BMSC cells alleviate liver injury induced by ulcerative colitis via repairing the intestinal-liver barrier and activating hepatocyte growth factor.

Ulcerative colitis (UC), which belongs to inflammatory bowel diseases (IBD), frequently induces liver inflammation and injury. Previous studies have proved that bone marrow-derived mesenchymal stem cells (BMSCs) can suppress inflammation and improve intestinal mucosal injury in colitis, however, the effects of BMSCs on colitis-induced liver injury and the underlying molecular mechanisms remain unclear. Here, we investigated the effects and mechanisms of BMSCs in acute ulcerative colitis BALB/c mice, which were induced by 4 % dextran sodium sulphate (DSS).

Prognostic Model and Immune Infiltration of Ferroptosis Subcluster-Related Modular Genes in Gastric Cancer.

Background: Gastric cancer (GC) is one of the gastrointestinal tumors with the highest mortality rate. The number of GC patients is still high. As a way of iron-dependent programmed cell death, ferroptosis activates lipid peroxidation and accumulates large reactive oxygen species.

[Mechanism of bone marrow-derived mesenchymal stem cell-promoted apoptosis of hepatic stellate cells].

Objective: To explore the role of the Rho pathway in the hepatocyte growth factor (HGF) paracrine signal-mediated bone marrow-derived mesenchymal stem cell (BMSC) promotion of apoptosis of hepatic stellate cells (HSCs).

Methods: A BMSC-HSC co-culture system was established using plates with transwell inserts. Dynamic changes in response to pretreatment with the c-met blocker PHA665752 and the Rho pathway inhibitor Y-27632 were observed under an inverted phase contrast microscope at 24, 48 and 72 h of culture.

[Activation of hepatocyte growth factor promotes apoptosis of hepatic stellate cells via the Rho pathway].

Objective: To investigate the role of activated hepatocyte growth factor (HGF) in apoptosis of hepatic stellate cells (HSCs) and in modulating the Rho signaling pathway.

Methods: HSCs were divided into the following groups: blank control, consisting of HSCs without treatment; two treatment controls, consisting of HSCs exposed to exogenous HGF at 50 ng/ml and HSCs exposed to exogenous HGF activator (HGFA) at 70 ng/ml; three experimental groups, consisting of HSCs exposed to both exogenous HGF and HGFA, HSCs pre-incubated with the HGF inhibitor c-met at 500 ng/ml for 6 hours and then exposed to exogenous HGF and HGFA, and HSCs pre-incubated with the Rho pathway inhibitor Y-27632 at 10 ng/ml and then exposed to exogenous HGF and HGFA. Activation status of the cultured HSCs was determined by change in expression of alpha-smooth muscle actin (SMA).

[Activation of hepatocyte growth factor-induced apoptosis in hepatic stellate cells].

Objective: To determine whether apoptosis is induced in rat hepatic stellate cells (HSCs) in response to activation of the hepatocyte growth factor (HGF) by hepatocyte growth factor activator (HGFA) by using a co-culture system of bone marrow mesenchymal stem cells (BMSCs) and HSCs.

Methods: In this study, cells were divided into the following five groups: HSC control group: HSCs co-cultured with fibroblast cells; HSCs blank group: HSCs cultured alone; BMSCs blank group: BMSCs cultured alone; Experimental group: BMSCs + HSCs; HGFA intervention group: HSCs treated with 70 ng/mL of HGFA. The culture systems were established in culture plates with transwell inserts, and cells were assessed at 24, 48, and 72 h of growth.