Swerilactones H-K (1-4), which are four novel lactones with an unprecedented C29 skeleton, were isolated from Swertia mileensis (Qing-Ye-Dan), an endemic Chinese herb used for treating viral hepatitis. Their structures were determined by extensive spectroscopic and X-ray crystallographic diffraction analyses. Swerilactones H-K exhibit potent anti-hepatitis B virus activity against HBV DNA replication with IC(50) values ranging from 1.53 to 5.34 μM. For the first time, a plausible biogenetic pathway for swerilactones H-K, together with the previously reported swerilactones A-D is proposed. From a biogenetic point of view, swerilactones A-D are ascribed as secoiridoid dimers, and swerilactones H-K as secoiridoid trimers.

Swerilactones A (1) and B (2), two novel lactones with an unprecedented 6/6/6/6/6 pentacyclic ring system, were isolated from the traditional Chinese herb of Swertia mileensis with activity against the hepatitis virus. Their structures and relative stereochemistry were elucidated based on spectroscopic methods and further confirmed by X-ray single crystal diffraction analysis. In vitro antihepatitis B virus (HBV) assay on Hep G 2.2.15 cell line showed that compound 1 inhibited HBsAg and HBeAg secretion with IC(50) values of 3.66 and 3.58 mM, respectively.

The present study was designed to assess the antiarthritic potential of ECF in collagen-induced arthritis (CIA) and explore its underlying mechanism. Methods. In vitro, lymphocyte proliferation assay was measured by CCK-8 kit. In vivo, the therapeutic potential of ECF on CIA was investigated; surface marker, Treg cell, and intracellular cytokines (IL-17A and IFN-γ) were detected by flow cytometry. Th1 cell differentiation assay was performed, and mRNA expression in interferon-γ-related signaling was examined by q-PCR analysis. Results. In vitro, ECF markedly inhibited the proliferation of splenocytes in response to ConA and anti-CD3. In vivo, ECF treatment reduced the severity of CIA, inhibited IFN-γ and IL-6 secretion, and decreased the proportion of CD11b+Gr-1+ splenic neutrophil. Meanwhile, ECF treatment significantly inhibited the IFN-γ expression in CD4+T cell without obviously influencing the development of Th17 cells and T regulatory cells. In vitro, ECF suppressed the differentiation of naive CD4+ T cells into Th1. Furthermore, ECF intensely blocked the transcriptional expression in interferon-γ-related signaling, including IFN-γ, T-bet, STAT1, and STAT4. Conclusion. Our results indicated that ECF exerted antiarthritic potential in collagen-induced arthritis by suppressing Th1 immune response and interferon-γ-related signaling.