To improve water solubility and bioavailability, curcumin (Cur) was encapsulated by liposomes (Cur-Lip), which was further coated with thiolated chitosan (CSSH) to form liposomal hydrogels (CSSH/Cur-Lip gel). The hydrogels were thermosensitive with in situ injectable performance, which were fluidic at room temperature and gelled quickly at 37 °C. The cumulative release ratio of the 200 μM CSSH/Cur-Lip gel was 31.57 ± 1.34% at 12 h, which could effectively delay the release of curcumin. Worthily, the resilient hydrogels were compressive even after five cycles of compression. The cytotoxicity test indicated that the liposomal hydrogels had good cytocompatibility, but after encapsulation of curcumin, MCF-7 cells were suppressed and killed dramatically after 72 h. The in vivo breast cancer recurrence experiment showed that the CSSH/Cur-Lip gel inhibited breast cancer recurrence after tumors were resected, and the tissue of defect in the CSSH/Cur-Lip gel group was repaired. The results showed that the drug-loaded liposomal hydrogels can deliver curcumin continuously and exerted an excellent tumoricidal effect in vitro and in vivo. The injectable, in situ-formable, and thermosensitive CSSH/Cur-Lip gel can be designed as a promising novel drug delivery vehicle to be used as carriers for local accurate and sustained drug delivery to minimize burst release and as tissue engineering scaffolds for tissue regeneration after tumor resection.

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Long-term studies have shown that virus infection affects the energy metabolism of host cells, which mainly affects the function of mitochondria and leads to the hydrolysis of ATP in host cells, but it is not clear how virus infection participates in mitochondrial energy metabolism in host cells. In our study, HUVEC cells were infected with HSV-1, and the differentially expressed genes were obtained by microarray analysis and data analysis. The viral gene encoding protein UL16 was identified to interact with host protein ANT2 by immunoprecipitation and mass spectrometry. We also reported that UL16 transfection promoted oxidative phosphorylation of glucose and significantly increased intracellular ATP content. Furthermore, UL16 was transfected into the HUVEC cell model with mitochondrial dysfunction induced by d-Gal, and it was found that UL16 could restore the mitochondrial function of cells. It was first discovered that viral protein UL16 could enhance mitochondrial function in mammalian cells by promoting mitochondrial metabolism. This study provides a theoretical basis for the prevention and treatment of mitochondrial dysfunction or the pathological process related to mitochondrial dysfunction.