The effect of ginger powder and Chinese herbal medicine on production performance, serum metabolites and antioxidant status of laying hens under heat-stress condition.

This study was done to evaluate the effects of Chinese herbal medicine (CHM) and ginger powder on layers-production performance, serum metabolites and antioxidant status under heat stress condition. Two hundred and fifty Lohmann layers were randomly divided into 5 different, including two controls and three experimental groups (H1, H2, and H3). Control groups were fed the basic diet without supplementation, while, the feed of three experimental groups was supplemented with 3.32 g CHM, 10 g ginger powder, and 10 g ginger powder+ 3.32 g CHM per kg of diet, respectively. Results showed that feed consumption and production rate were decreased in the HC group, while, feed intake and production significantly improved when birds were given supplemented diet. The production rate and feed intake of the H3 group were even significantly higher than the NC group. The birds that received supplemented diet had higher glucose level compared to HC. Triglycerides and serum cholesterol had significantly decreased level in supplemented groups compared to HC. Fungal catalase (CAT) level was significantly improved in H2 and H3 groups. Nitric oxide (NO), glutathione peroxidase (GSH-PX) and Total Protein (T-AOC) level were significantly improved in supplemented groups. Findings showed that ginger powder and CHM could be a viable alternative to the synthetic antibiotic in poultry feed.

Navicularines A-C: New diterpenoid alkaloids from Aconitum naviculare and their cytotoxic activities.

Three new bisditerpenoid alkaloids, navicularines A-C (1-3), and three known ones (4-6), were isolated from the ground parts of Aconitum naviculare. Their structures were elucidated by spectroscopic methods. All the new compounds were tested against five cell lines (HL-60, SMMC-7721, A-549, MCF-7, SW480). It was found that navicularine B exhibited certain cytotoxic activities in vitro, with IC50 values of 13.50, 18.52, 17.22, 11.18, and 16.36µM, respectively.

Scutellaria barbata D. Don extract inhibits the tumor growth through down-regulating of Treg cells and manipulating Th1/Th17 immune response in hepatoma H22-bearing mice.

BACKGROUND: Previous studies showed Scutellaria barbata D. Don extract (SBE) is a potent inhibitor in hepatoma and could improve immune function of hepatoma H22-bearing mice. However, the immunomodulatory function of SBE on the tumor growth of hepatoma remains unclear. This study aimed to investigate the anti-tumor effects of SBE on hepatoma H22-bearing mice and explore the underlying immunomodulatory function. METHODS: The hepatoma H22-bearing mice were treated by SBE for 30 days. The effect of SBE on the proliferation of HepG2 cells in vitro, the growth of transplanted tumor, the cytotoxicity of natural killer (NK) cells in spleen, the amount of CD4+CD25+Foxp3+ Treg cells and Th17 cells in tumor tissue, and the levels of IL-10, TGF-ß, IL-17A, IL-2, and IFN-γ in serum of the hepatoma H22-bearing mice was observered. IL-17A was injected to the SBE treated mice from day 9 post H22 inoculation to examine its effect on tumor growth. RESULTS: SBE treatment inhibited the proliferation of HepG2 cells in vitro with a dose-dependent manner and significantly suppressed the tumor growth of hepatoma H22-bearing mice. Meanwhile, it increased NK cells' cytotoxicity in spleen, down-regulated the amount of CD4+CD25+Foxp3+ Treg cells and Th17 cells in tumor tissue, and decreased IL-10, TGF-ß, and IL-17A levels (P < 0.01) whereas increased IL-2 and IFN-γ levels (P < 0.01) in the serum of hepatoma H22-bearing mice. Moreover, administration of recombinant mouse IL-17A reversed the anti-tumor effects of SBE. CONCLUSION: SBE could inhibit the proliferation of HepG2 cells in vitro. Meanwhile, SBE also could inhibit the growth of H22 implanted tumor in hepatoma H22-bearing mice, and this function might be associated with immunomodulatory activity through down-regulating of Treg cells and manipulating Th1/Th17 immune response.