Related Gene Signaling Pathway Huangputongqiao Capsule Learning And Memory In Rats With Vascular Dementia And Fas / FasL In Effect

Objectives To observe the changes of Fas-FasL pathway of apoptosis, NO-cGMP signal pathway,cAMP-protein kinase A(PKA)-cAMP-responsive element binding protein (CREB) pathway andgene expressions related to learning and memory, and the effects of HTC intervention on theabove pathways and related genes for probing into inner mechanisms of HTC on improvingvascular dementia. Methods The model of middle cerebral artery occlusion with threads for vascular dementia in rats wasmade. The model rats were devided into 3 groups, 15 rats in each group, which were the modelgroup, HTC group and Duxil group and fed with the different drugs of same volume. Proteinexpressions of Fas/FasL,NF-κB,PKA,CREB,c-fos and c-jun in neurons were detected withimmuno-histochemical method, the content of NO and the activitiy of NOS with colorimetryand the contents of cAMP and cGMP with radioimmunity method. The data was processed withSPSS 11.0 for Windows software. Results 1. Effects of HTC on Protein Expressions of Fas and FasL in Neurons of Rats withVascular Dementia After 4 weeks, the positive cell counts were conspicuously decreased in HTC group. Theexpression of NF-κB was remarkably decreased in HTC group, which was markedly differentcompared with model group (P<0.01). 2. Effects of HTC on Protein Expressions of cAMP,PKA,CREB,c-fos and c-jun inNeurons of Rats with Vascular Dementia The content of cAMP was elevated in HTC group, expressions of PKA and CREB wereincreased in HTC group, and an abundance of c-fos and c-jun proteins expressed in HTCgroup, which were markedly different compared with model group (P<0.01). 3. Effects of HTC on the content of cGMP and NO and activities of NOS in neurons ofrats with vascular dementia After 4 weeks, the content of cGMP and NO and activities of NOS in neurons of rats wereincreased in model group compared with the blank control group, and increased in Chinesemedicine group, which are markedly different compared with the model group. Conclusions HTC markedly lowered protein expressing of Fas, and depressed the neuronal apoptosisinduced by Fas-Fasl signal pathway. HTC may improve learning and memory through loweringprotein expression of NF-κB as to protect neurons and depress neuronal apoptosis. HTCelevated the expressions of cAMP, PKA and CREB, and may activate the signal pathway ofcAMP-PKA-CREB and start up and regulating certain gene expressions (eg, c-fos, c-jun, etc)associated with learning and memory. HTC may reduce neuronal apoptosis induced by NOpathway and decrease neuronal toxicity as to protect neurons by lowering the content of NOand the activity of NOS. The mentioned above could be important mechanisms for treatment ofvascular dementia.