Abstract

Introduction: Hyperhomocysteinaemia (HHcy) is an established risk factor for cardiovascular, cerebrovascular, peripheral vascular diseases and neurodegenerative disease. The effect of this HHcy on vascular diseases could potentially cause vascular pathology features. Experimental studies have demonstrated that Hcy can be neurotoxic to brain, hippocampus area. 

Methods: The present study was conducted to compare the possible neuroprotective effects of different herbal cocktail in HHcy-induced rats’ brain cerebrovascular dysfunction model. Rats were divided into nine groups: Group I - Controls received the same volume of saline solution (0.5 mL/100 g of body weight). Group II served as HHcy and received homocysteine 0.03 μmol/g of b.w. daily for 30 days. Group III served as HHcy and received homocysteine 0.03 μmol/g of b.w. + Artemisia Judaica extract (AJ) (50 mg/kg per oral by oral feeding needle with tuberculin syringe) daily for 30 days. Group IV served as HHcy and received homocysteine 0.03 μmol/g of b.w.+ Panax ginseng extract (PG) (50 mg/kg per oral by oral feeding needle with tuberculin syringe) daily for 30 days. Group V served as HHcy and received homocysteine 0.03 μmol/g of b.w. + Polygonum multiflorum extract (PM) (400 mg/kg per oral by oral feeding needle with tuberculin syringe) daily for 30 days. Group VI served as HHcy and received homocysteine 0.03 μmol/g of b.w. + AJ + PG with the same dose of previous group daily for 30 days. Group VII served as HHcy and received homocysteine 0.03 μmol/g of b.w. + AJ + PM with the same dose of the previous group daily for 30 days. Group VIII served as HHcy and received homocysteine 0.03 μmol/g of b.w. + PG + PM with the same dose of the previous group daily for 30 days. Group IX served as HHcy and received homocysteine 0.03 μmol/g of b.w. + AJ + PG + PM with the same dose of previous group daily for 30 days. The hippocampus of brain samples was collected at the end of the experiment and measuring oxidative stress markers (CAT, SOD, MDA and NO), inflammatory mediators (IL-6 and BDNF), histopathological examination and comet assay.

Results: Revealed data showed that the homocysteine induces SOD, CAT depletion, and an increase in AChE, MDA, NO, IL-6, and BDNF. A mixture of PG and PM or the individual treatments showed an ameliorative response for all parameters. In general, oxidative stress parameters, inflammatory mediator, neurotrophic factor, pathological examination and comet were degenerate against HHcy but did not differ significantly compared to AJ group.

Conclusion: Better physiological and histological characteristics were in PG and PM and their combination groups compared with HHcy and ameliorated nearly the control group.