Postoperative adhesion is a common post-surgery complication formed between the surface of the body cavity, ranging from a layer of connective tissue to a fibrous bridge containing blood vessels and nerve tissue. Despite achieving a lot of progress, the mechanisms of adhesion formation still need to be further studied. In addition, few current treatments are consistently effective in the prevention of postoperative adhesion. Hydrogel is a kind of water-expanding crosslinked hydrophilic polymer network generated by a simple reaction of one or more monomers. Due to the porous structure, hydrogels can load different drugs and control the drug release kinetics. Evidence from existing studies has confirmed the feasibility and superiority of using hydrogels to counter postoperative adhesions, primarily due to their outstanding antifouling ability. In this review, the current research status of hydrogels as anti-adhesion barriers is summarized, the character of hydrogels in the prevention of postoperative adhesion is briefly introduced, and future research directions are discussed.

Reactive oxygen species (ROS)‐mediated sonodynamic therapy (SDT) holds increasing potential in treating deep‐seated tumor owing to the high tissue‐penetration depth. However, the inevitable accumulation of sonosensitizers in normal tissues not only make it difficult to realize the in situ SDT, but also induces sonodynamic effects in normal tissues. Herein, this work reports the passivation and selective activation strategies for the sonodynamic and near‐infrared (NIR) imaging performances of an intelligent antitumor theranostic platform termed Cu‐IR783 nanoparticles (NPs). Owing to the ruptured coordination bond between IR783 with Cu ions by responding to tumor microenvironment (TME), the selective activation of IR783 only occurred in tumor tissues to achieve the visualized in‐situ SDT. The tumor‐specific released Cu ions not only realized the cascade amplification of ROS generation through Cu⁺‐mediated Fenton‐like reaction, but also triggered cuproptosis through Cu⁺‐induced DLAT oligomerization and mitochondrial dysfunction. More importantly, the immunosuppressive TME can be reversed by the greatly enhanced ROS levels and high‐efficiency cuproptosis, ultimately inducing immunogenic cell death that promotes robust systemic immune responses for the eradication of primary tumors and suppression of distant tumors. This work provides a distinct paradigm of the integration of SDT, CDT, and cuproptosis in a controlled manner to achieve visualized in‐situ antitumor therapy.

Purpose: Renal cell carcinoma (RCC) is known to be highly radioresistant but the mechanisms associated with radioresistance have remained elusive. We found DOC-2/DAB2 interactive protein (DAB2IP) frequently downregulated in RCC, is associated with radioresistance. In this study, we investigated the underlying mechanism regulating radioresistance by DAB2IP and developed appropriate treatment. Experimental Design: Several RCC lines with or without DAB2IP expression were irradiated with ionizing radiation (IR) for determining their radiosensitivities based on colony formation assay. To investigate the underlying regulatory mechanism of DAB2IP, immunoprecipitation-mass spectrometry was performed to identify DAB2IP-interactive proteins. PARP-1 expression and enzymatic activity were determined using qRT-PCR, Western blot analysis, and ELISA. In vivo ubiquitination assay was used to test PARP-1 degradation. Furthermore, in vivo mice xenograft model and patient-derived xenograft (PDX) model were used to determine the effect of combination therapy to sensitizing tumors to IR. Results: We notice that DAB2IP-deficient RCC cells acquire IR-resistance. Mechanistically, DAB2IP can form a complex with PARP-1 and E3 ligases that is responsible for degrading PARP-1. Indeed, elevated PARP-1 levels are associated with the IR resistance in RCC cells. Furthermore, PARP-1 inhibitor can enhance the IR response of either RCC xenograft model or PDX model. Conclusions: In this study, we unveil that loss of DAB2IP resulted in elevated PARP-1 protein is associated with IR-resistance in RCC. These results provide a new targeting strategy to improve the efficacy of radiotherapy of RCC.

Molecular hydrogen (H₂) has been previously reported playing an important role in ameliorating damage caused by acute radiation. In this study, we investigated the effects of H₂ on the alterations induced by low‐dose long‐term radiation (LDLTR). All the mice in hydrogen‐treated or radiation‐only groups received 0.1 Gy, 0.5 Gy, 1.0 Gy, and 2.0 Gy whole‐body gamma radiation, respectively. After the last time of radiation exposure, all the mice were employed for the determination of the body mass (BM) observation, forced swim test (FST), the open field test (OFT), the chromosome aberration (CA), the peripheral blood cells parameters analysis, the sperm abnormality (SA), the lymphocyte transformation test (LTT), and the histopathological studies. And significant differences between the treatment group and the radiation‐only groups were observed, showing that H₂ could diminish the detriment induced by LDLTR and suggesting the protective efficacy of H₂ in multiple systems in mice against LDLTR.

The small intestine is one of the most sensitive organs to irradiation injury, and the development of high effective radioprotectants especially with low toxicity for intestinal radiation sickness is urgently needed. Monophosphoryl lipid A (MPLA) was found to be radioprotective in our previous study, while its effect against the intestinal radiation injury remained unknown. In the present study, we firstly determined the intestinal apoptosis after irradiation injury according to the TUNEL assay. Subsequently, we adopted the immunofluorescence technique to assess the expression levels of different biomarkers including Ki67, γ-H2AX, and defensin 1 in vivo. Additionally, the inflammatory cytokines were detected by RT-PCR. Our data indicated that MPLA could protect the intestine from ionizing radiation (IR) damage through activating TLR4 signal pathway and regulating the inflammatory cytokines. This research shed new light on the protective effect of the novel TLR4 agonist MPLA against intestine detriment induced by IR.

Monophosphoryl lipid a attenuates radiation injury through TLR4 activation Monophosphoryl lipid a attenuates radiation injury through TLR4 activation