[Research progress of mesenchymal stem cell-derived extracellular vesicles in liver diseases].

Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) transport and transmit intercellular information and play an essential role in physiological and pathological processes. MSC-EVs, MSC-EVs-microRNA, and genetically modified MSC-EVs are involved in the onset and progression of different liver diseases and play a role in reducing liver cell damage, promoting liver cell regeneration, inhibiting liver fibrosis, regulating liver immunity, alleviating liver oxidative stress, inhibiting liver cancer occurrence, and others. Hence, it will replace MSCs as a research hotspot for cell-free therapy. This article reviews the research progress of MSC-EVs in liver diseases and provides a new basis for cell-free therapy of clinical liver diseases.

Intestinal epithelial cells express galectin-9 in patients with food allergy that plays a critical role in sustaining allergic status in mouse intestine.

BACKGROUND AND AIMS: Mechanisms in sustaining the allergic hypersensitivity status in the body are unclear. Galectin-9 (Gal-9) has strong immune regulatory capacity. The present study aims to elucidate the role of Gal-9 in sustaining allergic status in the intestine. METHODS: Duodenal biopsies were obtained from 20 patients with peptic ulcer and food allergy (FA). The expression of Gal-9 in intestinal tissue was examined at both protein level and mRNA level. Two coculture systems with intestinal epithelial cells (IEC) and mast cells, or dendritic cells (DC) and T cells were established to investigate the source of Gal-9 in the intestine and the mechanism by which Gal-9 modulated DC's phenotyping and sustained the T helper 2 polarization. RESULTS: Normal IEC showed mild expression of Gal-9 that was markedly enhanced in patients with FA. Mast cells had the capability to induce IEC to produce Gal-9 via releasing tryptase that activated the proteinase-activated receptor 2 on IEC. Gal-9 activated DC to produce TIM4 (T-cell immunoglobulin mucin domain) via ligating TIM3 on DC via activating the cyclic guanosine monophosphate (cGMP) pathway. In a mouse FA model, blocking Gal-9 inhibited the allergic hypersensitivity status and the antigen-specific Th2 response in the intestine. CONCLUSIONS: IEC-derived Gal-9 contributes to sustaining the allergic status in the intestine.

Psychological stress induces eosinophils to produce corticotrophin releasing hormone in the intestine.

BACKGROUND AND AIMS: Psychological stress plays an important role in an array of intestinal disorders. Corticotrophin releasing hormone (CRH) is involved in the pathogenic process induced by psychological stress. The peripheral sources of CRH remain to be further understood. This paper aims to identify the sources of CRH in the intestine. METHODS AND RESULTS: Mice were treated with chronic restraint stress. A double-labelling approach was taken to localise CRH expression in immune cells (including dendritic cells, mast cells, lymphocytes, enterochromaffin cells and eosinophils) in the intestine by confocal microscopy and flow cytometry. As CRH was identified in eosinophils, a cell line of eosinophil, EoL-1 cells were treated with an array of putative stress mediators. The results showed that substance P (SP) induced the expression/release of CRH in eosinophils via neurokinin receptor 1 and 2. Co-culturing SP-primed eosinophils with the mast cell line, HMC-1 cells, we found that HMC-1 cells were activated by eosinophil-derived CRH that further induced T84 monolayer barrier dysfunction, which was further confirmed by a mouse model study. CONCLUSION: Eosinophils express CRH in the jejunum in response to psychological stress. SP and its receptors mediate the effect of stress in the CRH expression in eosinophils. Eosinophil-derived CRH activates mast cells to induce the jejunum epithelial barrier dysfunction.

[Studies on saponins from the leaves of Panax japonicus var. bipinnatifidus(Seem.)Wu et Feng].

Two new saponins, bipinnatifidusoside F1(XII) and F2(XIII), were isolated along with eleven known saponins from the dried leaves of Panax japonicus var.bipinnatifidus(Seem.)Wu et Feng collected in the Range of Qinling Mountains in China. By spectrometric analysis(FAB-MS,1H and 13CNMR,1H-1H COSY), their structures were elucidated as dammar-25(26)-ene-3 beta, 12 beta, 20(S),24 zeta-tetraol-(20-O-beta-D-glucopyranosyl)-3-O- beta-D-glucopyranosyl(1-2)-beta-D-glucopyranoside (bipinnatifidusodie F1) and dammar-22(23) ene-3 beta, 12 beta, 20(S),24 zeta-tetraol-(20-O-beta-D-glucopyranosyl)-3-O-beta- D-glucopyranosyl(1-2)-beta-D-glucopyranoside (bipinnatifidusoside F2), respectively. The known saponins were identified as ginsenoside F1,F2,F3,Rg2,Re,Rd,Rb1,Rb3, 24(S)-pseudoginsenoside F11, panasenoside and majoroside F1. Compared with bipinnatifidusoside F2, majoroside F3 was corrected as dammar-22(23)-ene-3 beta, 12 beta,20(S),24 zeta-tetraol-(20-O-beta-D- glucopyranosyl)-3-O-beta-D-glucopyranoside.

[Further study on dammarane saponins of leaves of Panax japonicus var. major collected in Quinling Mountains China].

In continuation of our studies on the leaves of Panax japonicus var. major (Burk.) Wu et Feng, two new dammarane saponins are isolated. By means of FAB-MS and 13CNMR, their structures were elucidated as dammar-22(23)-ene-3 beta, 6 alpha, 12 beta, 20(S), 24 section-pentaol- (20-O-beta-D-glucopyranosyl)-6-O-alpha-L-rhamnopyranosyl (1-2)-beta-D- glucopyranoside (majorosids F5) and dammar-23(24)-ene-3 beta, 6 alpha, 12 beta, 20(S), 25-pentaol-(20-O-beta-D- glucopyranosyl)-6-O-alpha-L-rhamnopyranosyl(1-2)-beta-D-glucopyranoside (majoroside F6).