Novel BODIPY photosensitizers were developed for imaging-guided photodynamic therapy. The introduction of a strong electron donor to the BODIPY core through a phenyl linker combined with the twisted arrangement between the donor and the BODIPY acceptor is essential for reducing the energy gap between the lowest singlet excited state and the lowest triplet state (DE ST ), leading to a significant enhancement in the intersystem crossing (ISC) of the BODIPYs. Remarkably, the BDP-5 with the smallest DE ST (ca. 0.44 eV) exhibited excellent singlet oxygen generation capabilities in both organic and aqueous solutions. BDP-5 also displayed bright emission in the far-red/near-infrared region in the condensed states. More importantly, both in vitro and in vivo studies demonstrated that BDP-5 NPs displayed a high potential for photodynamic cancer therapy and bioimaging.

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Boron-dipyrromethene (BODIPY) dyes have aroused considerable interest in cancer theranostics over the past decade because of robust photochemical properties. Although a large number of BODIPY photosensitizers (PSs) containing heavy atoms have been reported, the development of heavy-atom-free BODIPY PSs for oncologic photodynamic therapy (PDT) has been limited mainly by the uncertainty in intersystem crossing (ISC) mechanisms, unbalanced phototoxic effectiveness and fluorescence quantum yields, and aggregation-caused quenching effects. In addition, the lack of extensive in vivo studies of heavy-atom-free BODIPY PSs continues to limit clinical application. Herein, novel heavy-atom-free BODIPY-phenoxazine triads (BDP-8/BDP-9) that generate efficient excited triplet states via radical pair intersystem crossing (RP-ISC) followed by triplet charge recombination were developed for use in fluorescence image-guided PDT. BDP-8/BDP-9 exhibited high molar absorption coefficients, prominent aggregation-induced emission, and excellent singlet oxygen generation capability upon light irradiation. The corresponding BODIPY nanoparticles (BDP-8/BDP-9 NPs) with bright red emission, considerable phototoxicity, and excellent tumor-targeting ability were simply prepared by encapsulating BDP-8/BDP-9 PSs in a polymeric matrix. More importantly, the results of both in vitro and in vivo experiments demonstrated the considerable potential of BDP-8 NPs for image-guided photodynamic cancer therapy. This study may inspire the development of potential BODIPY-based nanoagents for cancer theranostics.

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Atopic dermatitis (AD) is an inflammatory skin disease caused by an imbalance between Th1 and Th2 cells. AD patients suffer from pruritus, excessive dryness, red or inflamed skin, and complications such as sleep disturbances and depression. Although there are currently many AD treatments available there are insufficient data on their long-term stability and comparative effects. Moreover, they have limitations due to various side effects. Multipotent mesenchymal stem cells (M-MSCs) might have potential for next-generation AD therapies. MSCs are capable of immune function regulation and local inflammatory response inhibition. M-MSCs, derived from human embryonic stem cells (hESC), additionally have a stable supply. In L507 antibody array, M-MSCs generally showed similar tendencies to bone marrow-derived mesenchymal stem cells (BM-MSCs), although the immunoregulatory function of M-MSCs seemed to be superior to BM-MSCs. Based on the characteristics of M-MSCs on immunoregulatory functions, we tested a M-MSC conditioned media concentrate (MCMC) in mice with AD lesions on their dorsal skin. MCMC significantly decreased RNA expression levels of inflammatory cytokines in the mouse dorsal skin. It also suppressed serum IgE levels. In addition, significant histopathologic alleviation was identified. In conclusion, secretions of M-MSCs have the potential to effectively improve AD-related inflammatory lesions. M-MSCs showed potential for use in next-generation AD treatment.

Abstract. Troglitazone (TGZ) is a synthetic peroxisome proliferator-activated receptor γ (PPARγ) ligand that exhibits potential antitumor effects on a number of cancer subtypes, including prostate cancer. However, little is known about the effect of TGZ on metastasis in prostate cancer. The aim of the present study was to determine the inhibitory effect and mechanism underlying TGZ on cell growth, migration and invasion using the prostate cancer PC-3 cell line. Cellular migration and invasion were evaluated by performing a wound healing assay and Matrigel assay, respectively. The expression levels of mRNA and protein were determined by reverse transcription-quantitative polymerase chain reaction and western blotting. The results demonstrated that TGZ dose-dependently inhibited cell migration and invasion of PC-3 cells. The present study also revealed that TGZ increased the mRNA and protein levels of E-cadherin and glutathione peroxidase 3 (GPx3) in human prostate cancer PC-3 cells. In addition, GW9662, a PPARγ antagonist, attenuated the increased mRNA and protein levels of E-cadherin and GPx3, suggesting that the PPARγ-dependent signaling pathway was involved. Taken together, these results suggested that the anti-migration and anti-invasion effect of TGZ on PC-3 prostate cancer cells is, at least in part, mediated via upregulation of E-cadherin and GPx3. The present study also concluded that PPARγ may be used as a potential remedial target for the prevention and treatment of prostate cancer cell invasion and metastasis.