Tribovoltaic Effect Strengthened Microwave Catalytic Antibacterial Composite Hydrogel.

Microwave (MW) therapy is an emerging therapy with high efficiency and deep penetration to combat the crisis of bacterial resistance. However, as the energy of MW is too low to induce electron transition, the mechanism of MW catalytic effect remains ambiguous. Herein, a cerium-based metal-organic framework (MOF) is fabricated and used in MW therapy.

Engineering Dynamic Defect of Ce /Ce -Based Metal-Organic Framework through Ultrasound-Triggered Au Electron Trapper for Sonodynamic Therapy of Osteomyelitis.

Defect engineering is an important way to tune the catalytic properties of metal-organic framework (MOF), yet precise control of defects is difficult to achieve. Herein, a cerium-based MOF (CeTCPP) is decorated with Au nanoparticles. Under ultrasound irradiation, Au nanoparticles can precisely turn 1/3 of the pristine Ce nodes into Ce .

The recent progress on metal-organic frameworks for phototherapy.

Some infectious or malignant diseases such as cancers are seriously threatening the health of human beings all over the world. The commonly used antibiotic therapy cannot effectively treat these diseases within a short time, and also bring about adverse effects such as drug resistance and immune system damage during long-term systemic treatment. Phototherapy is an emerging antibiotic-free strategy to treat these diseases.

A novel STAT3 inhibitor W2014-S regresses human non-small cell lung cancer xenografts and sensitizes EGFR-TKI acquired resistance.

Constitutive activation of signal transducer and activator of transcription 3 (STAT3) is a common feature in human non-small cell lung cancer (NSCLC). STAT3 plays an important role in cancer progression as a driver oncogene and acquired resistance of targeted therapies as an alternatively activated pathway. W2014-S with pharmacophore structure of imidazopyridine, which was firstly reported to be utilized in STAT3 inhibitor discovery, was screened out as a potent STAT3 inhibitor from a library of small molecules.

Revisiting signal transducer and activator of transcription 3 (STAT3) as an anticancer target and its inhibitor discovery: Where are we and where should we go?

As a transcription factor, STAT3 protein transduces extracellular signals to the nucleus and then activates transcription of target genes. STAT3 has been well validated as an attractive anticancer target due to its important roles in cancer initiation and progression. Identification of specific and potent STAT3 inhibitors has attracted much attention, while there has been no STAT3 targeted drug approved for clinical application.

Chlojaponilactone B Attenuates Lipopolysaccharide-Induced Inflammatory Responses by Suppressing TLR4-Mediated ROS Generation and NF-κB Signaling Pathway.

The lindenane-type sesquiterpenoid chlojaponilactone B (), isolated from , has been reported to possess anti-inflammatory properties. The present study aimed to further explore the molecular mechanisms underlying the anti-inflammatory activity of . RNA-seq analyses revealed the significant changes in the expression levels of genes related to multiple inflammatory pathways upon treatment of lipopolysaccharide (LPS)-induced RAW 264.

sFRP1 has a biphasic effect on doxorubicin-induced cardiotoxicity in a cellular location-dependent manner in NRCMs and Rats.

Doxorubicin (Dox) is an effective anticancer drug, however, its clinical application is restricted by the life-threatening cardiotoxic effects. Secreted Frizzled-related protein 1 (sFRP1) has been reported to participate in both the cancer and cardiovascular diseases and was one of the differential expression genes in normal hearts compared with Dox-treated hearts. Thus, it is important to reveal the potential role of sFRP1 in Dox-induced cardiotoxicity.

Poly(ADP-ribose) polymerase 1 induces cardiac fibrosis by mediating mammalian target of rapamycin activity.

Cardiac fibrosis is involved in nearly all forms of heart diseases and is characterized by excessive deposition of extracellular matrix proteins by cardiac fibroblasts (CFs). We and others have reported the possibility of poly(ADP-ribose) polymerase 1 (PARP1), the founding subtype of the PARPs enzyme family, as a novel therapeutic target of heart diseases. The cardiac fibrotic induction of mammalian target of rapamycin (mTOR) is mainly due to collagen expression, Smad3- and p53/JNK-mediated apoptosis.