Abstract The effects of α-linolenic acid (ALA) on the proliferation and adhesion of probiotics would be investigated in the present study. Effects of ALA on intestinal flora were studied by animal fecal anaerobic fermentation system in vitro, which were analyzed by high-throughput sequencing. Results showed that treatment with ALA could promote the proliferation of probiotics Lactobacillus and Bifidobacterium, and inhibit the growth of harmful bacteria Enterococcus and E. coli. ALA restored the abnormal intestinal flora caused by high-fat diet, which was beneficial to the improvement of intestinal flora structure. In addition, adhesive characteristics of probiotics to epithelial colon cells NCM460 were detected by plate counting and Gram staining, which indicated that ALA promoted adhesion of probiotics to colonic cells. In conclusion, ALA could promote the proliferation and adhesion of intestinal probiotics, which provides a basis for ALA to exert the healthy activities of intestinal probiotics.

Abstract The effects of 6-gingerol on adhesive ability of probiotics to colonic epithelial cells in vitro were explored. Two strains of probiotics were Lactophilus acidophilus and Bifidobacterium bifidum. NCM 460 cells (normal colonic epithelial cells) and Caco-2 cells (colon cancer cells) were used in this study. Effect of 6-gingerol (5, 10, 15, 20, 25, 30, 35, 40 μg/mL on NCM 460 cells and effect of 6-gingerol (10, 25, 50, 75, 100, 125, 150, 175 μg/mL) on Caco-2 cells were investigated. MTT assay was adopted to analyze cell proliferation. Methods of Gram staining and plate counting were used to analyze the probiotic adhesion to colonic epithelial cells. Results showed that 6-gingerol had no inhibitory effect on colonic epithelial cells within the non-cytotoxic dose range. 6-gingerol could promote the adhesion of probiotics to colon epithelial cells in a dose-dependent manner, which would be benefit for probiotics to exert continuous probiotic activity in the intestinal tract.

Abstract The inhibitory effects of ginger essential oil (GEO) on chemically-induced cutaneous inflammation were investigated. Three kind of experimental murine models, such as xylene-induced ear edema model, carrageenan-induced paw edema model and 2,4-dinitrofluorobenzene (DNFB)-induced allergic contact dermatitis (ACD) model were exploited to evaluate the anti-inflammatory effect of GEO. Results showed that GEO lowered the ear swelling rate induced by xylene and decreased paw edema rate induced by carrageenan of mice with cutaneous inflammation significantly. Treatment with GEO significantly inhibited DNFB-induced ear swelling degree and rate, and alleviated the inflammatory symptoms of ear skin lesions of ACD model mice markedly. Treatment with GEO decreased the gene expression of the inflammatory cytokines of auricular tissues such as TLR-2, TLR-4, TNF-α, IFN-γ, IL-1β, IL-8, and increased the gene expression of cytokine IL-4 significantly. In conclusion, GEO has anti-inflammatory and protective effect on chemically-induced cutaneous inflammation.

OBJECTIVES:Our study aimed to investigate the impact of fatigue on the severity of stroke and to explore the underlying mechanisms.METHODS:Fatigued male rats underwent middle cerebral artery occlusion and the infarcted brain area was determined. Then, coagulation parameters were assessed in the fatigued group and a control group. In addition, the level of fibrinogen was determined in rats deprived of sleep for various numbers of days. To study whether interleukin-6 was involved in fibrinogen synthesis during fatigue, we also measured levels of interleukin-6 in rats deprived of sleep for various numbers of days. Furthermore, brain injury by middle cerebral artery occlusion was measured in wild-type mice, interleukin-6-/- mice and wild-type mice treated with bezafibrate.RESULTS:More severe cerebral infarction was observed in the fatigued rats, resulting in an infarct ratio of 23.4%. The infarct ratio was significantly increased in the fatigued rats compared with that in the control group (8%, p<0.05). The level of fibrinogen was increased significantly in the fatigued rats compared with that in the control group. In addition, a marked reduction in fibrinogen level was observed in the fatigued interleukin-6-/- mice compared to their wild-type counterparts, whereas no difference was observed between fatigued wild-type mice and interleukin-6-/- rats treated with recombinant human interleukin-6. The reduction in brain injury due to middle cerebral artery occlusion during fatigue was observed in interleukin-6-/- mice and wild-type mice treated with bezafibrate.CONCLUSION:Fatigue could increase stroke severity and was associated with the interleukin-6-induced expression of fibrinogen.