Anxiety is an ailment causing personal, social and economic burden. Some drugs are available to provide symptomatic assistance for the treatment of anxiety and attempts are being made to find new therapeutic entities and subside associated adverse effects. Approaching natural sources, the current study aims to investigate the anxiolytic effects of cardamonin and its effect on the brain GABAergic system. The anxiolytic effects of various dose of cardamonin were investigated using the elevated plus maze apparatus and possible motor disabilities were evaluated trough open field test. Possible impact on GABAergic system was investigated using the ELISA. Fourteen days treatment with cardamonin (5.0 and 10.0 mg/kg, i.p.) in mice significantly (p < 0.0001) increased and the percentages of open arm entry and open arm time compared to respective vehicle control group. Cardamonin show no influence on gross locomotor movement in open field test. Treatment with cardamonin significantly (p < 0.0001) increased levels of GABA in brain of treated mice compared to control mice. This study provided evidence on the anxiolytic potency of the cardamonin and revealed its action mechanism of regulating the GABA level in mouse brain.
Background: Neutrophils are one of the components of innate immune system that defend against infectious microorganisms through various antimicrobial capabilities, including microorganism phagocytosis and by releasing bactericidal agents from intracellular secretory granules into the phagosome or to the cell exterior. Activated neutrophils represent the main source of myeloperoxidase (MPO), superoxide (SO) and subsequently derived oxygen metabolites. The current study was carried out with the aim to investigate the effect of cardamonin on N-Objective: formyl-methionyl-leucyl-phenyl-alanine (fMLP) and opsonized zymosan (OZ) stimulated SO generation in neutrophils and their degranulation measured as MPO release. pectrophotometry was used Materials and Methods: S to evaluate the effect of cardamonin (0.1 to 100.0 OZ (0.5 mg/ml) or fMLP (0.1 μmol/l) on μmol/l) stimulated SO generation and MPO release in neutrophil cells. Superoxide formation was measured in isolated neutrophils as superoxide dismutase inhibitable reduction of cytochrome c and the activity of MPO was assayed by determining the oxidation of-dianisidine in the presence of hydrogen peroxide. It is evident from one way ANCOVA o Results: followed by post-hoc test that cardamonin dose-dependently (1.0 to 100.0 significantly decreased (p < 0.05) SO μmol/l) generation and MPO release after each stimulus (fMLP or OZ). Our results indicate that cardamonin Conclusion: could support resolution of inflammation through decreased activity of neutrophils, respiratory burst and i.e. degranulation by inhibiting MPO release and by decreasing the generation of SO and the subsequently derived reactive oxygen species.
Table S1. Predicted activity of all the molecules based on hypotheses of FFAR-1 Title Predicted activity 1 Predicted activity 2 Predicted activity 3 Predicted activity 4 Predicted activity 5 6i salaski 0.
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