Objective To observe the effects of puromycin aminonucleoside (PAN) and dexamethasone (DEX) on the expression and distribution of pedocin in vitro, and to explore the possible mechanism of DEX in improving proteinuria. Methods Mouse podecyte cells (MPCs) in control group were cultured with RPMI-1640 plus 0.02% DMSO, and were subjected to PAN treatment alone (PAN group) or PAN plus DEX (DEX group) for 8, 24,48 hours respectively. The pedocyte morphology was observed by phase-contrast microscope, and was analyzed by Image J. The distribution, mRNA and protein expression of podocin were detected by indirect immunocytofluorescence, semi-quantitative RT-PCR and Western blot, respectively. Results The well-developed arborization and interconnection of podocytes were found in control group. PAN treatment led to significant shrinkage of pedocytes with decreased distribution at 43% of control group at 8 h, 10% at 24 h and 5.7% at 48 h (P<0.01), respectively, together with podocyte foot process retraction as well as effacement and loss of cell contact. RT-PCR revealed podoein mRNA expression prone to decrease. Western blot showed podoein protein expression was significantly decreased and immunocytochemistry revealed podoein expression was disappeared in the cellular membrane after PAN treatment. DEX significantly prevented the shrinkage of podcytes, with decreased area at 43.9% of control at 8 h, 26.2% at 24 h and 29.6% at 48 h (P<0.05), respectively, and up-regulated the mRNA and protein expression of podocin at 48 h (P<0.05). The abnormal distribution of podocin was also alleviated by DEX. Conclusion DEX exerts a direct action on podocyte via stabilizing mRNA, protein expression and distribution of podocin, which may be associated with the improvement of proteinuria.

This study was aimed to observe the effect of Bai-Zhu Fu-Ling (BZFL) Decoction in different proportion-ing on VIP and VIPR1 in Crohn's disease (CD) rats with spleen deficiency syndrome, in order to further explore the immunologic mechanism of BZFL Decoction on CD. The CD rat model with spleen deficiency syndrome was estab-lished using exhaustion and hunger. The model rats were treated by BZFL Decoction with different proportioning, and immunohistochemistry (IHC) was used to detect the expression of VIP and its receptor in colon tissues. The results showed that comparing to the blank control group, the level of VIP and its receptor of the model group significantly increased (P< 0.05). Comparing to the model group, the level of VIP and its receptor in BZFL Decoction B5 group (Rhizoma A tractylodis Macrocephalae:Poria = 12:15), B6 group (Rhizoma A tractylodis Macrocephalae:Poria = 15:12) and B7 group (Rhizoma A tractylodis Macrocephalae:Poria = 18:9) was significantly decreased (P< 0.05). It was con-cluded that the effect of BZFL Decoction of B5 group, B6 group and B7 group was better than other groups in VIP and its receptor which can regulate the VIP and its receptor, inhibit the releasing of inflammatory factors and reduce intestinal inflammation injury.

Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in podocyte mito-chondrial dysfunction. Methods Cultured podocytes were injured by AngiotensinⅡ(AngⅡ).Cells were harvest-ed after 0 h,24 h and 48 h after AngⅡstimulating.Immunofluorescence staining was used to observe the disrup-tion of actin cytoskeleton,as well as the distribution of Cabin1.Western bolt was applied to detect the level of cyto-chrome c and Cabin1 protein in podocytes. Results AngⅡremarkably caused podocyte damage in a time depen-dent manner. Phalloidin staining displayed strong and long bundles of intracellular actin filaments in untreated cells. AngⅡ induced the loss of the cytoplasmic cytoskeleton and the reorganized of actin cytoskeleton at 24 and 48h. In normal podocytes,Cabin1 evenly localized in the cytoplasm and nuclei. AngⅡinduced strong staining of Cabin1 in podocytes nuclei. Cytochrome c and Cabin1 protein expression apparently increased in AngⅡ injuried podocyte.Ctyochrome c protein obviously increased in cells at 24 h and 48 h after AngⅡstimulating,which were as 1.51 and 1.87 times as the normal control group(P < 0.05). Similarly,the expression of Cabin1 were as 1.33 and 1.67 times respectively in 24 h and 48 h while compared to the normal control group(P < 0.05). Conclu-sion Cabin1 was overexpressed during podocyte mitochondrial dysfunction.It could be a crucial factor which regu-lates mitochondrial function during podocyte damage.

Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.

Objective To investigate the function and molecular mechanism of tacrolimus in podocyte injury and restoration.Methods Cultured podocytes were stimulated by Angiotensin Ⅱ (Ang Ⅱ) or Ang Ⅱ plus tacrolimus.Cells were collected at different time points (0 h,12 h and 24 h).The distribution of F-actin was observed after immunofluorescence staining,and the protein expression of nephrin and podocin were detected by Western Blot (WB).Results In normal control podocytes,F-actin was arranged in cytoplasm powerfully.Ang Ⅱ induced the disruption and discontinuity of F-actin.Tacrolimus inhibited the effect of Ang Ⅱ,stabilized the regular arrangement the F-actin.Compared to normal cells,the protein expression of nephrin in Ang Ⅱ group significantly decreased at 24 h after stimulation (0.76 ± 0.32 in AngⅡ group vs.1.18 ± 0.40 in normal group,P ＜ 0.05).And tacrolimus stabilized the expression of nephrin protein (1.00 ± 0.19 in treatment group vs.0.76 ± 0.32 in Ang Ⅱ group,P ＜ 0.05).Ang Ⅱ and tacrolimus did not affect the expression of podocin protein.Conclusion Tacrolimus inhibits podocyte injury induced by Ang Ⅱ,stabilizes the regular arrangement of cytoskeleton and protein expression of nephrin.

Alzheimer's disease (AD) is a complex neurodegenerative disease. Its pathogenesis involves many factors such as environment, heredity, aging, diet, personal preference and underlying diseases. And the complex pathogenic factors of AD lead to many social and economic problems such as delayed diagnosis, difficulty of drug research and development, low cure rate and high cost of care. In this paper, the relationship between AD disease progression and its risky diseases such as metabolic diseases, chronic inflammatory diseases and cardiovascular diseases was analyzed based on energy metabolism abnormalities. The role of energy metabolism signal/path abnormality activity in the course of risk disease to AD disease was analyzed. Finally, it is suggested that the prevention and treatment of risk disease evolution and adjustment of abnormal energy metabolism signals may be effective strategies for the treatment of AD.

It is great value to analyze the pathogenesis of Alzheimer's disease for the formulation and research of prevention and treatment strategies. The change of zang-fu meridians and collaterals is the essential rule of the pathogenesis of internal injury and miscellaneous diseases. Based on the analysis of the physiological basis of the aging changes of zang-fu meridians and the relationship between dementia and the abnormal function of zang-fu meridians and collaterals, this paper systematically explored the relationship between the changes of zang-fu meridians and the pathogenesis of dementia. It is considered that the change of zang-fu meridians and collaterals is the basic law of its pathogenesis development. Therefore, it is proposed that strengthening Qi is the essential principle throughout the whole process of dementia, and dredging channels and collaterals and maintaining normal function of meridians and collaterals are the key to block the pathogenesis evolution of dementia.

