Preventive Efficiency of Chelidonium majus Ethanolic Extract Against Aflatoxin B1 Induced Neurochemical Deteriorations in Rats.

<b>Background and Objective:</b> Aflatoxins affect many species including humans and animals, therefore the present study was designed to investigate the protective effect of <i>Chelidonium majus</i> Ethanolic Extract (CMEE) on neurotoxicity induced by Aflatoxin B₁ (AFB1) in rats. <b>Materials and Methods:</b> Four groups of male Albino rats were treated orally for 28 days as follows: (1) Control group was daily given DMSO-PBS buffer (1.0 mL per rat), (2) CMEE (300 mg kg¹/day) dissolved in DMSO-PBS buffer, (3) AFB1 (80 µg kg¹/day) dissolved in DMSO-PBS buffer and (4) Received daily AFB1 (300 mg kg¹) in combination with CMEE (300 mg kg¹). <b>Results:</b> CMEE exhibits antioxidant activity <i>in vitro</i> and neuroameliorative efficiency <i>in vivo</i> as its administration in combination with AFB1 succeeded significantly in down regulating the elevated levels of inflammatory and apoptotic markers and restoring the values of neurochemical markers (AChE-ase, dopamine and serotonin) that were deteriorated by AFB1 intake. <b>Conclusion:</b> In conclusion, the neuroprotective effect of CMEE may be mediated through its antioxidant and free radical scavenging activity that proved from the data<i> </i>of ferric-reducing power ability and DPPH radical scavenging activity.

Cardioprotective and Antioxidant Efficiency of Balanites aegyptiaca Extract Against Doxorubicin® Complication.

<b>Background and Objective:</b> The use of Doxorubicin^® (Doxo) in the treatment of different tumours is restricted due to its cardiotoxicity. The objective of this study was to determine the protective effect of<i> Balanites aegyptiaca</i> extract against cardiotoxicity induced by Doxorubicin^® in male rats. <b>Materials and Methods:</b> Adult male rats (140-160) were parted into 6 groups (10 animals each) as follows: Group (1) Normal rats the control, group (2) Rats were administered BAE (200 mg kg¹) orally for 4 weeks, group (3) Rats were treated IP with the anticancer drug (Doxorubicin^®) at the dose of (0.5 mg kg¹) for 4 weeks, group (4) Administrated orally with BAE in combination with Doxo injection for 4 weeks, group (5) Rats orally with BAE before intoxication with Doxo for 4 weeks and finally group (6) Animals post-administration of BAE for 4 weeks after intoxication with Doxo. After 4 weeks of injections. <b>Results:</b> Revealed that BAE succeeded to decline the Doxorubicin cardiotoxicity, this was evidenced by the significant reduction of serum LDH, CK-MB, total cholesterol, triglycerides, HDL, TNF-α, IL-1ß and IL-6 as well as cardiac MDA and nitric oxide levels coupled with marked improvement in serum LDL, PON1 as well as cardiac GSH, SOD and CAT. Moreover, the BAE induced prominent regeneration of the cardiac muscle. <b>Conclusion:</b> <i>Balanites aegyptiaca</i> extract may be a promising cardio-protector against Doxorubicin^® toxicity mediated through their antioxidant and radical scavenging activities.

The Estimation of the Anti-neurotoxic Effect of Costus Ethanolic Extract against Bifenthrin-Intoxication in Male Rats.

BACKGROUND AND OBJECTIVE: Pyrethroidsare a group of synthetic pesticides similar to the natural pesticide pyrethrum, which is produced by chrysanthemum flowers. Bifenthrin is one of the pyrethroids that are widely used pesticide in households and to control crop vectors. The main goal of this work was to investigate the possible ameliorating effect of Costus Ethanolic Extract (CEE) against neurotoxicity induced by bifenthrin in adult-male rats. MATERIALS AND METHODS: Rats were arranged randomly to 4 groups (8 rats each) as next. Group 1) control rats orally received 0.5 mL water for consecutive 30 days; group 2) healthy rats orally received CEE (200 mg kg) for consecutive thirty days; group 3) rats treated orally with 7 mg kg-1 day-1 bifenthrin for consecutive 30 days and group 4) included rats treated with bifenthrin for consecutive 30 days followed by administration with CEE another consecutive 30 days. RESULTS: The results showed that CEE succeeded to decline the neurotoxicity-induced by bifenthrin; this was evidenced by the significant reduction in TNF-α, IL- 1ß, MDA and nitric oxide levels in cortex, hippocampus and striatum concomitant with marked improvement in the values of GSH, dopamine, serotonin, AChE-ase, SOD, GPx and catalase that were diminished by bifenthrin intoxication. CEE improved also cognitive impairment and the deficits in motor coordination induced by bifenthrin. CONCLUSION: CEE was found successful, to a great extent, to counteract the bifenthrin-induced brain oxidative stress and neurochemical deteriorations and possesses a protective potential against brain-induced neurotoxicity. Therefore, it may be a promising supplement for the amelioration of BF-neurotoxicity.