Pan Hong, Shen Yang, Zhai Guohong, Li Xiaobing, Wu Qin, Fang Chao, Shi Jingshan, Shi Fuguo
Key Laboratory of Basic Pharmacology of Ministry of Education & Joint International Research Laboratory of Ethnomedicine of Ministry of Education, School of Pharmacy, Zunyi Medical University, Zunyi 563003, China; Hongqiao International Institute of Medicine, Tongren Hospital and State Key Laboratory of Oncogenes and Related Genes, Department of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Key Laboratory of Basic Pharmacology of Ministry of Education & Joint International Research Laboratory of Ethnomedicine of Ministry of Education, School of Pharmacy, Zunyi Medical University, Zunyi 563003, China.
Biochem Pharmacol. 2025 Sep;239:117042. doi: 10.1016/j.bcp.2025.117042. Epub 2025 Jun 6.
Dendrobine, a neuroprotective alkaloid, exhibited complex pharmacokinetics characterized by multiple peaks and continuous concentration plateaus in rats, particularly for dendrobine and its major metabolite N-demethylated dendrobine (N-deM dendrobine), but not for dendrobine N-oxide. This study elucidated the disposition mechanism underlying the multiple peaks phenomena through systematic investigation of tissue distribution, excretion, enteral reabsorption, and intestinal biotransformation. Key findings revealed that glucuronide N-deM dendrobine and glucuronide N-deM dendrobine N-oxide were major biliary metabolites, undergoing deglucuronidation and reduction in the jejunum to regenerate N-deM dendrobine for intestinal reabsorption. Interestingly, substantial quantities of dendrobine and its N-oxide were secreted into the gastric lumen through ion trapping, with dendrobine N-oxide functioning as a temporary storage form that underwent retro-reduction to dendrobine, facilitating subsequent intestinal reabsorption. The reabsorbed dendrobine was predominantly metabolized in the liver, yielding N-deM dendrobine and its glucuronide conjugates, dendrobine N-oxide, along with other metabolites, thereby facilitating enterohepatic recycling. In contrast, the reabsorbed N-deM dendrobine was primarily distributed into systemic circulation. Antibiotic-induced inhibition of intestinal biotransformation partially abolished the multiple peaks, suggesting that gut microbiota significantly influenced the pharmacokinetics of dendrobine and its metabolites. In conclusion, dendrobine and dendrobine N-oxide abundantly underwent gastric secretion-enteral reduction-reabsorption, resulting in multiple peaks of dendrobine. The reabsorbed dendrobine also supported the enterohepatic recycling of N-deM dendrobine through hepatic metabolism, driving its pharmacokinetic multiple peaks. The enterohepatic recycling of glucuronide metabolites of N-deM dendrobine was partially responsible for multiple peaks of N-deM dendrobine.
石蒜碱是一种具有神经保护作用的生物碱,在大鼠体内呈现出复杂的药代动力学特征,表现为多个峰和持续的浓度平台,特别是石蒜碱及其主要代谢产物N-去甲基石蒜碱(N-deM石蒜碱),但石蒜碱N-氧化物并非如此。本研究通过对组织分布、排泄、肠内重吸收和肠道生物转化的系统研究,阐明了多峰现象背后的处置机制。主要研究结果表明,N-去甲基石蒜碱葡萄糖醛酸苷和N-去甲基石蒜碱N-氧化物葡萄糖醛酸苷是主要的胆汁代谢产物,在空肠中进行葡萄糖醛酸苷水解和还原,以再生N-去甲基石蒜碱用于肠内重吸收。有趣的是,大量的石蒜碱及其N-氧化物通过离子捕获分泌到胃腔中,石蒜碱N-氧化物作为一种临时储存形式,经过逆向还原为石蒜碱,促进随后的肠内重吸收。重吸收的石蒜碱主要在肝脏中代谢,产生N-去甲基石蒜碱及其葡萄糖醛酸结合物、石蒜碱N-氧化物以及其他代谢产物,从而促进肝肠循环。相比之下,重吸收的N-去甲基石蒜碱主要分布到体循环中。抗生素诱导的肠道生物转化抑制部分消除了多个峰,表明肠道微生物群显著影响了石蒜碱及其代谢产物的药代动力学。总之,石蒜碱和石蒜碱N-氧化物大量经历胃分泌-肠内还原-重吸收,导致石蒜碱出现多个峰。重吸收的石蒜碱还通过肝脏代谢支持N-去甲基石蒜碱的肝肠循环,推动其药代动力学多峰。N-去甲基石蒜碱葡萄糖醛酸代谢产物的肝肠循环部分导致了N-去甲基石蒜碱的多峰现象。