Objective: Based on the Chinese Medicine Heritage Auxiliary Platform (V2.5) software, to analyze the differences in prescriptions for the treatment of Alzheimer's disease and Vascular dementia in the literature of the past five years, and to find the rules of prescription. Methods: Screening CNKI, VIP, and Wan fang data for nearly 5 years to find the prescriptions for the treatment of Alzheimer's disease and Vascular dementia, and constructing a prescription database through the Chinese Medicine Heritage Auxiliary Platform (V2.5) software, and utilizing the Data mining algorithms such as association rules and entropy clustering of the software. Compare the frequency of medication, the drug.s natural, flavor and channel tropism, the common drug pairs, the potential drug pairs, and the differences in the new prescriptions used in the treatment of senile dementia and vascular dementia. Results: 13 of the top 20 high frequency herbs used in AD and VD are the same, the other is different. Its common pathogenesis reflect the interaction of deficiency, stasis and phlegm, while the difference shows that AD focuses on spleen and kidney deficiency, insufficiency of essence and blood, but VD focuses on the interaction of phlegm blood stasis and toxic turbidity obstruction in collaterals. They both use warm herbs in nature and flavor, but AD mainly use sweet and warm herbs, followed by calm and cold herbs, while VD mainly use bitter and warm herbs, followed by cold and calm herbs; The channel tropisms both are mainly liver channel, followed by heart channel, spleen channel and kidney channel. In addition, 16 potential medicine pairs, 7 new prescriptions, 26 new prescriptions and 13 new prescriptions were found. Conclusion:Prescriptions for AD and VD have similarities and differences, with emphasis on each other, suggesting that the former focuses on warming Yang and invigorating spleen, while the latter focuses on resolving phlegm and removing blood stasis, detoxifying and awakening the brain.

Objective: To investigate the effects of compatibility of Radix Ginseng and Radix Scutellariae (CRH) on learning and memory ability in multi-infarct dementia (MID) model rats and to explore the mechanism from the perspective of brain energy. Methods: We established MID rat model by thrombus injection, and learning and memory ability of MID rats was evaluated by Morris water maze; HE staining was used to observe the pathological changes in hippocampal CA1 region of rats; the contents of ATP, ADP and AMP in brain tissues were determined by highperformance liquid chromatography; flow cytometry was used to detect the changes of mitochondrial swelling and mitochondrial membrane potential in hippocampus of rats. Results: Compared with the rats in model group, the escape latency was significantly shortened in both high and low dose groups (P ＜ 0.05) . The times of crossing the platform were increased in both high and low dose groups (P ＜ 0.05) . The disorder of cell arrangement and loss of number of cell layers were significantly improved in high and low dose groups (P ＜ 0.05) . The degree of mitochondria swelling was significantly reduced in low dose group (P ＜ 0.05) . The decreasing trend of mitochondrial membrane potential was improved (P ＜0.05), and the energy charge of brain tissue was increased in high dose group rats (P ＜ 0.05) . Conclusion: CRH improved the cognitive decline and increased the concentration of energy charge in MID rats which was in relation to protect mitochondrial damage and improve brain energy, and further protect neurons.

Objective: To investigate the effects of Kaixin Powder on learning and memory, ATP/AMP ratio, GABA andiNOS levels in rats with multiple infarct dementia. Methods: The rat model of multi-infarct dementia was established bymicro-thromboembolism. Morris water maze and opening experiment were used to evaluate learning and memoryfunction. The pathological changes of hippocampal CA1 area were evaluated by HE staining. The contents of ATP andAMP in brain tissue were determined by HPLC. The content of γ-aminobutyric acid and iNOS in peripheral blood weredetected by ELISA kit. Results: Compared with the rats of model group, rats of Kaixin Powder group can significantlyshorten the escape latency, increase the number of crossing platforms, Results: Compared with the model group, increasethe standing times in the opening experiment, prolong the exercise time, shorten the resting time, improve the nerve celldamage in the hippocampal CA1 area, and significantly increase the ratio of ATP/AMP of brain tissue, decreased brainGABA content and serum iNOS content (P ＜ 0.05) . Conclusion: Kaixin Powder has the effect of improving learning andmemory function and abnormal motor behavior in rats with multiple infarct dementia. The mechanism is related toreducing GABA and i NOS content in brain tissue, increasing ATP/AMP ratio in brain tissue and improving energysupply in brain tissue.