This study was carried out to evaluate the detoxifying effects of aqueous extract of Moringa Oleifera on sodium fluoride-induced neurotoxicity in male Wister rats. Design: Randomized controlled study. Animals: Forty rats Procedures: Rats were allocated into four equal groups (10 each). Basically, each group received the same basal diet for 30 days. The first group was not received additional treatment (negative control). However, the second group received 20 mg/kg b.wt sodium fluoride daily (positive control), the third group received sodium fluoride at a dose of 20 mg/kg b.wt and Moringa Oleifera at 300 mg/kg daily, and the fourth group received sodium fluoride at a dose of 20 mg/kg b.wt and Moringa Oleifera 500 mg/kg daily using a stomach tube. Results: Dopamine and serotonin were significantly increased in Moringa Oleifera treated rats at 300 and 500 mg/kg in comparison with rats treated with sodium fluoride, but the higher dose of M. Oleifera achieved the best result (1.23±0.13 vs. 0.31±0.013) and (2.95±0.019 vs. 0.91±0.016) respectively. TAC, SOD, catalase were significantly increased in Moringa Oleifera treated rats at 300 and 500 mg/kg in comparison with rats treated with sodium fluoride, versed with MDA significantly decreased in Moringa Oleifera treated rats Also, to improve the anatomical structure of the disease in the brain reduces heavy bleeding and neurodegenerative changes, and maintains normal nerve cells, improves antioxidant ability as a whole. Conclusion and clinical relevance:Collectively, our results indicate that Moringa Oleifera watery extract has a detoxifying effect on NaF induced neurotoxicity via improving neurotransmitters andantioxidant activity.
Investigating the effect of green tea extract (GTE) on the testicular damage induce d by cadmium chloride CdCl2 in male rats. Design: Random iz e d controlle d study. Animals : 40 male Wistar rats. Procedures: Rats were randomly divided into four groups: A) control group (each rat daily received pellet diet); B) GTE group each rat daily received pellet diet as well as 3 ml of 1.5 % w/v GTE, C) CdCl2 group each rat was I/P injected a single dose of 1 mg/kg CdCl2, then daily received pellet diet, and D) CdCl2+GTE group each rat was I/P injected a single dose of 1 mg/kg CdCl2 then daily received pellet diet as well as 3 ml of 1.5 % w/v GTE. After 30 days, blood samples were collected for hormonal assays (testosterone, FSH, and LH). In addition, both testes were collected; one of them was used for quantification of 17-beta hydroxysteroid dehydrogenase III (17β-HSDIII) gene expression using a real-time PCR. The other testis was used for determination of catalase and reduced glutathione; GSH, Nitric oxide (NO) and malondia lde hyde (MDA) levels. Results: CdCl2 decreased serum testosterone levels and its synthesis pathway (17β-HSDIII testicular gene expression). While antioxidants catalase and GSH were reduced, oxidants MDA were enriched in the testes of CdCl2-poisoned rats.This CdCl2-promoted testicular dysfunction was corre cte d via the adminis tra tion of GTE to male rats. Conclusion and clinical relevance: GTE could be used as a remedy for protecting against CdCl2-induce d testicula r damage in male rats.
Objective: Investigating the effect of green tea extract (GTE) on the testicular damage induced by cadmium chloride CdCl2 in male rats. Design: Randomized controlled study. Animals: 40 male Wistar rats. Procedures: Rats were randomly divided into four groups: A) control group (each rat daily received pellet diet); B) GTE group each rat daily received pellet diet as well as 3 ml of 1.5 % w/v GTE, C) CdCl2 group each rat was I/P injected a single dose of 1 mg/kg CdCl2, then daily received pellet diet, and D) CdCl2+GTE group each rat was I/P injected a single dose of 1 mg/kg CdCl2 then daily received pellet diet as well as 3 ml of 1.5 % w/v GTE. After 30 days, blood samples were collected for hormonal assays (testosterone, FSH, and LH). In addition, both testes were collected; one of them was used for quantification of 17-beta hydroxysteroid dehydrogenase III (17β-HSDIII) gene expression using a real-time PCR. The other testis was used for determination of catalase and reduced glutathione; GSH, Nitric oxide (NO) and malondialdehyde (MDA) levels. Results: CdCl2 decreased serum testosterone levels and its synthesis pathway (17β-HSDIII testicular gene expression). While antioxidants catalase and GSH were reduced, oxidants MDA were enriched in the testes of CdCl2-poisoned rats. This CdCl2-promoted testicular dysfunction was corrected via the administration of GTE to male rats. Conclusion and clinical relevance: GTE could be used as a remedy for protecting against CdCl2-induced testicular damage in male rats.
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