RESUMEN
Acute lung injury and its severe form acute respiratory distress syndrome are lethal lung diseases. So far, effective therapy for the diseases is deficient and the prognosis is poor. Recently, it was found activating nuclear factor erythroid 2-related factor 2 could attenuate the injury including inflammation, oxidative stress, and apoptosis in those diseases. To discover novel therapy, we have evaluated safflor yellow A and explored the underlying mechanisms using Beas-2B cells injured by lipopolysaccharide. As a result, safflor yellow A could improve the viability of Beas-2B cells treated with lipopolysaccharide. Further investigations have revealed safflor yellow A suppressed oxidative stress induced by lipopolysaccharide via reducing reactive oxygen species and malondialdehyde, and elevating superoxide dismutase, catalase, and glutathione peroxidase. Meanwhile, the inflammation resulting from lipopolysaccharide was ameliorated through decreasing the pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1ß, and interleukin-6. It was also found nuclear factor κB was inactivated by safflor yellow A. In addition, safflor yellow A downregulated cysteinyl aspartate specific proteinase-3 and Bcl-2-associated X protein and upregulated B-cell lymphoma-2 to inhibited apoptosis of Beas-2B cells induced by lipopolysaccharide. The activation of nuclear factor erythroid 2-related factor 2 was observed in Beas-2B cells, which was associated with the protective effects of safflor yellow A. And molecular docking elucidated safflor yellow A interacted with Kelch-like ECH-associated protein 1 to activate nuclear factor erythroid 2-related factor 2. These results can provide evidences for the discovery of novel therapy for further evaluation of safflor yellow A in the treatment of acute lung injury and acute respiratory distress syndrome.
RESUMEN
Nasopharyngeal carcinoma (NPC) is a malignant disease that threatens the health of humans. To find effective agents for the inhibition of Epstein-Barr virus (EBV) infection, which is associated with NPC, a phytochemical investigation of Ganoderma lucidum was carried out in the present study. Five triterpenoids were identified, including ganoderic acid A (compound 1), ganoderic acid B (compound 2), ganoderol B (compound 3), ganodermanontriol (compound 4), and ganodermanondiol (compound 5), on the basis of spectroscopic analysis. An inhibition of EBV antigens activation assay was implemented to elucidate the triterpenoids from G. lucidum and potentially prevent NPC. All the triterpenoids showed significant inhibitory effects on both EBV EA and CA activation at 16 nmol. At 3.2 nmol, all the compounds moderately inhibited the activation of the two antigens. The activity of telomerase was inhibited by these triterpenoids at 10 µM. Molecular docking demonstrated that compound 1 was able to inhibit telomerase as a ligand. In addition, the physicochemical properties of these compounds were calculated to elucidate their drug-like properties. These results provided evidence for the application of these triterpenoids and whole G. lucidum in the treatment of NPC.
RESUMEN
OBJECTIVE: To investigate the relation between levels of intercellular adhesion molecule-1, interleukin-6 and airway hyperresponsiveness in patients with allergic rhinitis. METHODS: Fifty-four patients with allergic rhinitis (AR) and 20 controls were included in the study. The levels of intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in nasal lavage fluid, gathered 1 hour after specific allergen nasal provocation test (SANPT), were detected by sandwich enzyme-linked immunosorbent assay (ELISA) technique. The pulmonary function (FEV1) and nonspecific bronchial provocation test were measured in 54 patients with AR, 36 patients with AR and bronchial asthma (BA) and 20 controls. At the same time, the correlation between levels of ICAM-1 and IL-6 in nasal lavage fluid and pulmonary function (FEV1) was studied. RESULTS: The levels of ICAM-1 and IL-6 in nasal lavage fluid from patients with AR were (272.75 +/- 32.25) pg/ml and (52.11 +/- 16.54) pg/ml, significantly higher than those the controls, which were (158.82 +/- 33.88) pg/ml and (25.64 +/- 10.14) pg/ml (P < 0.01). The pulmonary function (FEV1) in patients with AR and BA was (78.82 +/- 7.41)%. It was obviously lower than that in patients with AR [(83.90 +/- 4.87)%], much lower than that in normal controls [(90.25 +/- 4.69)%]. The difference among them was significant. In patients with AR, the positive percentage of bronchial provocation test was 64.81%, in patients with AR and BA, it was 83.33% in normal controls, it was 0. The differences among them had very significant meaning. The levels of ICAM-1 and IL-6 in nasal provocation fluid had closely negative correlation with pulmonary function (FEV1), r = -0.7071, -0.6248, P < 0.01. CONCLUSIONS: The close correlation was observed in upper and lower airway for allergic inflammation. The pulmonary function of patients with AR was lower, and 64. 8% of them had airway hyperresponsiveness, so that they had the potent possibility to have bronchial asthma.