RESUMEN
Background: Cynara scolymus has bioactive constituents and has been used for therapeutic actions. The present study was undertaken to investigate the mechanisms underlying pain-relieving effects of the hydroethanolic extract of C. scolymus (HECS). Methods: The antinociceptive activity of HECS was assessed through formalin and acetic acid-induced writhing tests at doses of 50, 100 and 200 mg/kg intraperitoneally. Additionally, naloxone (non-selective opioid receptors antagonist, 2 mg/kg), atropine (non-selective muscarinic receptors antagonist, 1 mg/kg), chlorpheniramine (histamine HH1-receptor antagonist, 20 mg/kg), cimetidine (histamine H2-receptor antagonist, 12.5 mg/kg), flumazenil (GABAA/BDZ receptor antagonist, 5 mg/kg) and cyproheptadine (serotonin receptor antagonist, 4 mg/kg) were used to determine the systis implicated in HECS-induced analgesia. Impact of HECS on locomotor activity was executed by open-field test. Determination of total phenolic content (TPC) and total flavonoid content (TFC) was done. Evaluation of antioxidant activity was conducted iploying 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radical scavenging assay. Results: HECS (50, 100 and 200 mg/kg) significantly indicated dose dependent antinociceptive activity against pain-related behavior induced by formalin and acetic acid (P < 0.001). Pretreatment with naloxone, atropine and flumazenil significantly reversed HECS-induced analgesia. Antinociceptive effect of HECS riained unaffected by chlorpheniramine, cimetidine and cyproheptadine. Locomotor activity was not affected by HECS. TPC and TFC of HECS were 59.49 ± 5.57 mgGAE/g dry extract and 93.39 ± 17.16 mgRE/g dry extract, respectively. DPPH free radical scavenging activity (IC50) of HECS was 161.32 ± 0.03 µg/mL. Conclusions: HECS possesses antinociceptive activity which is mediated via opioidergic, cholinergic and GABAergic pathways.
RESUMEN
The aim of the current study was to determine protective effects of betaine on depressive-like behaviors in zinc oxide nanoparticles (ZnO NPs) exposed mice. Forty male mice randomly allocated into four experimental groups. Group 1 kept as control and groups 2-4 received oral administration of betaine (30 mg/kg), ZnO NPs (600 mg/kg), and ZnO NPs (600 mg/kg) 1 h after pre-administration of betaine (30 mg/kg) for 7 days, respectively. Then, forced swimming test (FST), tail suspension test (TST), open field test (OFT), and rotarod tests were done. Furthermore, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) levels were determined. Hippocampal tissue samples were collected for histopathological assessment. According to the results, treatment with ZnO NPs significantly increased immobility time in the FST and TST (P<0.05). Betaine significantly decreased immobility time in the FST and TST (P<0.05). Pretreatment with betaine significantly decreased ZnO NPs-induced alterations in the FST and TST (P<0.05). The duration of staying on the rotarod and the numbers of crossings in the OFT significantly decreased in the mice that received ZnO NPs (P<0.05). These results were significantly improved in betaine+ZnO NPs treated mice as compared to the ZnO NPs group (P<0.05). Treatment with ZnO NPs significantly increased serum MDA level while decreased SOD and GPx compared to the control group (P<0.05). These changes were effectively ameliorated by pretreatment with betaine compared to the ZnO NPs group (P<0.05). No significant effect on serum TAC level was observed in all groups (PË0.05). Administration of ZnO NPs decreased the thickness of hippocampus and pyramidal neurons in the hippocampal dentate gyrus (DG) and CA1 regions were sparsely arranged. Pretreatment with betaine caused an improvement in the histological features of the hippocampus when compared with ZnO NPs-treated mice. Taken together, these results suggest that betaine has protective role against ZnO NPs-induced toxicity in mice.