Article
HPLC determination of polydatin in rat biological matrices: application to pharmacokinetic studies.
School of Pharmacy, Second Military Medical University, Shanghai Key Laboratory for Pharmaceutical Metabolites Research, No. 325, Guohe Road, Shanghai 200433, PR China.
Journal of Pharmaceutical and Biomedical Analysis (impact factor:
2.97).
04/2006;
41(1):240-5.
DOI:10.1016/j.jpba.2005.08.027
pp.240-5
Source: PubMed
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Citations (0)
- Cited In (1)
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Article: Polydatin up-regulates Clara cell secretory protein to suppress phospholipase A2 of lung induced by LPS in vivo and in vitro.
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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
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Keywords
2,3,5,4'-tetrahydroxychrysophenine-beta-d-glucoside
C18 reversed-phase column
concentration ranges
interferences
internal standard
intravenous administration
liquid-liquid extraction
mobile phase
PD
pharmacokinetics
plasma samples
quantification limits
rats
reversed-phase high-performance liquid chromatographic
sample pretreatment
tissue homogenates
various matrices