Recent evidence demonstrates that a double dose of Jasminoidin (2�JA) ismore effective than Jasminoidin (JA) in cerebral ischemia\ntherapy, but its dosage-effect mechanisms are unclear. In this study, the software GeneGo MetaCore was used to perform pathway\nanalysis of the differentially expressed genes obtained in microarrays of mice belonging to four groups (Sham, Vehicle, JA, and\n2�JA), aiming to elucidate differences in JA and 2�JA�s dose-dependent pharmacological mechanism from a system�s perspective.\nThe top 10 enriched pathways in the 2�JA condition were mainly involved in neuroprotection (70% of the pathways), apoptosis and\nsurvival (40%), and anti-inflammation (20%), while JA induced pathways were mainly involved in apoptosis and survival (60%),\nanti-inflammation (20%), and lipid metabolism (20%). Regarding shared pathways and processes, 3, 1, and 3 pathways overlapped\nbetween the Vehicle and JA, Vehicle and 2�JA, and JA and 2�JA conditions, respectively; for the top ten overlapped processes these\nnumbers were 3, 0, and 4, respectively.The common pathways and processes in the 2�JA condition included differentially expressed\ngenes significantly different from those in JA. Seven representative pathways were only activated by 2�JA, such as Gamma-Secretase\nregulation of neuronal cell development. Process network comparison indicated that significant nodes, such as alpha-MSH, ACTH,\nPKR1, and WNT, were involved in the pharmacological mechanism of 2�JA. Function distribution was different between JA and\n2�JA groups, indicating a dosage additive mechanism in cerebral ischemia treatment. Such systemic approach based on wholegenome\nmultiple pathways and networks may provide an effective and alternative approach to identify alterations underlining\ndosage-dependent therapeutic benefits of pharmacological compounds on complex disease processes.
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