciences Central South UniversityChangsha 410013China Hunan Key Laboratory of Diagnostic and Therapeutic Drug Research for Chronic Diseases Central South UniversityChangsha 410013China Sir William Dunn School of Pathology University of OxfordOxford OX13REUK xiangya Hospital of Central South University Changsha 410013China Institute of Physiological Chemistry and Pathobiochemistry University of MünsterMünster 48149Germany

Bacterial biofilm-associated infection was one of the most serious threats to human health. However, effective drugs for drug-resistance bacteria or biofilms remain rarely reported. Here, we propose an innovative strategy to develop a multifunctional antimicrobial agent with broad-spectrum antibacterial activity by coupling photosensitizers (PSs) with antimicrobial peptides (AMPs). This strategy capitalizes on the ability of PSs to generate reactive oxygen species (ROS) and the membrane-targeting property of AMPs (KRWWKWIRW, a peptide screened by an artificial neural network), synergistically enhancing the antimicrobial activity. In addition, unlike conventional aggregation-caused quenching (ACQ) photosensitizers, aggregation-induced emission (AIE) PSs show stronger fluorescence emission in the aggregated state to help visualize the antibacterial mechanism. In vitro antibacterial experiments demonstrated the excellent killing effects of the developed agent against both Gram-positive (G^(+)) and Gram-negative (G^(–)) bacteria. The bacterial-aggregations induced ability enhanced the photoactivatable antibacterial activity against G^(–) bacteria. Notably, it exhibited a significant effect on destroying MRSA biofilms. Moreover, it also showed remarkable efficacy in treating wound infections in mice in vivo. This multifunctional antimicrobial agent holds significant potential in addressing the challenges posed by bacterial biofilm-associated infections and drug-resistant bacteria.

关键词： Photodynamic therapy Antimicrobial peptides Multidrug-resistant bacteria Aggregation-induced emission Anti-biofilm

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Extracellular vesicles from human urine-derived stem cells delay aging through the transfer of PLAU and TIMP1

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Acta Pharmaceutica Sinica B 2024年第3期14卷 1166-1186页

作者： Shanshan Rao Zehui He Zun Wang Hao Yin Xiongke Hu Yijuan Tan Tengfei Wan Hao Zhu Yi luo Xin Wang Hongming Li Zhenxing Wang Xinyue Hu Chungu Hong Yiyi Wang Mingjie luo Wei Du Yuxuan Qian Siyuan Tang Hui Xie Chunyuan Chen Department of Orthopedics Movement System Injury and Repair Research CenterXiangya HospitalCentral South UniversityChangsha 410008China Hunan Key Laboratory of Angmedicine Changsha 410008China xiangya School of Nursing Central South UniversityChangsha 410013China Department of Pediatric Orthopedics Hunan Children’s HospitalUniversity of South ChinaChangsha 410007China Department of Respiratory Medicine Xiangya HospitalCentral South UniversityChangsha 410008China School of Nursing Xinjiang Medical UniversityUrumqiXinjiang 830000China Department of Rehabilitation Xiangya HospitalCentral South UniversityChangsha 410008China National Clinical Research Center for Geriatric Disorders Xiangya HospitalCentral South UniversityChangsha 410008China

Aging increases the risks of various diseases and the vulnerability to *** senescence is a hallmark of aging that contributes greatly to aging and aging-related *** study demonstrates that extracellular vesicles from human urine-derived stem cells(USC-EVs)efficiently inhibit cellular senescence in vitro and in *** intravenous injection of USC-EVs improves cognitive function,increases physical fitness and bone quality,and alleviates aging-related structural changes in different organs of senescence-accelerated mice and natural aging *** anti-aging effects of USC-EVs are not obviously affected by the USC donors’ages,genders,or health *** analysis reveals that USC-EVs are enriched with plasminogen activator urokinase(PLAU)and tissue inhibitor of metalloproteinases 1(TIMP1).These two proteins contribute importantly to the anti-senescent effects of USC-EVs associated with the inhibition of matrix metalloproteinases,cyclin-dependent kinase inhibitor 2A(P16INK4a),and cyclin-dependent kinase inhibitor 1A(P21cip1).These findings suggest a great potential of autologous USC-EVs as a promising anti-aging agent by transferring PLAU and TIMP1 proteins.

