[Determination of six active ingredients in different parts of Belamcanda chinensis and Iris tectorum and their anti-inflammatory activity].

In order to explore the anti-inflammatory activity and active ingredient basis from the leaves of the Belamcanda chinensis and Iris tectorum, we established an HPLC method for simultaneous determination of six anti-inflammatory active ingredient contents in the root of the B. chinensis and I. tectorum as well as their leaves with different dry methods, and the anti-inflammatory effects of the extract were studied by the mouse ear swelling experiment. The HPLC analysis was performed on an Agilent WondaSil© C18-WR(4.6 mm×250 mm，5 µm)，with isocratic elution of acetonitrile-0.1% ortho-phosphoric acid solution at a flow rate of 1. 0 mL·min⁻¹ and the detection was carried out at 265 nm. The chemical compositions of the B. chinensis and I. tectorum are similar but the contents of them are obviously different. Both rhizome and leaf extract of B. chinensis and I. tectorum had inhibitory effects on inflamed mice induced by dimethylbenzene and had anti-inflammatory effects by animal experiment, which could lay the material and active foundation for the development of the non-medicinal parts of the B. chinensis and I. tectorum.

Increased accumulation of hypoxia-inducible factor-1α with reduced transcriptional activity mediates the antitumor effect of triptolide.

BACKGROUND: Hypoxia-inducible factor-1α (HIF-1α), a critical transcription factor to reduced O2 availability, has been demonstrated to be extensively involved in tumor survival, aggressive progression, drug resistance and angiogenesis. Thus it has been considered as a potential anticancer target. Triptolide is the main principle responsible for the biological activities of the Traditional Chinese Medicine tripterygium wilfordii Hook F. Triptolide possesses great chemotherapy potential for cancer with its broad-spectrum anticancer, antiangiogenesis, and drug-resistance circumvention activities. Numerous biological molecules inhibited by triptolide have been viewed as its possible targets. However, the anticancer action mechanisms of triptolide remains to be further investigated. Here we used human ovarian SKOV-3 cancer cells as a model to probe the effect of triptolide on HIF-1α. RESULTS: Triptolide was observed to inhibit the proliferation of SKOV-3 cells, and meanwhile, to enhance the accumulation of HIF-1α protein in SKOV-3, A549 and DU145 cells under different conditions. Triptolide did not change the kinetics or nuclear localization of HIF-1α protein or the 26 S proteasome activity in SKOV-3 cells. However, triptolide was found to increase the levels of HIF-1α mRNA. Unexpectedly, the HIF-1α protein induced by triptolide appeared to lose its transcriptional activity, as evidenced by the decreased mRNA levels of its target genes including VEGF, BNIP3 and CAIX. The results were further strengthened by the lowered secretion of VEGF protein, the reduced sprout outgrowth from the rat aorta rings and the inhibitory expression of the hypoxia responsive element-driven luciferase reporter gene. Moreover, the silencing of HIF-1α partially prevented the cytotoxicity and apoptosis triggered by triptolide. CONCLUSIONS: The potent induction of HIF-1α protein involved in its cytotoxicity, together with the suppression of HIF-1 transcriptional activity, indicates the great therapeutic potential of triptolide as an anticancer drug. Meanwhile, our data further stress the possibility that HIF-1α functions in an unresolved nature or condition.