A new triterpenoid saponin, named 3-O-β-d-glucopyranosyl-(1 → 3)-β-d-xylopyranosyl-(1 → 2)-[α-l-rhamnopyranosyl-(1 → 3)]-β-d-glucopyranosyl-(1 → 4)-[β-d-glucopyranosyl-(1 → 2)]-α-l-arabinopyranosyl-3β,16α,28,30-tetrahydroxy-olean-12-ene (1), along with four known triterpenoids (2-5), was isolated from the rhizomes of Ardisia gigantifolia. Their structures were elucidated by spectroscopic methods. Compounds 1-4 showed cytotoxic activity against Hela, EJ, BCG, and HepG-2 cell lines. The percentage of early apoptotic cells after treatment with 1 was significantly increased compared with control cells (p < 0.05).

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As one of the most prospective delivery systems of insoluble drugs, nanocrystal has attracted more and more attention from pharmaceutical researchers. Nanoparticles with prominent different particle diameters were obtained to solve the problem of solubility and evaluate the positive effects of quercetin in vitro. The newly prepared nanocrystals were investigated by several methods including dynamic light scattering (DLS) and transmission electron microscopy (TEM). The particle sizes of the quercetin nanocrystals A (quercetin/NCs-A), quercetin nanocrystals B (quercetin/NCs-B) and quercetin nanocrystals C (quercetin/NCs-C) were 3.089±0.162 μm, 677.2±9.7 nm and 169.8± 0.3 nm respectively. The crystalline state of quercetin was detected by X-ray powder diffraction (XRPD) and differential scanning calorimetry (DSC) analyses and no change was observed after the process of reducing sizes. An accelerated quercetin dissolution rate was achieved through the nanocrystal technique. In conclusion, nanocrystals could significantly increase the equilibrium solubility of quercetin In Vitro. In addition, the particle size also had an important effect on the dissolution behavior of quercetin.

Phagocytic ability of macrophage is responsible for tuberculosis infection. Nicotine has been shown to attenuate the phagocytic ability of macrophage; however, the underlying mechanism remains unclear. Here, we demonstrated that nicotine increased the message RNA (mRNA) and protein expression of signal regulatory protein alpha (SIRPα) and enhanced the stability of SIRPα mRNA in macrophage. Nicotine decreased the expression of microRNA (miR)-296-3p, which directly targeted the 3′-untranslated region (3′-UTR) of SIRPα mRNA in macrophage. Furthermore, nicotine inhibited the phagocytic ability of macrophage by regulating the miR-296-3p–SIRPα axis. Moreover, nicotine decreased miR-296-3p expression via increasing c-Myc expression in macrophage. Together, we found that nicotine attenuate the phagocytic ability of macrophage by regulating the c-Myc-miR-296-3p–SIRPα signal.