关键词： Extracellular vesicles Urine-derived stem cells Cellular senescence Anti-aging PLAU TIMP1 Senescence-accelerated mice Natural aging mice

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紫菀酮对体外破骨细胞分化和活性的影响及作用机制研究

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中医正骨 2023年第6期35卷 24-35页

作者：苏珮茹罗香雅余丽娜曾春平周琳广州医科大学附属第五医院广东广州510700 华北理工大学公共卫生学院河北唐山063210

目的:探讨紫菀酮对体外破骨细胞分化和活性的影响及作用机制。方法:①分析紫菀酮对核因子κB受体活化因子配体(receptor activator of nuclear factorκB ligand,RANKL)诱导Raw 264.7细胞向破骨细胞分化的影响。将Raw 264.7细胞分为空... 详细信息

目的:探讨紫菀酮对体外破骨细胞分化和活性的影响及作用机制。方法:①分析紫菀酮对核因子κB受体活化因子配体(receptor activator of nuclear factorκB ligand,RANKL)诱导Raw 264.7细胞向破骨细胞分化的影响。将Raw 264.7细胞分为空白对照组、阳性对照组、紫菀酮1μmol·L^(-1)干预组、紫菀酮2.5μmol·L^(-1)干预组、紫菀酮5μmol·L^(-1)干预组和紫菀酮10μmol·L^(-1)干预组,空白对照组加入完全培养基,阳性对照组加入含25 ng·mL^(-1)RANKL的完全培养基,其余各组分别加入含有相应浓度紫菀酮及25 ng·mL^(-1)RANKL的完全培养基,培养5 d后进行抗酒石酸酸性磷酸酶(tartrateresistant acid phosphatase,TRAP)染色,统计各组破骨细胞数;②分析紫菀酮对Raw 264.7细胞活力的影响。将Raw 264.7细胞分为空白对照组、紫菀酮1μmol·L^(-1)干预组、紫菀酮2.5μmol·L^(-1)干预组、紫菀酮5μmol·L^(-1)干预组和紫菀酮10μmol·L^(-1)干预组,空白对照组加入完全培养基,其余各组分别加入含有相应浓度紫菀酮的完全培养基,分别培养48 h、120 h后测定各组细胞活力;③分析紫菀酮对破骨细胞纤维状肌动蛋白环形成的影响。将Raw 264.7细胞分为空白对照组、阳性对照组、紫菀酮5μmol·L^(-1)干预组和紫菀酮10μmol·L^(-1)干预组,空白对照组加入完全培养基,阳性对照组加入含25 ng·mL^(-1)RANKL的完全培养基,紫菀酮5μmol·L^(-1)干预组和紫菀酮10μmol·L^(-1)干预组分别加入含有相应浓度紫菀酮及25 ng·mL^(-1)RANKL的完全培养基,培养5 d后采用鬼笔环肽和4’,6二脒基2苯基吲哚染色,观察各组破骨细胞纤维状肌动蛋白环形成情况。④分析紫菀酮对核因子κB(nuclear factorκB,NFκB)转录活性的影响。将稳定转染pGL4.32[luc2P/NFκBRE/Hygro]载体的RAW 264.7细胞分为空白对照组、阳性对照组和紫菀酮10μmol·L^(-1)干预组,空白对照组及阳性对照组加入完全培养基,紫菀酮10μmol·L^(-1)干预组加入终浓度为10μmol·L^(-1)紫菀酮的完全培养基;培养2 h后,阳性对照组及紫菀酮10μmol·L^(-1)干预组分别加入RANKL溶液,使培养基中RANKL的终浓度为25 ng·mL^(-1);继续培养6 h后,检测各组细胞荧光素酶的荧光强度。⑤分析紫菀酮对核因子κB抑制蛋白激酶α亚基(inhibitor of nuclear factor kappaB kinase subunitα,IκBα)蛋白表达的影响。将Raw 264.7细胞分为阳性对照组和紫菀酮10μmol·L^(-1)干预组,每组6孔,分别编号1~6。待细胞贴壁后,阳性对照组加入完全培养基,紫菀酮10μmol·L^(-1)干预组加入终浓度为10μmol·L^(-1)紫菀酮的完全培养基,继续培养2 h后,在2组的1号孔加入RANKL溶液使RANKL终浓度为25 ng·mL^(-1),在1号孔加入RANKL溶液后30 min、40 min、50 min、55 min,分别在2号、3号、4号、5号孔加入RANKL溶液至RANKL终浓度为25 ng·mL^(-1)。在1号孔加入RANKL后60 min,收集各孔细胞,采用蛋白印迹法检测IκBα蛋白的表达量。⑥分析紫菀酮对破骨细胞特异性基因转录的影响。将Raw 264.7细胞分为阳性对照组、紫菀酮5μmol·L^(-1)干预组和紫菀酮10μmol·L^(-1)干预组。阳性对照组加入含25 ng·mL^(-1)RANKL的完全培养基,紫菀酮5μmol·L^(-1)干预组和紫菀酮10μmol·L^(-1)干预组分别加入含有相应浓度紫菀酮和25 ng·mL^(-1)RANKL的完全培养基,培养5 d后,收集各组细胞,采用实时定量PCR检测组织蛋白酶K、空泡型ATP酶d2亚基(vacuolar ATPase subsnit D2,VATPase d2)、TRAP的mRNA表达量。⑦分析紫菀酮对活化T细胞核因子c1(nuclear factor of activated T cells c1,NFATc1)蛋白表达的影响。将Raw 264.7细胞分为阳性对照组和紫菀酮10μmol·L^(-1)干预组,每组4孔,分别编号1~4。待细胞贴壁后,阳性对照组加入完全培养基,紫菀酮10μmol·L^(-1)干预组加入终浓度为10μmol·L^(-1)紫菀酮的完全培养基。

