黄芩苷、栀子苷及其配伍治疗局灶性脑缺血的海马基因表达：一项基因网络功能分析

The compound traditional Chinese medicine Qingkailing,which is an ingredient used to treat cerebral ischemia,has been limited to studies concerning single genes or single pathways.Interactions and pharmacological mechanisms of the compound ingredients(baicalin and jasminoidin) remain poorly understood.In the present study,baicalin and jasminoidin,as well as the combination,were used to separately treat mouse models of cerebral ischemia.cDNA microarray analyses of 374 cerebral ischemia-related genes were utilized to determine changes in gene-expression profiles.Arraytrack 3.40 and Ingenuity Pathway Analysis(IPA) databases were utilized to analyze changes in gene molecular functions and network path functions.Baicalin or jasminoidin alone effectively reduced infarct area,and the combination resulted in significantly better outcomes.IPA showed inhibited cell apoptosis in the baicalin group and Ca2+ channel regulation in the jasminoidin group.The combination of baicalin and jasminoidin activated HTR3A and F5 expression,regulated Ca2+ channels,activated kappa light polypeptide gene enhancer inhibitor IKBKG in B cells to control IkB kinase/nuclear factor-kB cascade,suppressed activation of inflammatory cytokine interleukin-6 receptors and activated transduction of guanine-nucleotide-binding protein(G protein) signal.Results suggested that the combination of baicalin and jasminoidin resulted in similar molecular mechanisms to baicalin and jasminoidin alone.However,novel pharmacological actions of compatibility were detected,demonstrating significant protection against cerebral ischemia.

Baicalin and jasminoidin effects on gene expression and compatibility in the hippocampus following focal cerebral ischemia

The compound traditional Chinese medicine Qingkailing, which is an ingredient used to treat cerebral ischemia, has been limited to studies concerning single genes or single pathways. Interactions and pharmacological mechanisms of the compound ingredients (baicalin and jasminoidin) remain poorly understood. In the present study, baicalin and jasminoidin, as well as the combination, were used to separately treat mouse models of cerebral ischemia. cDNA microarray analyses of 374 cerebral ischemia-related genes were utilized to determine changes in gene-expression profiles. Arraytrack 3.40 and Ingenuity Pathway Analysis (IPA) databases were utilized to analyze changes in gene molecular functions and network path functions. Baicalin or jasminoidin alone effectively reduced infarct area, and the combination resulted in significantly better outcomes. IPA showed inhibited cell apoptosis in the baicalin group and Ca2+ channel regulation in the jasminoidin group. The combination of baicalin and jasminoidin activated HTR3A and F5 expression, regulated Ca2+ channels, activated kappa light polypeptide gene enhancer inhibitor IKBKG in B cells to control IkB kinase/nuclear factor-kB cascade, suppressed activation of inflammatory cytokine interleukin-6 receptors and activated transduction of guanine-nucleotide- binding protein (G protein) signal. Results suggested that the combination of baicalin and jasminoidin resulted in similar molecular mechanisms to baicalin and jasminoidin alone. However, novel pharmacological actions of compatibility were detected, demonstrating significant protection against cerebral ischemia.