Materials displaying room‐temperature phosphorescence (RTP) have been attracting wide attention in recent years due to their distinctive characteristics including long emissive lifetime and large Stokes shift, and their various applications. Most synthesized RTP materials are metal complexes that display enhanced intersystem crossing and crystallization is a common way to restrict nonradiative transition. Amorphous metal‐free RTP materials, which do not rely on expensive and toxic metals and can be prepared in a straightforward fashion, have become an important branch of the field. This Minireview summarizes recent progress in amorphous RTP materials according to the approaches used to immobilize phosphors: host–guest interactions, molecule doping, copolymers, and small‐molecule self‐assembly. Some existing challenges and insightful perspectives are given at the end of the Minireview, which should benefit the future design and development of amorphous metal‐free RTP materials.

In order to selectively target malignant cells and eliminate severe side effects of conventional chemotherapy, biocompatible and redox-responsive hollow nanocontainers with tumor specificity were fabricated. The mechanized nanocontainers were achieved by anchoring mechanically interlocked molecules, i.e., [2]rotaxanes, onto the orifices of hollow mesoporous silica nanoparticles via disulfide bonds as intermediate linkers for intracellular glutathione-triggered drug release. The [2]rotaxane employed was mainly composed of U.S. Food and Drug Administration approved tetraethylene glycol chains, α-cyclodextrin, and folic acid. In this study, folate groups on the mechanized hollow nanocontainers act as both the tumor-targeting agents and stoppers of the [2]rotaxanes. Detailed investigations showed that anticancer drug doxorubicin loaded mechanized nanocontainers could selectively induce the apoptosis and death of tumor cells. The drug-loaded nanocontainers enhanced the targeting capability to tumor tissues in vitro and inhibited the tumor growth with minimal side effects in vivo. The present controlled and targeted drug delivery system paves the way for developing the next generation of nanotherapeutics toward efficient cancer treatment.

Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) is characterized by uncontrolled progressive lung inflammation. Macrophages serve a key role in the pathogenesis of ALI/ARDS. Macrophage pyroptosis is a process of cell death releasing the proinflammatory cytokines interleukin (IL)-1β and IL-18. It was hypothesized that macrophage pyroptosis may partially account for the uncontrolled lung inflammation of ALI/ARDS. In the present study, greater macrophage pyroptosis in lipopolysaccharide (LPS)-treated macrophages and the ALI/ARDS mouse model was observed. The expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing (NLRP)3 and IL-1β and cleavage of caspase-1 were significantly elevated following LPS treatment accompanied by greater activation of p38 mitogen-activated protein kinase (MAPK) signaling in vitro and in vivo. However, blocking p38 MAPK signaling through the inhibitor SB203580 significantly suppressed the acute lung injury and excessive lung inflammation in vivo, consistent with the reduced expression of the NLRP3 inflammasome and IL-1β and cleavage of caspase-1. Pretreatment of the rat NR8383 macrophage cell line with SB203580 significantly decreased the population of caspase-1+PI+ pyroptotic cells and expression of NLRP3/IL-1β. However, a larger population of Annexin V+PI- apoptotic cells was observed following blocking of the p38 MAPK signaling pathway. The results indicated that blockage of p38 MAPK signaling pathway skewed macrophage cell death from proinflammatory pyroptosis towards non-inflammatory apoptosis. These effects may contribute to attenuated acute lung injury and excessive inflammation in the SB203580-treated mice. The results may provide a novel therapeutic strategy for the treatment of uncontrolled lung inflammation in patients with ALI/ARDS.