Acute mesenteric ischemia (AMI) defines a complex of conditions characterized by an interruption of the splanchnic circulation, leading to insufficient oxygen delivery or utilization to fill the metabolic needs of the visceral organs. Early diagnosis and immediate therapy are the cornerstones of early ischemia to reach a successful outcome and are necessary to reduce the high mortality. Although there is still lack of specific biomarkers to assist the diagnosis of AMI in clinical practice, there are several biomarkers with high specificity, may become a potential tools in early diagnosis of AMI, including intestinal fatty acid binding protein (I-FABP), a-glutathione S-transferase (a-GST), D-dimer, L- and D-lactate, citrulline, ischemia modified albumin, procalcitonin (PCT). However, they use in clinical limited duo to the many studies about these makers finished with small patient populations, and heterogeneous among these populations. This review describes the etiology of AMI, the current most studied promising biomarkers, the current research situation and future of biomarker research.

Objective: We have previously found that mesenchymal stem cell (MSC) therapy can ameliorate phosgene-induced acute lung injury (ALI). Moreover, exosomes can be used as a cell-free alternative therapy. In the present study, we aimed to assess the effect of MSC-derived exosomes on phosgene-induced ALI. Methods: MSC-derived exosomes were isolated from MSCs through ultracentrifugation. Sprague-Dawley (SD) rats were exposed to phosgene at 8.33 g/m³ for 5 min. MSC-derived exosomes were intratracheally administered and rats were sacrificed at the time points of 6, 24 and 48 h. Results: Compared with the phosgene group, MSC-derived exosomes reversed respiratory function alterations, showing increased levels of TV, PIF, PEF and EF50 as well as decreased levels of RI and EEP. Furthermore, MSC-derived exosomes improved pathological alterations and reduced wet-to-dry ratio and total protein content in BALF. MSC-derived exosomes reduced the levels of TNF-α, IL-1β and IL-6 and increased the IL-10 level in BALF and plasma. MSC-derived exosomes suppressed the MMP-9 level and increased the SP-C level. Conclusions: MSC-derived exosomes exerted beneficial effects on phosgene-induced ALI via modulating inflammation, inhibiting MMP-9 synthesis and elevating SP-C level.

Acute lung injury (ALI) and its more serious form [acute respiratory distress syndrome (ARDS)] are devastating diseases that lead to high morbidity and mortality rates in patients in intensive care units. ALI is caused by numerous direct or indirect factors, including trauma and sepsis. However, the underlying mechanism associated with the pathophysiological process of ALI has yet to be fully elucidated. As our understanding of mitochondrial biology continuously progresses, mitochondria have been largely considered as biosynthetic, bioenergetic and signaling organelles that have a critical role in the processes of cellular development, proliferation and death, and novel insights into how mitochondrial dysfunction affects the pathogenesis of different diseases have been garnered. According to current research models, functional characteristics of mitochondria are recognized to affect the function of cells and organs in ALI. The aim of the present review is therefore to discuss mitochondria and their role in ALI, and to consider how they may serve as potential therapeutic targets for this disease.

This study aimed to investigate the expression of miRNA‐21 during intestinal barrier dysfunction induced by intestinal ischemia reperfusion. Forty SPF SD rats were divided into 5 groups randomly. Intestinal ischemia‐reperfusion injury (IRI) was induced by mesenteric artery occlusion for 1 h and reperfusion for 1 h, and the rats were sacrificed at 1, 3, 6 and 12 h after reperfusion. Fresh intestine tissues were immediately isolated for the measurement of transepithelial electrical resistance (TER). The levels of cytokines, ICAM‐1, DAO, iFABP and MPO in serum were determined by ELISA. Intestinal tight junction proteins occludin and claudin‐1 were detected by immunofluorescence analysis and Western blot analysis. miR‐21 expression in intestinal tissues was measured by RT‐PCR. Compared with sham group, the levels of pro‐inflammatory cytokines TNF‐α and IL‐6 and ICAM‐1, DAO, iFABP and MPO increased while IL‐10 level decreased in intestinal ischemia‐reperfusion group. In addition, the levels of intestinal tight junction proteins occludin and claudin‐1 decreased while miR‐21 level increased in intestinal ischemia‐reperfusion group, compared with sham group. In conclusion, miR‐21 expression is upregulated during intestinal barrier dysfunction induced by IRI. miR‐21 may play an important role in the regulation of intestinal barrier function.

Animals exposed to phosgene (Psg) result in acute lung injury (ALI). We have recently reported that angiopoietin-1 (Ang1) reduces inflammation and vascular hyperpermeability in ALI animals. In this study, we examined whether the beneficial effects of adenovirus-delivered Ang1 (Ad/Ang1) on inflammatory responses in Psg-induced ALI rats are due to the suppression of the nuclear factor-kappa B (NF-κB) and p38 mitogen-activated protein kinase (MAPK) pathways, which play crucial roles in inflammatory responses in ALI. We demonstrated that Psg increased Ang2 and inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-4 (IL-4), IL-6, IL-8, and IL-10, in the serum and bronchoalveolar lavage fluid of ALI rats, determined by ELISA. Ang1 inhibits pro-inflammatory mediators (TNF-α, IL-6 and IL-8) and has no effect on anti-inflammatory mediators (IL-4 and IL-10). Furthermore, the inhibitory action of Ang1 was mediated by the suppression of the NF-κB and p38 MAPK pathways, leading to the attenuation of inflammatory responses of ALI. Thus, Ad/Ang1 may provide a useful tool for the effective treatment in Psg-induced ALI.