RESUMEN
Luteolin, which is a natural flavonoid, has anti-inflammatory, antioxidant, and anticancer properties. Numerous studies have proven that luteolin inhibits the growth of many types of cancer cells by promoting apoptosis, autophagy, and cell cycle arrest in tumour cells. However, in vivo research on this topic has been limited. In addition, other studies have shown that luteolin exerts a good inhibitory effect on apoptosis-resistant cancer cells. While existing studies have not completely elucidated the mechanism underlying this phenomenon, we assume that luteolin, which is a natural compound that exerts its effects through various mechanisms, may have the potential to inhibit tumour growth. In our study, we proved that luteolin exerted a good inhibitory effect on the proliferation of colon cancer cells according to CCK8 and EdU fluorescence assays, and the same conclusion was drawn in animal experiments. In addition, we found that luteolin, which is an antioxidant, unexpectedly promoted oxidative stress as shown by measuring the levels of oxidative balance-related indicators, such as reactive oxygen species (ROS), SOD, H2O2 and GSH. However, the decreased oxidation of luteolin-treated HT-29 cells after treatment with the active oxygen scavenger NAC did not reverse the inhibition of cell growth. However, the Caspase1 inhibitor VX765 did reverse the inhibition of cell growth. Western blotting analysis showed that luteolin treatment increased the expression of Caspase1, Gasdermin D and IL-1ß, which are members of the pyroptosis signalling pathway, in colon cancer cells. We further intuitively observed NLRP3/Gasdermin D colocalization in luteolin-treated HT-29 cells and mouse tumour tissues by immunofluorescence. These results suggest that luteolin inhibits the proliferation of colon cancer cells through a novel pathway called pyroptosis. This study provides a new direction for the development of natural products that inhibit tumour growth by inducing pyroptosis.
RESUMEN
In the conventional method of microskin autografting, aggressive early excision is adopted, followed by coverage with a microskin-allograft complex to close extensive burn wounds. However, early excision is always associated with a defect of viable tissue, resulting in massive blood loss and causing high risk to aged patients or those with other systemic diseases. We developed a new method in which an eschar thinning operation was first adopted, followed by raising granulation tissue and microskin autografting, which was covered by a Vaseline-based moisture dressing. A total of 52 patients were included in this study and randomly assigned to the control group (n=26) and the experimental group (n=26) for the conventional method and the new method, respectively. The re-epithelisation rate on the 21st day after autografting indicated that there was no significant difference between both groups. There was also no significant difference between the two groups when the re-epithelialisation rate was compared with the type of organisms cultured. However, the Vancouver Burn Skin Score (VBSS) results demonstrated a significant improvement of cosmetic appearance in the experimental group (score=2.1) as compared to the control group (score=3.9). The new method also showed other advantages, including less blood loss, shorter surgical duration and lower cost of surgery. From this prospective study, it can be concluded that the new method can be an alternative to the conventional microskin autografting procedure.