Sesamin promotes angiogenesis and accelerates wound healing in rats via alleviates TBHP-induced apoptosis in human umbilical vein endothelial cells.

Acute stress induces tissue damage through excessive cellular apoptosis. In our study, the effects of sesamin on apoptosis and wound healing were investigated. The angiogenesis effect of sesamin was evaluated by the abilities of adherence, migration and tube formation in human umbilical vein endothelial cells (HUVECs). Our data demonstrated that treatment with sesamin dose-dependently promoted the proliferation, adherence, migration and enhanced their angiogenic ability in vitro. Moreover, the increased apoptosis in HUVECs, which stimulated by tert-butyl hydroperoxide (TBHP) was significantly attenuated by the sesamin treatment. Furthermore, we revealed that neogenesis of granulation tissue and deposition and remodeling of the collagen matrix were accelerated by the administration of sesamin in our in vivo study. These results confirm that sesamin accelerates wound healing at least partly through its antiapoptotic effects on endothelial cells at the injury site. Thus, sesamin represents a potential therapeutic medicine for vessel injury-related wounds.

Determination of cepharanthine in rat plasma by LC-MS/MS and its application to a pharmacokinetic study.

CONTEXT: Cepharanthine (CPA) has been reported to possess a wide range of pharmacological activities. OBJECTIVE: This study investigates the pharmacokinetic characteristics after oral or intravenous administration of CPA by using a sensitive and rapid LC-MS/MS method. MATERIALS AND METHODS: A sensitive and rapid LC-MS/MS method was developed for the determination of CPA in Sprague-Dawley rat plasma. Twelve rats were equally randomized into two groups, including the intravenous group (1 mg/kg) and the oral group (10 mg/kg). Blood samples (250 µL) were collected at designated time points and determined using this method. The pharmacokinetic parameters were calculated. RESULTS: The calibration curve was linear within the range of 0.1-200 ng/mL (r = 0.999) with the lower limit of quantification at 0.1 ng/mL. After 1 mg/kg intravenous injection, the concentration of CPA reached a maximum of 153.17 ± 16.18 ng/mL and the t1/2 was 6.76 ± 1.21 h. After oral administration of 10 mg/kg of CPA, CPA was not readily absorbed and reached Cmax 46.89 ± 5.25 ng/mL at approximately 2.67 h. The t1/2 was 11.02 ± 1.32 h. The absolute bioavailability of CPA by oral route was 5.65 ± 0.35%, and the bioavailability was poor. DISCUSSION AND CONCLUSIONS: The results indicate that the bioavailability of CPA was poor in rats, and further research should be conducted to investigate the reason for its poor bioavailability and address this problem.