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Panax notoginseng is used as a therapeutic agent to stop haemorrhages and a tonic to promote health in Chinese medicine. Currently saponins of P. notoginseng (PNS) are especially given attentions for their hemorheological properties. The pharmacokinetic profiles of the main PNS are still not accurately investigated. Therefore, our preliminary aim is to elucidate the pharmacokinetic features of ginsenoside Rb1 (Rb1) and ginsenoside Rg1 (Rg1), two of the main PNS in rats. Firstly, quantitive analysis of Rb1 and Rg1 in saponins of P. notoginseng was studied and the most suitable assay method by HPLC for blood sample were established. Then Rb1 and Rg1 in the same serum were determined after administering PNS to rats. The decline of Rb1 in serum could be described by a two-compartment model. The half-life of α phase was 23.40 min and that of β phase was 17.96 h. Rb1 was absorbed from the digestive tract and the bioavailability via P.O. was 4.35%. The pharmacokinetics of Rg1 in rats also could be described by a two-compartment model. The half-lives of Rg1 were 24.23 min for α phase and 14.13 h for β phase. Rg1 could be absorbed in the digestive tract and the oral bioavailability was 18.40%. Both of the low oral bioavailability of Rb1 and rapid reduction of Rg1 in blood indicated that formula modification is necessary. [Copyright &y& Elsevier]

Ethnopharmacological relevance Houttuynia cordata (HC) has been used as a folk therapy to treat pulmonary infections. This study aimed to determine the role and mechanism of action of polysaccharides isolated from HC (HCP) in lipopolysaccharide (LPS)-induced ALI in the mice. Materials and methods LPS was delivered by the intratracheal route to Balb/c mice 2 h before HCP (40, 80 and 160 mg/kg) administration. Results The number of total cells, protein and tumor necrosis factor-α (TNF-α) concentrations in bronchoalveolar lavage fluid, the wet/dry weight ratio (w/d) of lungs and pulmonary pathology of each mouse were analyzed, it was found that HCP significantly alleviated ALI induced by LPS. Moreover, in lungs of mice, it was found that the infiltration of inflammatory cells, the expression of Toll-like receptor 4 and complement deposition were significantly decreased by HCP treatment. In vitro assays showed that C5a, a complement activation product, induced significant macrophage migration and treatment with HCP prevented it. The in vitro results also proved that LPS increased nitric oxide and pro-inflammatory cytokines (TNF-α, interleukin-6, and interleukin-1β) production, and HCP antagonized these effects of LPS. It was also found that HCP alone augmented secretion of some pro-inflammatory cytokines. Conclusion These results indicate that HCP may alleviate LPS induced lung inflammatory injury, which may be associated with its inhibitory effect on the over activation of complement and macrophages. This suggests a potential role to treat ALI. [ABSTRACT FROM AUTHOR]