Tu-Jia medicine is an important part of traditional Chinese medicine (TCM).“San-Yuan doctrine”is the guiding ideology of Tu-Jia medicine, but there is no systematic exposition of its literature origin. This paper ar-gued that“San-Yuan doctrine”of Tu-Jia medicine was originated in the“San-Yuan”of Taoism. Its formation was closely related to the impact of Taoism and Tu-Jia culture, the understanding of human physiology and pathology in Tu-Jia medicine. This paper expounded the origin of“San-Yuan doctrine”, the guiding ideology of Tu-Jia medi-cine and Taoism culture through citing a number of theoretical bases. First of all, the concept of“San-Yuan”in Tu-Jia medicine originated in Taoism. Secondly, legends about the Lord Lao-Zi and Medicine King Bodhisattva in Tu-Jia medicine were closely related with Taoism. Moreover, there existed important links between Tu-Jia medicine and Taoist medicine. For example, both of them are aware of the importance of brain. The reason, I think, is firstly due to the penetration of Taoism in Tu-Jia culture. Taoism culture has a profound influence on Tu-Jia culture. Sec-ondly, the understanding of human physiology and disease in Tu-Jia medicine is closely related to“three”. There-fore, Tu-Jia medicine took“San-Yuan doctrine”as its own guiding ideology. It is of great significance to the study of ethnic minority medicine culture and inheriting its academic thoughts by the study of Tu-Jia medicine origin.

Objective To investigate the effects of Gastrodin on AKT/NLRP3 pathway in BV-2 microglial pyroptosis model.Methods BV-2 microglia were divided into normal control group and model group(1 μg·mL-1 LPS+10 μmol·L-1 Nigericin),Gastrodin group(10,100 μg·mL-1 Gastrodin),inhibitor control group(10 μmol·L-1 LY294002),inhibitor group(100 μg·mL-1 Gastrodin+10 μmol·L-1 LY294002),using 1 μg·mL-1 LPS combination 10 μmol·L-1 Nigericin co intervened to induce pyroptosis of BV-2 microglia.CCK-8 observed the effect of Gastrodin on cell activity,and western blot detected p-AKT,NLRP3,ASC,caspase-1,IL-1β expression,immunofluorescence detection of NLRP3,p-AKT protein expression,Real-time PCR observation of IL-1β mRNA content.Molecular docking was used to determine the binding sites of Gastrodin to p-AKT1/2/3 and NLRP3 proteins.Results Compared with the control group(0 μg·mL-1 Gastrodin),0.1-1000 μg·mL-1 Gastrodin had no significant effect on BV-2 cell activity(P>0.05).In the western blot experiment,compared with the normal group,the expression p-AKT,NLRP3,ASC,caspase-1,IL-1β in model group was significantly increased(P<0.01);Compared with the model group,the expression of p-AKT,NLRP3,ASC,caspase-1,IL-1β in Gastrodin group decreased(P<0.05 or P<0.01).In immunofluorescence,the expression of NLRP3 in model group was significantly higher than that in normal group(P<0.01);Compared with the model group,the expression of p-AKT and NLRP3 in Gastrodin group decreased significantly(P<0.01);Compared with Gastrodin group,the expression of p-AKT and NLRP3 in the inhibitor group decreased(P<0.01).In the Real-time PCR experiment,compared with the normal group,IL-1β mRNA content in model group cells increased significantly(P<0.01);Compared with the model group,IL-1β mRNA content in Gastrodin group cells decreased(P<0.01).In the LDH content test,compared with the normal group,the LDH activity in the model group cells increased significantly(P<0.01);Compared with the model group,the intervention of 100 μg·mL-1 Gastrodin can reduce the LDH activity in the pyroptosis cells(P<0.01).In molecular docking,Gastrodin had the binding ability with AKT1/2/3 and NLRP3,with the binding energy range of(-6.6)-(-6.8),and the binding mode included hydrogen bond,van der Waals force,etc.Conclusion Gastrodin can improve the pyroptosis of BV-2 microglia by inhibiting AKT/NLRP3 pathway.

Objective:To explore the mechanism of Dabuyuanjian in Against alzheimer's disease(AD)through network phar-macology and molecular docking technology,and to verify the molecular mechanism discovered by animal experiments.Methods:Net-work pharmacology was used to analyze the active ingredients and targets of AD in the treatment of large supplementary yuan decoc-tion.The core components of the drug were verified by molecular docking with the core protein by using AutoDock and PyMOL soft-ware.AD model mice were treated with Dabuyuanjian,and the core pathways which discovered were verified.Results:A total of 80 active ingredients and 107 disease targets were screened out.Dabuyuanjian had 95 targets in the treatment of AD,of which 35 were core targets.GO enrichment found that it mainly involved in programmed cell death process,apoptosis process and signal transduction regulation,etc.KEGG signaling pathway enrichment found that it mainly involved PI3K/Akt signaling pathway,Wnt signaling pathway,AMPK signaling pathway,etc.Morris water maze experiment showed that Dabuyuanjian could reduce the escape latency of AD mice,and increase the number of crossing platform and time's target quadrant.Immunohistochemistry(IHC)showed that Dabuyuanjian could increase the number of positive labeled-NeuN cells in the hippocampal CA3 region of AD mice.Immunofluores-cence(IF)showed that Dabuyuanjian could inhibit the expression levels of(GFAP)and ionized calcium-binding protein 1(IBA1)in the hippocampal CA3 region of AD mice.Western blot experiments showed that Dabuyuanjian could increase the expression levels of phosphorylated adenylate-activated protein kinase α(AMPKα)and silent information regulator 1(SIRT1)in the hippocampus of AD mice.Conclusion:This study explores the mechanism of Dabuyuanjian against AD,and find that Dabuyuanjian can improve cognitive impairment,neuron loss and neuroinflammation via activating AMPK/SIRT1 signaling pathway of AD.

AIM:To investigate the effects of Cong Rong San(CRS)on neuronal injury and endoplasmic re-ticulum stess(ERS)in rat models of Alzheimer disease.METHODS:Sixty male Sprague-Dawley rats(2 months old)were randomly divided into control(CON),model(MOD),low-dose CRS(CRSD),medium-dose CRS(CRSZ),high-dose CRS(CRSG),and memantine hydrochloride(MJG)groups.Morris water maze experiments were used to assess learning and memory in the rats.The morphology of neurons in the CA1 region of the hippocampus was examined using HE and Nissl staining,and the morphology of the endoplasmic reticulum in hippocampal cells was observed by transmission electron microscopy.Neuronal apoptosis in the CA1 region of the hippocampus was evaluated by TUNEL staining,while Western blot was used to assess the protein expression of glucose-regulated protein 78(GRP78),B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),caspase-3,protein kinase R-like endoplasmic reticulum kinase(PERK),p-PERK,activating transcription factor 4(ATF4)and C/EBP homologous protein(CHOP)in rat hippocampal tissues.RE-SULTS:Compared with those in the MOD group,rats in the CRSZ and CRSG groups showed improved learning and mem-ory,together with reduced hippocampal neuronal loss,PERK-ATF4-CHOP activity,and the expression of the pro-apoptot-ic proteins Bax and caspase-3,while the expression of the anti-apoptotic protein Bcl-2 was increased.CONCLUSION:Treatment with Cong Rong San was found to mitigate cognitive impairment,as well as damage and apoptosis in hippocam-pal neurons,in rat models of Alzheimer disease,possibly by inhibition of endoplasmic reticulum stress.