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Microorganism invasion is still a severe threat for wound healing, which usually induces severe complications and cannot be eradicated completely. Thus, a biodegradable nanomaterial for guarding against bacteria-associated wound infection and accelerating wound healing is of vital importance. Here, black phosphorus nanosheets (BPs) were successfully decorated with cationic carbon dots (CDs) through an in situ growth strategy. The BPs@CDs exhibit photon-responsiveness and contact-responsiveness as an antibacterial agent, which shorten wound healing time. Moreover, the BPs@CDs show available photothermal and photodynamic therapy via exploring their photothermal properties and the ability of singlet-oxygen (1O2) production. Astonishingly, the BPs@CDs could possess antibacterial activity even without laser illumination due to an electrostatic attraction between bacteria and cationic CDs on the surface of BPs. This chemical therapy causes the antibacterial process to occur more accurately and for a faster 1O2 release to kill bacteria than in a normal process. Importantly, BPs@CDs display outstanding cytocompatibility and hemocompatibility. In vitro and in vivo investigations demonstrate that the BPs@CDs have enhanced antibacterial effect and can significantly accelerate skin tissue regeneration and wound closure. Given their antibacterial triple-combination therapy and excellent physicochemical properties, the broad application of BPs@CDs in bacteria-associated wound management is anticipated.

Specific chemical reactions only happen in the tumor region and produce abundant special chemicals to in situ trigger a train of biological and pathological effects that may enable tumor-specific curative effects to treat cancer without causing serious side effects on normal cells or organs. Chemodynamic therapy (CDT) is a rising tactic for cancer therapy, which induces cancer cell death via a localized Fenton reaction. However, the tumor therapeutic effect is limited by the efficiency of the chemical reaction and relies heavily on the catalyst. Here, we constructed hollow porous carbon coated FeS2 (HPFeS2@C)-based nanocatalysts for triple-enhanced CDT. Tannic acid was encapsulated in HPFeS2@C for reducing Fe3+ to Fe2+, which had a better catalytic activity to accelerate the Fenton reaction. Afterward, glucose oxidase (GOx) in nanocatalysts could consume glucose in the tumor microenvironment and in situ synchronously produce H2O2, which could improve Fenton reaction efficiency. Meanwhile, the consumption of glucose could lead to the starvation effect for cancer starvation therapy. The photothermal effects of HPFeS2@C could generate heat, which further sped up the Fenton process and implemented synergetic photothermal therapy/starvation therapy/CDT. The biodistribution of nanoparticles was investigated by multimodal magnetic resonance, ultrasound, and photoacoustic imaging. These nanocatalysts could trigger the catalytic Fenton reaction at a high degree, which might provide a good paradigm for nanocatalytic tumor therapy.

Chronic cystitis is characterized by the hyperplasia and fibrosis of the bladder wall as well as attenuated compliance of the bladder. To further unravel its underlying molecular mechanism, the role of NFκB-JMJD3 signaling pathway in cystitis induced bladder fibrosis was investigated. Jmjd3 and Col1/3 expression was detected in a cystitis mouse model that was developed by intraperitoneal injection of cyclophosphamide (CYP). Human bladder smooth muscle cells (hBSMCs) were stimulated in vitro with lipopolysaccharide (LPS), and the cell proliferation and collagen accumulation were detected using EdU, CCK8, flow cytometry, qPCR, western blotting and immunofluorescence assays. Furthermore, the effects of NFκB and JMJD3 on cell proliferation and collagen accumulation were investigated using its selective antagonists, JSH23 and GSK-J4, respectively. CYP induced cystitis significantly increased Jmjd3, Col1 and Col3 expression in the bladder muscle cells. Furthermore, LPS stimulation markedly activated NFκB signaling and elevated JMJD3 expression in hBSMCs, and the activation of NFκB-JMJD3 signaling significantly promoted cell proliferation and collagen accumulation by upregulating CCND1 and COL1/3 expression, respectively. Our study reveals the critical role of NFκB-JMJD3 signaling in cystitis induced bladder reconstruction by regulating hBSMC proliferation and extracellular matrix (ECM) deposition, and these findings provide an avenue for effective treatment of patients with cystitis.

Specific chemical reactions only happen in the tumor region and produce abundant special chemicals to in situ trigger a train of biological and pathological effects that may enable tumor-specific curative effects to treat cancer without causing serious side effects on normal cells or organs. Chemodynamic therapy (CDT) is a rising tactic for cancer therapy, which induces cancer cell death via a localized Fenton reaction. However, the tumor therapeutic effect is limited by the efficiency of the chemical reaction and relies heavily on the catalyst. Here, we constructed hollow porous carbon coated FeS