关键词：骨质疏松破骨细胞细胞分化紫菀酮体外研究技术信号传导 NFκB 组织蛋白酶K 腺苷三磷酸酶抗酒石酸酸性磷酸酶 NFATC转录因子

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Co-alteration of Myc and RTK-RAS pathways defines a liver-metastatic propensity and immune-cold subgroup of pancreatic adenocarcinoma

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Genes & Diseases 2024年第3期11卷 47-50页

作者： Yuyuan Zhang Ziyang Zu Hui Xu Siyuan Weng Yuqing Ren Quan Cheng Peng luo Jian Zhang Zaoqu Liu Xinwei Han Department of Interventional Radiology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan450052China Interventional Institute of Zhengzhou University ZhengzhouHenan450052China Interventional Treatment and Clinical Research Center of Henan Province ZhengzhouHenan 450052China Department of Hepatobiliary and Pancreatic Surgery The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan 450052China Department of Respiratory and Critical Care Medicine The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan450052China Department of Neurosurgery Xiangya HospitalCentral South UniversityChangshaHunan 410008China Department of Oncology Zhujiang HospitalSouthern Medical UniversityGuangzhouGuangdong 510280China

Co-altered pathways refer to the phenomenon where multiple biological pathways exhibit aberrant changes simultaneously within the same tumor *** phenomenon can facilitate a better understanding of the mechanism and evolution of tumors and serve as a biological marker for diagnosing,classifying,and treating tumors.1 However,the nature of alteration occurrence and the impact on pancreatic adenocarcinoma(PAAD)remain *** SELECT algorithm was originally designed to systematically assess the evolutionary dependencies and their impact between altered genes in cancer for anticipating drug resistance and proposing alternative ***,to better characterize the etiology of PAAD and develop an improved risk assessment strategy,2 by utilizing SELECT,we identified a co-altered pathway subgroup of PAAD that demonstrated an elevated risk for unfavorable prognosis,a propensity for liver metastasis,and an immunologically cold microenvironment.

关键词： adenocarcinoma elevated alteration

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Cytokines-activated nuclear IKKα-FAT10 pathway induces breast cancer tamoxifen-resistance

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Science China(Life Sciences) 2024年第7期67卷 1413-1426页

作者： Xueyan Chen Weilin Wu Ji-Hak Jeong Matjaz Rokavec Rui Wei Shaolong Feng Werner Schroth Hiltrud Brauch Shangwei Zhong Jun-Li luo Department of Oncology Xiangya HospitalCentral South UniversityChangsha 410008China Department of Molecular Medicine The Scripps Research InstituteJupiter 33458USA Dr.Margarete Fischer-Bosch-Institute of Clinical Pharmacology Stuttgart 70376Germany iFIT Cluster of Excellence University of TübingenTübingen 72074Germany The Cancer Research Institute and the Second Affiliated Hospital Henyang Medical SchoolUniversity of South ChinaHengyang 421001China National Health Commission Key Laboratory of Birth Defect Research and Prevention Hunan Provincial Maternal and Child Health Care HospitalChangsha 410008China

Endocrine therapy that blocks estrogen signaling is the most effective treatment for patients with estrogen receptor positive(ER+)breast ***,the efficacy of agents such as tamoxifen(Tam)is often compromised by the development of *** we report that cytokines-activated nuclear IKKαconfers Tam resistance to ER+breast cancer by inducing the expression of FAT10,and that the expression of FAT10 and nuclear IKKαin primary ER+human breast cancer was correlated with lymphotoxinβ(LTB)expression and significantly associated with relapse and metastasis in patients treated with adjuvant ***αactivation or enforced FAT10 expression promotes Tam-resistance while loss of IKKαor FAT10 augments Tam *** induction of FAT10 by IKKαis mediated by the transcription factor Pax5,and coordinated via an IKKα-p53-miR-23a circuit in which activation of IKKαattenuates p53-directed repression of ***,our findings establish IKKα-to-FAT10 pathway as a new therapeutic target for the treatment of Tam-resistant ER+breast cancer.

关键词： nuclear IKKα breast cancer Tam-resistance FAT10 Pax5 lymphotoxin nuclear IKKα-FAT0 pathway

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