Serum p-amyloid peptide(Aβ)40 and Ap42 levels in patients with type 2 diabetes mellitus (T2DM)and atherosclerosis(AS)were detected by ELISA.The results showed that serum Ap40 level in T2DM group was significantly higher than that in the control group[(274.70±159.51 vs 162.63±87.58)pg/ml,P<0.05],especially in the diabetic patients accompanied with AS[(616.95±195.13)pg/m],P<0.01].Serum Ap40 level in simple AS group was also higher than that in control group[(318.52± 188.65)pg/ml,P<0.05].These results suggest that Ap40 is a risk factor of T2DM complicated with AS.However,there was no difference in serum Ap42 levels among various groups.

This study was designed to explone whether catalpol exerts a protective effects on kidney of diabetic rats and its possible mechanism.Insulin-like growth factor- I ( IGF- I ) and protein kinase B (PKB/Akt)mRNA and protein expression in kidney of diabetic rats were up-regulated as results of assessments by RT-PCR,immunohistochemistry and Western blot.Catalpol could partially reduce IGF- Ⅰ and Akt expressions in kidney of diabetic rats,and thus alleviate the damage of kidney.

Ginkgo biloba preparation is widely used as natural extract preparation both domestically and internationally, for myocardial infarction and cerebral infarction diseases in China; and mainly used to improve memory and treat dementia symptoms abroad. In recent years, there have been a large amount of reports on the treatment of ophthalmic diseases, mental diseases, kidney diseases and so on, however some of which have not uniform literature result. Therefore, it is necessary to summarize the reports on off-label use of Ginkgo biloba preparation. Among them, Ginkgo biloba preparation has a lot of controversy on brain diseases such as dementia and autism, mainly due to the mild effect, the difficulty in tracking long-term medication data for chronic diseases, and the subjective evaluation results of cognitive level, so more high-level research is needed to provide data support. In addition, Ginkgo biloba preparation has obvious protective effects on peripheral nerves and microvascular, and as an adjuvant drug in related diseases, it can effectively accelerate the recovery process of patients. This article summarizes various reports on Ginkgo biloba preparations, which can better clarify the product positioning and provide a reference for the selection of relevant treatment options.

BACKGROUNDThe mechanisms underlying diabetic encephalopathy are largely unknown, and no effective treatments are available. Catalpol has received much attention due to its numerous biological effects, especially in neuroprotective studies. The aim of this study was to investigate the effects of catalpol on cognitive functions in diabetic rats and the underlying mechanisms.

METHODSA rat model of diabetes was established by streptozotocin injection, followed by intraperitoneal infusion of catalpol after 10 weeks. Two weeks later, the Morris water maze was used to test the spatial learning performance. Nissl staining was performed to evaluate the morphological changes in the hippocampus. Expression of protein kinase Cγ (PKCγ) and caveolin-1 (Cav-1) in the hippocampus were assessed by reverse transcription PCR and Western blotting. Activities of anti-oxidative enzymes such as glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) and levels of malonaldehyde (MDA) were measured using commercial kits.

RESULTSSignificant hippocampal neuronal injury was observed in rats with streptozotocin-induced diabetes. Moreover, cognitive dysfunction was associated with markedly increased oxidative stress in the brain. Catalpol treatment significantly attenuated cognitive deficits, neuronal damage, and oxidative stress in the brain of diabetic rats. Biochemical analyses showed that catalpol reversed the down-regulation of PKCγ and Cav-1 expression in the diabetic rats.

CONCLUSIONSSpatial memory in diabetic rats is associated with the expression of PKCγ and Cav-1. Catalpol treatment markedly attenuated oxidative stress, reversed the alteration of PKCγ, Cav-1 and spatial memory deficits.

Animals ; Caveolin 1 ; metabolism ; Diabetes Mellitus, Experimental ; drug therapy ; metabolism ; physiopathology ; Hippocampus ; drug effects ; metabolism ; Iridoid Glucosides ; therapeutic use ; Male ; Neuroprotective Agents ; therapeutic use ; Oxidative Stress ; drug effects ; Protein Kinase C ; metabolism ; Rats ; Spatial Memory ; drug effects ; physiology