Terminalia catappa attenuates phenylhydrazine-induced anaemia and hepato-renal toxicity in male Wistar rat by boosting blood cells, modulation of lipoproteins and up-regulation of in vivo antioxidant armouries.

AIM: This study investigated the haematinic, antihyperlipidaemic, hepato-renal protective effects of Terminalia catappa aqueous leaf extract on male Wistar rats exposed to phenylhydrazine toxicity. METHODS: Animals were exposed to phenylhydrazine (PHZ) 50 mg/kg intraperitoneal for two consecutive days thereafter, treated with T. catappa extract (100 mg/kg and 200 mg/kg) orally for 21 days. After the experimentation, animals were sedated with ketamine (70 mg/kg) and euthanized by cervical dislodgement. Blood and organs were collected for haematology and biochemical studies following standard laboratory methods. RESULTS: Our study showed that T. catappa significantly increased erythrocytes, haemoglobin, haematocrit and high density lipoprotein as well as down-regulating leukocytes, thrombocytes, ALP AST, ALT creatinine, urea, total cholesterol as well as low density lipoprotein. The liver, kidney and spleen antioxidant defence were also up-regulated against the adverse effect caused by phenylhydrazine exposure. CONCLUSION: Terminalia catappa attenuated Phenylhydrazine-induced anaemia and hepato-renal toxicity in male Wistar rat by boosting blood cells, modulation of lipoproteins and up-regulation of in vivo antioxidant armouries.

Lead acetate induces hippocampal pyramidal neuron degeneration in mice via up-regulation of executioner caspase-3, oxido-inflammatory stress expression and decreased BDNF and cholinergic activity: Reversal effects of Gingko biloba supplement.

PURPOSE: It has been hypothesized that compounds with strong anti-oxidant activity might mitigate lead-induced neurotoxicity that resulted to neuronal degeneration.Ginkgo biloba supplement (GB-S) is a neuroactive supplement which has been reported to demonstrate neuroprotective effects. In this study, we investigated the reversal effect and the underlying mechanism of GB-S following lead-induced neurotoxicity in mice. METHODS: Male Swiss mice (n = 8) were pre-treated with lead acetate (100 mg/kg) for 30 min before GB-S (10 mg/kg and 20 mg/kg) or Ethylenediaminetetraacetic acid (EDTA) (50 mg/kg) intraperitoneally for 14 consecutive days. Memory impairment symptoms were evaluated on day 13 and 14 using Y-maze and Novel object recognition test (NORT) respectively. Thereafter, spectrophotometry, ELISA, immunohistochemistry and histomorphormetry were used to estimate the degree and expression of biomarkers of neuronal inflammation: oxido-inflammatory stress, apoptosis and degeneration in the hippocampus (HC). RESULTS: Lead acetate treatment significantly (p < 0.05) induced neurobehavioral impairment which was reversed by GB-S as evident in increased percentage alternation and discrimination index. GB-S significantly (p < 0.05) reduced lipid peroxidation and nitrite level, inhibited TNF-α and acetylcholinesterase activity and improved glutathione, catalase and superoxide dismutase activity in the HC. Moreover, GB-S inhibited hippocampal apoptosis via elevated expression of caspase-3 with marked increase level of brain derived neurotrophic factor (BDNF). Also, the histomorphormetric study showed that GB-S rescued death of pyramidal neurons (CA3) in the HC. CONCLUSION: Our findings however suggest that GB-S decreased memory impairment progression induced by lead acetate via mechanisms connected to inhibition of oxido-inflammatory stress mediators, restrained acetylcholinesterase activity, up-regulated BDNF/Caspase-3 expression and suppression of hippocampal pyramidal neuron degeneration in mice.

Long-term consumption of Moringa oleifera-supplemented diet enhanced neurocognition, suppressed oxidative stress, acetylcholinesterase activity and neuronal degeneration in rat's hippocampus.

OBJECTIVES: This study investigates protection against oxidative stress and memory enhancing potential of long-term consumption of Moringa oleifera leaves. METHODS: Male Wistar rat were fed with mixture of M. oleifera-supplemented diets (MOSD) partitioned in 1, 5, 10, and 20% continuously for 12 weeks. Object recognition test (ORT) and Morris water maze (MWM) was used for assessing neurocognition. Changes in body weight, Lipid peroxidation (MDA), Glutathione (GSH), Catalase (CAT) and Acetylcholinesterase (AChE) activity was assayed in the brain tissue. Histomorphometric of the hippocampus was also examined. RESULTS: The diets progressively increase the body weigh after the 12 weeks, improved spatial (MWM) and non-spatial (ORT) memory performance, protect against oxidative stress, inhibit AChE activity and suppresses neuronal degeneration in the hippocampus when stained with Cresyl violent stain. CONCLUSIONS: Conclusively, long-term consumption of MOSD shows strong protection against oxidative stress and hippocampal degeneration and improves neurocognition with dose dependent effect.