In the present study, the effects of aqueous, ethanolic and chloroformic extracts of Rosa damascena on pentylenetetrazol (PTZ)-induced seizures were investigated in mice.

To study the different effects of soy extract on pentylenetetrazole (PTZ)-induced seizures in the presence and absence of ovarian hormones in rats, and the gender-dependent differences in the effects of phytoestrogens on behavior.

Background: The effects of soy extract on memory as well as the oxidative damage to brain tissue induced by ischemia was investigated in ovariectomised (OVX) rats. Methods: The rats were divided into: 1) Sham; 2) OVX; 3) Sham‑Ischemia; 4) OVX‑Ischemia; 5) OVX-‑Ischemia-‑S 20; and 6) OVX-‑Ischemia-‑S 60. The common carotid artery was occluded (30 minutes), and it was then re-‑perfused. The OVX-‑Ischemia-‑S 20 and OVX-‑Ischemia-‑S 60 groups received 20 or 60 mg/kg of soy extract for eight weeks before the ischemia. Results: The Sham-‑Ischemia and OVX-‑Ischemia groups took a longer time to reach the platform while, spent a shorter time in the target quadrant (Q1) than the Sham and OVX. The escape latencies in the OVX-‑Ischemia-‑S 20 and OVX-‑Ischemia-‑S 60 groups were lower while, time spent in the Q1 was higher than that of the OVX-‑Ischemia. In the rotarod test, there were no significant differences between the groups. The hippocampal concentrations of malondialdehyde (MDA) in the Sham-‑Ischemia and OVX-‑Ischemia groups were higher than the Sham and OVX. Pre-‑treatment by 20 and 60 mg/kg of the extract reduced the MDA. Conclusion: It is suggested that soy prevents memory impairment and brain tissue oxidative damage due to ischemia in OVX rats.

To investigate the possible anticonvulsant effect of different extracts of Eugenia caryophyllata (clove) on pentylenetetrazole (PTZ)-induced seizures in mice.

OBJECTIVETo evaluate the effect of Nigella sativa (NS) extract on memory performance and its possible mechanisms in scopolamine (Sco)-induced spatial memory impairment model using Morris water maze test.

METHODSThirty-two male Wistar rats were randomly divided into four groups. The control group received saline instead of both NS extract and Sco. The Sco group was treated by saline for two weeks, and was injected by Sco (2 mg/kg, intraperitoneally) 30 min before each trail in Morris water maze test. Sco+NS 200 and Sco+NS 400 groups were daily treated by 200 or 400 mg/kg of NS (intraperitoneally) for two weeks, respectively, and were finally injected by Sco 30 min before Morris water maze test. The brains of animals were removed to determine the acetylcholinesterase (AChE) activity and oxidative stress criteria in cortical tissues.

RESULTSTime latency and path length in the Sco group were significantly higher than in the control group (P<0.01), while the Sco+NS 400 group showed a significantly shorter traveled path length and time latency compared with the Sco group (P<0.01). AChE activity in the cortical tissues of the Sco group was significantly higher than the control group (P<0.01), while AChE activity in the Sco+NS 200 and Sco+NS 400 groups was lower than the Sco group (P<0.01). Following Sco administration, malondialdehyde (MDA) concentrations were increased (P<0.01) in comparison with the control group, while cortical total thiol content decreased (P<0.01). Pretreatment with extracts caused a significant elevation in cortical total thiol content (P<0.01) and reduction in cortical MDA concentration (P<0.01) compared with the Sco group.

CONCLUSIONSHydro-alcoholic extract of NS prevents Sco-induced spatial memory deficits and decreases the AChE activity as well as oxidative stress of brain tissues in rats. Our results support the traditional belief about the beneficial effects of NS in nervous system. Moreover, further investigations are needed for better understanding of this protective effect.

Acetylcholinesterase ; metabolism ; Animals ; Ethanol ; chemistry ; Male ; Malondialdehyde ; metabolism ; Maze Learning ; drug effects ; Memory Disorders ; drug therapy ; physiopathology ; Nigella sativa ; chemistry ; Plant Extracts ; pharmacology ; therapeutic use ; Rats, Wistar ; Reaction Time ; drug effects ; Scopolamine Hydrobromide ; Spatial Memory ; drug effects ; Sulfhydryl Compounds ; metabolism ; Water ; chemistry

OBJECTIVEFlavonoids are present in foods such as fruits and vegetables. Several studies have demonstrated a relationship between the consumption of flavonoid-rich foods and prevention of human disease, including neurodegenerative disorders. We assessed the effect of rutin (quercetin-3-O-rutinoside) on oxidative stress in kainic acid (KA)-induced seizure.

METHODSThirty-six BALB/c mice were randomly divided into three groups. In the control group, saline (intra-peritoneal, i.p.) was administered for 7 d, and on the last day, KA (10 mg/kg, i.p.) was injected 30 min after administration of saline. In rutin groups, mice were pretreated with rutin (100 and 200 mg/kg, i.p.) for 7 d, and on the last day, KA (10 mg/kg, i.p.) was injected 30 min after administration of rutin. Subsequently, behavioural changes were observed in mice. Lipid peroxidation and oxidative stress were measured respectively in the early and late phases after KA-induced seizures.

RESULTSSeizure scores in the rutin groups were significantly lower than those in the control group (P < 0.01). Furthermore, rutin dose-dependently inhibited the number of wet-dog shakes (WDS) (P < 0.05). Malondialdehyde level in the hippocampus of the rutin groups was significantly lower than that in the hippocampus of the control group on days 1 and 21 after KA administration. In the rutin groups, the thiol levels observed on day 1 after KA administration were higher than that in the control group (P < 0.01).

CONCLUSIONThese results indicate that rutin has potential anticonvulsant and antioxidative activities against oxidative stress in KA-induced seizure in mice.

Animals ; Dose-Response Relationship, Drug ; Kainic Acid ; toxicity ; Lipid Peroxidation ; drug effects ; Male ; Mice ; Mice, Inbred BALB C ; Oxidative Stress ; drug effects ; Rutin ; pharmacology ; Seizures ; chemically induced ; metabolism ; Sulfhydryl Compounds ; analysis