This article focuses on the research of molecular mechanism of brain tumor treatment using the Jinlong capsule via system biology technology. Methods:Human Genome U133 Plus 2.0 gene chip was used to detect the genes of samples, in-cluding the brain tumor tissues of nude mice after Jinlong capsule intervention and those of blank control group mice. Differentially ex-pressed genes were identified based on fold change between the two groups. To identify the upstream regulators of the response signa-tures, the differentially expressed genes were subjected to interactome analysis by one-step overconnectivity test and multi-step hidden node algorithm. A set of genes preferentially connected to differentially expressed genes via direct interactions and pathways (called to-pologically significant genes) was generated. Concurrent pathway enrichment analysis on key pathways, processes, and functional units of both differentially expressed genes and topologically significant genes was performed to identify the most likely signaling pathways connecting regulators and effector genes. Finally, condition-specific networks (called causal network) were built to model molecular events by using a set of manually annotated protein interactions, pathways, and proteins and a toolkit of algorithms and filters on Meta-Core platform. Results:A total of 37 differentially expressed genes have been identified between Jinlong capsule-treated sample and ve-hicle sample with fold change of 2. Connection analysis identified 106 topologically significant genes. The main feature of the causal network is stimulation of neural cell specific genes that regulate normal cell physiology, particularly developmental processes and apop-tosis. Another important effect of the Jinlong capsule is its inhibition of the gene markers of interferon response, suggesting signaling in-hibition, followed by de-activation of immune response. Conclusion:Jinlong capsule exerts an anti-neoplastic effect by inducing stimu-lation of neural cell and by inhibiting interferon signal transduction.

China/epidemiology* ; Humans ; Pemphigoid, Bullous/epidemiology* ; Retrospective Studies

OBJECTIVE To study the effects of Dianxianqing granules on the tau protein in P301S mice by regulating mitophagy. METHODS Totally 36 P301S mice were randomly divided into model group， Dianxianqing granule group （12.48 g/kg）， donepezil hydrochloride group （positive control， 1.3 mg/kg）， with 12 mice in each group； another 10 C57BL6 mice were selected as control group. Administration groups were given relevant drug solutions intragastrically， and control group and model group were given constant volume of water intragastrically. The gavage volume was 20 mL/kg， once a day， for consecutive 5 months. During the experiment， the general condition of mice was observed in each group. After the last medication， the learning and memory ability was determined by Y maze test and Morris water maze test； HE staining was used to observe the morphological changes in brain tissue， and Nissl staining was used to observe the structure of neural cells and the number of Nissl bodies in cerebral tissue. Immunohistochemistry was used to detect the expressions of phospho-tau serine 202/threonine 205 （abbreviated as AT8） in brain tissue. Western blot assay was used to determine the expressions of mitophagy-associated proteins [PTEN-induced putative kinase-1 （PINK1）， Parkin， microtubule-associated protein 1 light chain 3B （LC3B）， p62]， synaptic-associated proteins [postsynaptic density protein-95 （PSD-95）， synaptophysin （SYP）， and growth-associated protein-43 （GAP-43）] and the phosphorylation of tau protein [expressed by the phosphorylation levels of serine 199 （Ser199） and Ser202] in brain tissue. RESULTS The mice in E-mail：lnzyxyqy2003@163.com model group showed symptoms such as white hair， decreased body mass， and lower limb paralysis， with incomplete hippocampal structures in their brain tissue， as well as incomplete cell membrane edges and cell structures； the spontaneous alternating response rate， the times of crossing platform， the number of Nissl bodies， the protein expressions of PINK1， Parkin， LC3B， SYP， GAP-43， and PSD-95 were decreased significantly， compared with control group； swimming latency （fourth and fifth day）， the protein expressions of AT8 and p62，the phosphorylation levels of Ser199 and Ser202 were increased or lengthened significantly， compared with control group （P＜0.05 or P＜0.01）. Compared with model group， the above symptoms and indexes of mice were improved significantly in administration groups （P＜0.05 or P＜0.01）. CONCLUSIONS Dianxianqing granules can effectively improve cognitive impairment in P301S mice，the mechanism of which may be associated with inducing mitochondrial autophagy， reducing the hyperphosphorylation of tau protein， up-regulating the expression of synaptic-associated proteins in brain tissue，and repairing damaged neural cells.