Mechanism of Jinrong granule in inhibiting the invasion of breast cancer cells by the CXCL-1-CXCR2/CCL20 pathway.

The purpose of this study was to explore the effect of the Jinrong granule on CXCL-1 and the mechanism of the Jinrong granule on the metastasis and apoptosis of breast cancer cell lines. MDA-MB-231 human breast cancer cell line was divided into a control group, Jinrong extract group, CXCL-1 group and Jinrong extract + CXCL-1 group. The proliferation, apoptosis and permeability of the cells in the experimental group were studied. The protein expression of CXCL-1 was detected by Western blot. On this basis, a bioinformatics method was used to analyze the mechanism of CXCL-1. The results of the CCK8 experiment showed that compared with the control group, the cell proliferation activity of the CXCL-1 treatment group was enhanced while that of the Jinrong granule group was decreased. Compared with that of the CXCL-1 treatment group, the cell proliferation rate of the CXCL-1 + Jinrong granule group was significantly lower. The results showed that CXCL-1 could inhibit apoptosis of breast cancer cells, while the Jinrong granule could reverse the inhibition of apoptosis induced by CXCL-1. The results showed that the Jinrong granule could inhibit the ability of CXCL-1 to promote the migration and proliferation of breast cancer cells. The Jinrong granule could reverse the promoting effect of CXCL-1 on breast cancer through the CXCL-1- CLCR2/CCL20 pathway. In conclusion, the Jinrong granule can inhibit the invasion of breast cancer cells through the CXCL-1-CLCR2/CCL20 pathway.

Lipoxin A4 alleviates lung injury in sepsis rats through p38/MAPK signaling pathway.

The aim of the study was to explore the effect of lipoxin A4 (LXA4) on lung injury in sepsis rats through the p38/mitogen-activated protein kinase (MAPK) signaling pathway. Sprague-Dawley rats were used for the study. The rat model of sepsis-induced acute lung injury was established via cecal ligation (Sepsis group, n=20). LXA4 (0.1 mg/kg) was injected at 6 h after modeling (Treatment group, n=20), and a The Control group (n=20) was also set up. The 7-day survival rate was 100% in The Control group, and LXA4 raised the survival rate of rats in the Sepsis group from 40% to 60% (P<0.01). Alveolar fluid clearance (AFC) significantly declined and the wet/dry weight (W/D) ratio of lung tissues rose remarkably in the Sepsis group compared with those in the Control group, while LXA4 restored AFC and reduced the W/D ratio of lung tissues (P<0.05), suggesting that LXA4 treatment reduces lung fluids and partially enhances AFC, thus lowering the W/D ratio of lung. The total cell count, polymorphonuclear neutrophils (PMN) percentage and concentration of tumor necrosis factor-α (TNF-α) and interleukin (IL)-6 in bronchoalveolar lavage fluid (BALF) were obviously increased in the Sepsis group compared with those in the Control group, while they were markedly decreased in the Treatment group (P<0.05). The activity of myeloperoxidase (MPO) in lung tissue homogenate was evidently higher in the Sepsis group than that in The Control group, while it was notably lower in the Treatment group than that in the Sepsis group after LXA4 treatment (P<0.05). Moreover, it was observed microscopically that the morphology of lung tissues was intact in the Control group. Finally, the results of Western blotting manifested that the p-p38/ MAPK protein expression was remarkably increased in the Sepsis group, indicating the activation of the p38/MAPK pathway, while it was remarkably decreased in the Treatment group, indicating the inhibited activity of the pathway (P<0.05). LXA4 has an anti-inflammatory effect on sepsis rats with lung injury, and such effect is related to the p38/MAPK signaling pathway.