Effect of Cinnamon and Turmeric Aqueous Extracts on Serum Interleukin-17F Level of High Fructose-Fed Rats.

BACKGROUND: Studies have indicated that extraweight and obesity induce chronic inflammation, which can lead to other diseases such as cancers. OBJECTIVE: To evaluate the effects of two weight-lowering and anti-inflammatory agents including cinnamon, and turmeric, on serum levels of interleukin-17 (IL-17) as a pro-inflammatory cytokine. METHODS: In this study, 64 rats were designated in eight groups. The control group received normal diet. The other groups were fed with normal diet plus high cinnamon (3 mg/ml), high turmeric (3 mg/ml), high-fructose solution (30%), fructose solution with low (0.15 mg/ml) and high doses (3 mg/ml) of cinnamon and turmeric three times per week. The serum level of IL-17F was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: High fructose consumption led to an increase in the weight and serum level of IL-17. While, feeding with cinnamon and turmeric caused to decline weight but, surprisingly increased IL-17F levels. CONCLUSION: Although, some studies have showed that cinnamon and turmeric supplementation decreased IL-17F under the standard diet, in the presence of high fructose diet and extraweight their effects were reversed and caused an increase in serum level of IL-17F.

Antioxidative and immunostimulatory effect of dietary cinnamon nanoparticles on the performance of Nile tilapia, Oreochromis niloticus (L.) and its susceptibility to hypoxia stress and Aeromonas hydrophila infection.

An experiment was conducted to evaluate the effect of dietary cinnamon nanoparticles (CNP) on the growth performance, antioxidant and digestive enzymes activities, and innate immunity of Nile tilapia, Oreochromis niloticus (L.). Fish (9.7 ±â€¯0.3 g) were fed on diets enriched with 0.0, 0.25, 0.5, 1.0, 3.0, 5.0, and 10.0 g CNP/kg diet for 8 weeks. After the feeding trial, fish were challenged against hypoxia stress or pathogenic bacteria (Aeromonas hydrophila) infection. Fish performance was significantly improved with increasing CNP levels over the control diet. Furthermore, only crude protein contents in whole-fish body were significantly higher in CNP-fed fish than those fed the control diet. Antioxidant-stimulated activity was observed with dietary CNP where malondialdehyde (MDA) level and activities of superoxide dismutase (SOD) and catalase (CAT) increased significantly, whereas glutathione peroxidase (GPx) activity decreased significantly in CNP-fed fish. Likewise, CNP supplementation induced the secretion of protease, lipase, and amylase, which were maximized at 3.0-10.0 g CNP/kg diet. All innate immunity variables i.e. nitrous oxide (NO), nitro blue tetrazolium (NBT), and lysozyme activity were significantly higher in CNP-fed fish than the control one. No fish mortality was observed during hypoxia stress among all treatments, but CNP administration protected the fish against A. hydrophila infection. No mortality was observed in fish fed 3.0-10.0 g CNP/kg diet after bacterial challenge; meanwhile the mortality of fish fed the control diet was 66.7%. This study evoked that dietary CNP enhanced the performance, antioxidant and digestive enzymes activity, and innate immunity of Nile tilapia and its optimum level is 3.0 g CNP/kg diet.

Cinnamaldehyde modulates LPS-induced systemic inflammatory response syndrome through TRPA1-dependent and independent mechanisms.

Cinnamaldehyde is a natural essential oil suggested to possess anti-bacterial and anti-inflammatory properties; and to activate transient receptor potential ankyrin 1 (TRPA1) channels expressed on neuronal and non-neuronal cells. Here, we investigated the immunomodulatory effects of cinnamaldehyde in an in vivo model of systemic inflammatory response syndrome (SIRS) induced by lipopolysaccharide. Swiss mice received a single oral treatment with cinnamaldehyde 1 h before LPS injection. To investigate whether cinnamaldehyde effects are dependent on TRPA1 activation, animals were treated subcutaneously with the selective TRPA1 antagonist HC-030031 5 min prior to cinnamaldehyde administration. Vehicle-treated mice were used as controls. Cinnamaldehyde ameliorated SIRS severity in LPS-injected animals. Diminished numbers of circulating mononuclear cells and increased numbers of peritoneal mononuclear and polymorphonuclear cell numbers were also observed. Cinnamaldehyde augmented the number of peritoneal Ly6C(high) and Ly6C(low) monocyte/macrophage cells in LPS-injected mice. Reduced levels of nitric oxide, plasma TNFα and plasma and peritoneal IL-10 were also detected. Additionally, IL-1ß levels were increased in the same animals. TRPA1 antagonism by HC-030031 reversed the changes in the number of circulating and peritoneal leukocytes in cinnamaldehyde-treated animals, whilst increasing the levels of peritoneal IL-10 and reducing peritoneal IL-1ß. Overall, cinnamaldehyde modulates SIRS through TRPA1-dependent and independent mechanisms.