In order to determine the chemical constituents of Cistanche deserticola cultured in Tarim desert,a systematically phytochemical investigation was carried out.The constituents were isolated by silica gel,Sephadex LH-20,MCI gel,ODS column chromatography,and semi-preparative HPLC.Their structures were determined on the basis of MS and NMR spectroscopic analyses,by chemical methods,and/or comparison with literature data.The anti-inflammatory activities of the isolates were evaluated for their inhibitory effects on the lipopolysaccharide(LPS)-induced nitric oxide(NO)production in BV-2 mouse microglial cells.Nine iridoids were isolated and identified as cistadesertoside A(1),cistanin(2),cistachlorin(3),6-deoxycatalpol(4),gluroside(5),kankanoside A(6),ajugol(7),bartsioside(8),and 8-epi-loganic acid(9).Compound 9 exhibited potent inhibition on the NO production with an IC_(50) value being 5.2 μmol·L^(-1),comparable to the positive control quercetin(4.3 μmol·L^(-1)).Compound 1 was a new iridoid,and compounds 5,6,and 8 were isolated from this species for the first time.
NAN Ze-DongZHAO Ming-BoZeng Ke-WuTIAN Shuai-HuaWANG Wei-NanJIANG YongTU Peng-Fei
The saponin ginsenoside Rk1 is a major compound isolated from ginseng.Ginsenoside Rk1 has been reported to have anti-inflammatory and anti-tumor properties and to be involved in the regulation of metabolism.However,the effect and mechanism of anti-inflammatory action of ginsenoside Rk1 has not been fully clarified.We investigated whether ginsenoside Rk1 could suppress the inflammatory response in lipopolysaccharide-stimulated RAW264.7 macrophages and to explore its mechanism of the action.RAW264.7 cells were treated with LPS(1 μg×mL^(–1))in the absence or the presence of Ginsenoside Rk1(10,20,and 40 μmol×L^(–1)).Then the inflammatory factors were tested with Griess reagents,ELISA,and RT-PCR.The proteins were analyzed by Western blotting.Ginsenoside Rk1 inhibited lipopolysaccharide-induced expression of nitric oxide(NO),interleukin(IL)-6,IL-1β,tumor necrosis factor(TNF)-α,and monocyte chemotactic protein(MCP)-1.Ginsenoside Rk1 inhibited the lipopolysaccharide-stimulated phosphorylation of NF-κB and janus kinase(Jak)2 and signal transducer and activator of transcription(Stat)3 at Ser727 and Tyr705.These data suggested that ginsenoside Rk1 could inhibit expression of inflammatory mediators and suppress inflammation further by blocking activation of NF-κB and the Jak2/Stat3 pathway in LPS-stimulated RAW264.7 cells.
The shortage of reference standards has become the bottleneck of quality control of TCMs.In this study,a series of strategies,including one single reference standard to determine multi-compounds(SSDMC),quantitative analysis by standardized reference extract(QASRE),and quantitative nuclear magnetic resonance
Objective:Baoyuan decoction(BYD)is a traditional Chinese formula with myocardial protection efficacy validated by modern pharmacological tests.The present study aimed to investigate the effect and mechanism of BYD on alleviating myocardial infarction(MI).Methods:Nuclear magnetic resonance-based serum and urinary metabolomics were employed to explore the metabolic regulation effects of BYD in rats with MI induced by left anterior descending ligation.Oxygen-glucose deprivation/recovery(OGD/R)model in H9c2 cells and multiple molecular biology approaches were used to clarify the underlying action mechanisms of BYD.Results:BYD treatment recovered the serum and urinary metabolite profiles of the MI rats toward normal metabolic status and significantly improved mitochondrial energy metabolism and apoptosis pathways perturbed by MI.Analysis of the molecular mechanism of BYD indicated that it suppressed OGD/R-induced H9c2 cell apoptosis in a concentration-dependent manner by inhibiting the mitochondria-dependent caspase-9/3-poly ADP-ribose polymerase pathway.Conclusions:Our results demonstrate that BYD protects against myocardial apoptosis via the mitochondrial metabolic and apoptosis pathways.They also provide novel insights into the clinical application of BYD for the treatment of ischemic heart diseases.
