Inducible nitric oxide synthase inhibitor, aminoguanidine improved Ki67 as a marker of neurogenesis and learning and memory in juvenile hypothyroid rats.

INTRODUCTION: In the present study, the effect of inducible nitric oxide (NO) synthase inhibitor, aminoguanidine (AG) on neurogenesis indicators, learning and memory, and oxidative stress status in juvenile hypothyroid (Hypo) rats was evaluated. METHOD: The studied groups were including: (a) Control, (b) Hypo, (c-e) Hypo-AG 10, Hypo-AG 20, and Hypo-AG 30. Hypothyroidism was induced in the groups 2-5 by adding propylthiouracil in drinking water (0.05%). AG (10, 20, or 30 mg/kg) was daily injected intraperitoneally in the groups 3-5. The rats of the groups 1 and 2 were injected by saline instead of AG. After 6 weeks treatment, Morris water maze (MMW) and passive avoidance (PA) tests were done. Deep anesthesia was then induced and the brain tissue was excised for biochemical parameters measuring. RESULTS: Ki67 as a maker of neurogenesis and thiol, superoxide dismutase (SOD), and catalase (CAT) as oxidative stress indicators were decreased in the brain of Hypo group, whereas malondialdehyde (MDA) and NO metabolites were enhanced. AG improved Ki67, thiol, CAT, and SOD while decreased MDA and NO metabolites. The escape latency in the MWM test increased in the Hypo group. The spending time in the target quadrant in the probe test of MWM and step-through latency in the PA test in the Hypo group was lower than Control group. AG reversed all the negative behavioral effects of hypothyroidism. CONCLUSION: These results revealed that AG improved neurogenesis, learning and memory impairments, and oxidative imbalance in the brain juvenile Hypo rats.

Nigella sativa prevented liver and renal tissue damage in lipopolysaccharide-treated rats.

Liver and renal dysfunction accompanying with the tissues' oxidative damage has been reported to occur during Inflammation. Nigella sativa has been well known for its antioxidant and anti-inflammatory effects. The aim of this study was to investigate preventive effects of N. sativa on liver and renal tissue damage in lipopolysaccharide (LPS) -treated rats. The rats were divided into five groups: (1) control; (2) LPS (1 mg/kg, IP, for 10 days), (3-5) N. sativa hydroethanolic extract (100, 200, or 400 mg/kg) before LPS. Compared to LPS group, treatment by the extract decreased alondialdehyde, nitric oxide (NO) metabolites, and interleukin-6 while increased thiol content and superoxide dismutase and catalase activities in both renal and liver tissues. N. sativa extract also decreased serum aspartate aminotransferase, alanine aminotrans-ferase, and alkaline phosphatase concentration, while it increased serum protein and albumin compared with LPS group. In LPS group, serum blood urea nitrogen and creatinine were higher than control group. The extract reversed the negative effects of LPS. The results demonstrated that the N. sativa prevented liver and renal tissue damage in LPS-treated rats. It is suggested that the effects are due to its antioxidant and anti-inflammatory effects.

The effects of tamoxifen on spatial and nonspatial learning and memory impairments induced by scopolamine and the brain tissues oxidative damage in ovariectomized rats.

BACKGROUND: Modulatory effects of tamoxifen (TAM) on the central nervous system have been reported. The effects of TAM on spatial and nonspatial learning and memory impairments induced by scopolamine and the brain tissues oxidative damage was investigated. MATERIALS AND METHODS: The ovariectomized (OVX) rats were divided and treated: (1) Control (saline), (2) scopolamine (Sco; 2 mg/kg, 30 min before behavioral tests), (3-5) Sco-TAM 1, Sco-TAM 3 and Sco-TAM 10. TAM (1, 3 or 10 mg/kg; i.p.) was daily administered for 6 weeks. RESULTS: In Morris water maze (MWM), both the latency and traveled distance in the Sco-group were higher than control (P < 0.001) while, in the Sco-TAM 10 group it was lower than Sco-group (P < 0.05). In passive avoidance test, the latency to enter the dark compartment was higher than control (P < 0.05 - P < 0.01). Pretreatment by all three doses of TAM prolonged the latency to enter the dark compartment compared to Sco-group (P < 0.05 - P < 0.001). The brain tissues malondialdehyde (MDA) concentration was increased while, superoxide dismutase activity (SOD) decreased in the Sco-group compared to control (P < 0.05 - P < 0.01). Pretreatment by TAM lowered the concentration of MDA while, increased SOD compared to Sco-group (P < 0.05 - P < 0.001). CONCLUSIONS: It is suggested that TAM prevents spatial and nonspatial learning and memory impairments induced by scopolamine in OVX rats. The possible mechanism(s) might at least in part be due to protection against the brain tissues oxidative damage.