In the bacterial infection of humans, sepsis is of great concern based on its high fatality rate. Correction of immune dysfunction by targeting dendritic cells (DCs) is a promising strategy for sepsis therapy. Royal jelly, a natural health product, is produced by worker bees for feeding queens. In the study, we evaluated whether royal jelly could attenuate LPS-induced immune dysfunction of DCs. We found that royal jelly reduced the expression levels of mature phenotype (MHCII, CD40, CD80, and CD86), activation marker (CD69), and inflammatory cytokines (TNF-α, IL-6, and IL-10) in LPS-induced DCs. In addition, royal jelly enhanced the endocytosis levels and abrogated allogeneic CD4 + T cell proliferation in LPS-induced DCs. Finally, we found that the Nrf2/HO-1 axis played a vital role in the inhibition of LPS-induced immune dysfunction of DCs by royal jelly. These results indicated that royal jelly had a potential application in sepsis therapy by regulating DC function.
Wen-lin Li,Ke Li,Wen-guang Chang,Hui Shi,Wen-xuan Zhang,Zi Wang,Wei Li
Background Although our previous work confirmed 20(R)-ginsenoside Rg3 (R-Rg3), which is an active ingredient in the Panax Ginseng C.A. Meyer, to have good anti-diabetic activity, its beneficial effect on diabetic retinal injury was found to be limited. Purpose This study aims to investigate the protective effects of R-Rg3 on diabetes-induced retinal injury and the associated molecular mechanisms of action. Methods Diabetic retinal injury was induced in mice using a combination of a high-fat diet (HFD) and intraperitoneal injection of streptozotocin (STZ). R-Rg3 (10 and 20 mg/kg) was subsequently administered for 6 weeks. The human retinal endothelial cells (HRECs) were subjected to high glucose (HG)-induced injury for the in vitro analysis and treated with R-Rg3 (4, 8, 16 μM), antioxidant N-Acetylcysteine (NAC, 1 mM) and Nrf2 inhibitor ML385 (5 μM). The mice retinas then underwent functional and histopathological analysis. Expression levels of proteins related to the Nrf2/HO-1 axis, tight junction proteins, endoplasmic reticulum (ER) stress and the apoptosis in retinal tissue and HRECs were determined by western blot. Expressions of ZO-1 and Nrf2 in the retina and HRECs were assessed by immunofluorescence. Additional evaluations included measuring body weights, fasting blood glucose (FBG), lipid levels and oxidative markers. Results The results showed 6 weeks of R-Rg3 treatment significantly restored the functional changes and redox system imbalance that was induced by HFD/STZ in mice. R-Rg3 was also found to significantly reduce retinal barrier damage and thickness changes resulting from hyperglycaemia exposure. At the same time, R-Rg3 also protected HRECs from HG-induced damage. R-Rg3 could also activate Nrf2/HO-1 axis and inhibit endoplasmic reticulum stress as a means of alleviating retinal endothelial cells apoptosis. The molecular docking results also demonstrated that R-Rg3 had a good binding ability with Nrf2. Conclusion Our study suggested Nrf2/HO-1 axis might be crucial for the ability of R-Rg3 to prevent diabetic retinal injury.
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