Metabolite lactic acid has always been regarded as a metabolic by-product rather than a bioactive molecule. Recently, this view has changed since it was discovered that lactic acid can be used as a signal molecule and has novel signal transduction functions both intracellular and extracellular, which can regulate key functions in the immune system. in recent years, more and more evidence has shown that lactic acid is closely related to the metabolism and polarization of macrophages. During inflammation, lactic acid is a regulator of macrophage metabolism, and it can prevent excessive inflammatory responses; in malignant tumors, lactic acid produced by tumor tissues promotes the polarization of tumor-associated macrophages, which in turn promotes tumor progression. in this review, we examined the relationship between lactic acid and macrophage metabolism. we further discussed how lactic acid plays a role in maintaining the homeostasis of macrophages, as well as the biology of macrophage polarization and the M1/M2 imbalance in human diseases. Potential methods to target lactic acid in the treatment of inflammation and cancer will also be discussed so as to provide new strategies for the treatment of diseases.
Catalytic
conversion of hydrogen peroxide (H2O2) to more
toxic hydroxyl radicals (•OH) is a good
choice for sterilization and anti-infection, but endogenous H2O2 is insufficient to achieve satisfactory sterilization
efficacy. Despite great efforts, designing and developing antimicrobial
materials that specifically and effectively self-supply H2O2 at the wound site remain as tremendous challenges.
Here, we report a pH-responsive copper peroxide-loaded wound dressing
made from copper hydroxide and gelatin sponge and then reacted with
H2O2. In vitro experiments show that the prepared
wound dressing has good bactericidal properties against Escherichia coli (E. coli), Staphylococcus aureus (S. aureus), and Pseudomonas aeruginosa (P. aeruginosa). Moreover, the as-prepared
wound dressing can release •OH specifically in the
bacterial-infected skin wound, rather than in normal tissues, and
in vivo skin wound-healing experiments proved that the synthesized
copper peroxide-loaded gelatin sponge could combat E. coli effectively; in addition, Cu2+ released from the gelatin sponge could stimulate angiogenesis and
collagen deposition simultaneously. The study provides a strategy
to improve antibacterial efficacy and reduce the toxic side effects
through the release of •OH by bacterial self-activation.
Hypoxia-induced epithelial-to-mesenchymal transition (EMT) could facilitate tumor progression. TIPE2, the tumor necrosis factor-α (TNF-α)-induced protein 8-like 2 (also known as TNFAIP8L2), is a member of the TNF-α-induced protein 8 (TNFAIP8, TIPE) family and has been involved in the development and progression of several tumors. However, the effects of TIPE2 on the EMT process in glioma cells and the underlying mechanisms of these effects have not been previously reported. In our study, we assessed the roles of TIPE2 in the EMT process in glioma cells in response to hypoxia. Our results indicated that TIPE2 expression was significantly decreased in human glioma cell lines. TIPE2 overexpression significantly inhibited hypoxia-induced migration and invasion, as well as suppressed the EMT process in glioma cells. Furthermore, TIPE2 overexpression prevented hypoxia-induced expression of β-catenin, cyclin D1, and c-myc in human glioma cells. In summary, these data suggest that TIPE2 overexpression inhibited hypoxia-induced Wnt/β-catenin pathway activation and EMT in glioma cells.
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