黄芩苷及以其为主要活性成分的中药复方临床应用广泛，如辅助治疗急、慢性肝炎等。环孢素广泛用于肝、肾移植患者的治疗，CYP3A被抑制是其血药浓度升高产生毒性反应的重要原因。迄今关于黄芩苷对环孢素人体药动学的影响仍知之甚少。本研究前期结果提示黄芩苷多次给药可降低大鼠肝CYP3A的表达和活性。为此，我们提出假说：黄芩苷可能通过核受体PXR、PPARα、FXR等抑制CYP3A表达而减慢环孢素代谢，增加其AUC。为了验证这一假说，我们将通过HepG2细胞系、人原代肝细胞、人体试验，采用ChIP、qRT-PCR、Western blot、荧光素酶报告基因、LC-MS等手段，从分子、细胞、整体等多方面探讨黄芩苷对健康志愿者及肝移植病人环孢素药动学的影响，明确黄芩苷抑制CYP3A的分子调控机制。本研究将为揭示黄芩苷对人CYP3A的作用和机制奠定基础，为黄芩苷及CYP3A底物药物的临床合理应用提供新的思路。

Baicalin monomer and Chinese medicine including baicalin as the main bioactive constituent are widely used in clinical therapy of many diseases, such as acute and chronic hepatitis. Cyclosporine is extensively metabolized by CYP3A and used in patients undergoing liver or renal transplantation as an immunosuppressant. Inhibition of CYP3A causes the variation of the plasma concentration, which in turn leads to unanticipated toxic reactions of cyclosporine. Little research is reported about baicalin’s effects on cyclosporine pharmacokinetics in human. Our earlier study showed that multiple doses of baicalin significantly decreased the expression and activity of CYP3A in rat liver. Based on that, we proposed that baicalin may represse the expression of CYP3A potentially through regulation of nuclear receptors including PXR, PPARα and FXR, decrease metabolism of cyclosporine and increase AUC in human. To test this hypothesis, we will employ the ChIP, qRT-PCR, western blot, luminescent assay and LC-MS to evaluate the effect of baicalin on cyclosporine pharmacokinetics in healthy volunteers and liver-transplant-patients, to explore the mechanism of CYP3A down-regulation induced by baicalin in HepG2 cells, primary human hepatocytes. The results of the study would be helpful for revealing the influence of baicalin on the CYP3A in human and providing direction on clinical reasonable application of baicalin and CYP3A substrate drugs.