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This study was conducted to assess whether Lactobacillus-containing probiotics could protect intestinal mucosa in rats during traumatic hemorrhagic shock and to determine its underlying mechanisms. Healthy male Sprague–Dawley rats (300 ± 20 g) were randomly divided into four groups. During the study, reverse transcription polymerase chain reaction, western blotting, and hematoxylin and eosin methods were used. There was a significant increase in the expression of toll-like receptor 4 (TLR4) in the rats that experienced traumatic hemorrhagic shock, along with increased mRNA of tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. Pretreatment with Lactobacillus-containing probiotics reduced TLR4 expression, decreased phosphorylation (Ser536) and acetylation (Lys310) of p65, and decreased TNF-α and IL-6 mRNA. The probiotics combined acetate Ringer’s group showed a less severe pathological manifestation compared to the other experimental groups. Lactobacillus-containing probiotics inhibited nuclear factor-kappa B signaling via the downregulation of TLR4, resulting in inflammatory homeostasis, which might be the mechanism whereby Lactobacillus protects the intestinal mucosa from damage caused by the traumatic hemorrhagic shock.

To explore the efficacy of microecopharmaceutics combined with early enteral nutrition support to the treatment of severe acute pancreatitis (SAP). A total of 26 patients diagnosed with SAP in our hospital were retrospectively reviewed. Microecopharmaceutics, the living microbial food supplements that are beneficial to the host by improving the balance of intestinal microorganisms, were combined with early enteral nutrition group, and used as the treatment group; and delayed enteral nutrition was used as the control group. Two weeks after both treatments, variables of C-reactive protein (CRP), albumin (Alb), total serum protein (TP), urinary amylase recovery time, hemodiastase recovery time, acute physiology and chronic health evaluation (APCHE) score, and hospitalisation time in both groups were compared. Alb and TP of the treatment group were significantly higher than those in the control group (p

JAK/STAT plays an important role in cytokine signal transduction and it is potentially involved in the proinflammatory response during the early phase of severe acute pancreatitis (SAP). However, whether JAK2 activity is upregulated and whether JAK2 inhibition plays a role in the maintenance of pancreatic homeostasis during SAP is incompletely understood. Here we show that JAK2/STAT3 activity is highly elevated in SAP and blockade of JAK2 by AG-490 protects against SAP-induced pancreatic inflammation and injury. Gene expression and ELISA studies showed that JAK2 inhibition altered the cytokine profiles in both the circulation and pancreases. Further analysis revealed that JAK2 inhibition restored the level of cytokines critical for macrophage polarization towards M2 macrophage. Our findings suggest that pharmacological targeting at JAK2/STAT signalling may be an effective choice of therapeutic interventions against SAP., Highlights • JAK2/STAT3 pathway is activated in rat model of severe acute pancreatitis (SAP). • Inhibition of JAK2 protects against SAP-induced damage and inflammation of pancreas. • JAK2 inhibition modulates cytokine profile in rats. • JAK2 inhibition restored the level of cytokines critical for M2 macrophage polarization.