HPLC determination of polydatin in rat biological matrices: application to pharmacokinetic studies.
ABSTRACT A reversed-phase high-performance liquid chromatographic (RPHPLC) method has been developed for the determination of polydatin (PD) in rat plasma, bile, urine, feces and tissue homogenates using 2,3,5,4'-tetrahydroxychrysophenine-beta-d-glucoside as an internal standard. The sample pretreatment included deproteinization for plasma samples and a liquid-liquid extraction for bile, urine, feces and tissue homogenates. Separation was obtained on a C18 reversed-phase column with the mobile phase consisting of methanol and water (35:65 v/v). The flow rate was 1 ml/min and the effluent was monitored at 310 nm. The method showed good linearity over the concentration ranges employed for various matrices (r > 0.998). The quantification limits of PD in rat plasma, bile, urine, feces and tissue homogenates were 0.0251, 0.126, 0.025 microg/ml, 0.189 and 0.0378 microg/g, respectively. The accuracy and precision of the method were less than 12.0% for the various matrices. No interferences from endogenous substances were found. The method was successfully applied to study the pharmacokinetics of PD in rats after intravenous administration.
Article: Polydatin up-regulates Clara cell secretory protein to suppress phospholipase A2 of lung induced by LPS in vivo and in vitro.[show abstract] [hide abstract]
ABSTRACT: Lung injury induced by lipopolysaccharide (LPS) remains one of the leading causes of morbidity and mortality in children. The damage to membrane phospholipids leads to the collapse of the bronchial alveolar epithelial barrier during acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Phospholipase A2 (PLA2), a key enzyme in the hydrolysis of membrane phospholipids, plays an important traumatic role in pulmonary inflammation, and Clara cell secretory protein (CCSP) is an endogenous inhibitor of PLA2. Our previous study showed that polydatin (PD), a monocrystalline extracted from a traditional Chinese medicinal herb (Polygonum cuspidatum Sieb, et Zucc), reduced PLA2 activity and sPLA2-IIA mRNA expression and mitigated LPS-induced lung injury. However, the potential mechanism for these effects has not been well defined. We have continued to investigate the effect of PD on LPS-induced expression of CCSP mRNA and protein in vivo and in vitro. Our results suggested that the CCSP mRNA level was consistent with its protein expression. CCSP expression was decreased in lung after LPS challenge. In contrast, PD markedly increased CCSP expression in a concentration-dependent manner. In particular, CCSP expression in PD-pretreated rat lung was higher than in rats receiving only PD treatment. These results indicated that up-regulation of CCSP expression causing inhibition of PLA2 activation may be one of the crucial protective mechanisms of PD in LPS-induced lung injury.BMC Cell Biology 07/2011; 12:31. · 2.59 Impact Factor