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-1β 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-1β. Overall, cinnamaldehyde modulates SIRS through TRPA1-dependent and independent mechanisms.
Morphine is a potent analgesic opioid used extensively for pain treatment. During the
last decade, global consumption grew more than 4-fold. However, molecular mechanisms
elicited by morphine are not totally understood. Thus, a growing literature indicates
that there are additional actions to the analgesic effect. Previous studies about
morphine and oxidative stress are controversial and used concentrations outside the
range of clinical practice. Therefore, in this study, we hypothesized that a
therapeutic concentration of morphine (1 μM) would show a protective effect in a
traditional model of oxidative stress. We exposed the C6 glioma cell line to hydrogen
peroxide (H2O2) and/or morphine for 24 h and evaluated cell
viability, lipid peroxidation, and levels of sulfhydryl groups (an indicator of the
redox state of the cell). Morphine did not prevent the decrease in cell viability
provoked by H2O2 but partially prevented lipid peroxidation
caused by 0.0025% H2O2 (a concentration allowing more than 90%
cell viability). Interestingly, this opioid did not alter the increased levels of
sulfhydryl groups produced by exposure to 0.0025% H2O2, opening
the possibility that alternative molecular mechanisms (a direct scavenging activity
or the inhibition of NAPDH oxidase) may explain the protective effect registered in
the lipid peroxidation assay. Our results demonstrate, for the first time, that
morphine in usual analgesic doses may contribute to minimizing oxidative stress in
cells of glial origin. This study supports the importance of employing concentrations
similar to those used in clinical practice for a better approximation between
experimental models and the clinical setting.
Inhibition of mushroom tyrosinase was observed with synthetic dihydropyrano[3,2-b]chromenediones. Among them, DHPC04 displayed the most potent tyrosinase inhibitory activity with a K value of 4 μm, comparable to the reference standard inhibitor kojic acid. A kinetic study suggested that these synthetic heterocyclic compounds behave as competitive inhibitors for the L-DOPA binding site of the enzyme. Furthermore, molecular modeling provided important insight into the mechanism of binding interactions with the tyrosinase copper active site.
Açai (Euterpe oleracea Mart.) fruit from the Amazon region in Brazil contains bioactive compounds such as α-tocopherol, anthocyanins (cyanidin 3-glycoside and cyanidin 3-rutinoside), and other flavonoids with antioxidant and anti-inflammatory properties. Moreover, the prebiotic activity of anthocyanins in modulating the composition of gut microbiota has emerged as an additional mechanism by which anthocyanins exert health-promoting effects. Açai consumption may be a nutritional therapeutic strategy for chronic kidney disease (CKD) patients since these patients present with oxidative stress, inflammation, and dysbiosis. However, the ability of açai to modulate these conditions has not been studied in CKD, and this review presents recent information about açai and its possible therapeutic effects in CKD.
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