Gossypium herbaceam extracts inhibited NF-κB activation to attenuate spatial memory impairment and hippocampal neurodegeneration induced by amyloid-β in rats

Amyloid-beta (A beta) is considered to be responsible for the pathogenesis of Alzheimer's disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment induced by A beta were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70 and 140 mg/kg exerted an improved effect on the learning and memory impairment in rats induced by intracerebroventricular (i.c.v.)injection of 10 mu g of A beta(25-35). Subsequently, the GHE afforded a beneficial action on promotion on the activity of glutathione peroxidase and catalase, as well as inhibition on the NF-kappa B activation in the hippocampus followed by the presence of A beta(25-35). Meanwhile, the number of degenerating neurons with an apoptotic feature was dramatically decreased in hippocampus after treatment with GHE, implicating that its antioxidant stress and inhibition of NF-kappa B activation could be involved in the mechanism underlying neuroprotection of GHE against A beta-induced cell death. These findings suggested that GHE might be a potential agent for treatment of Alzheimer's disease.