Heat stroke (HS) models in rats are associated with severe intestinal injury, which is often considered as the key event at the onset of HS. Probiotics can regulate the gut microbiota by inhibiting the colonization of harmful bacteria and promoting the proliferation of beneficial bacteria. Here, we investigated the preventive effects of a probiotic Bacillus licheniformis strain (BL, CMCC 63516) on HS rats as well as its effects on intestinal barrier function and gut microbiota. All rats were randomly divided into four groups: control (Con) + PBS (pre-administration with 1 ml PBS twice a day for 7 days, without HS induction), Con + BL group (pre-administration with 1 ml 1 × 108 CFU/ml BL twice a day for 7 days, without HS induction), HS + PBS (PBS, with HS induction), and HS + BL (BL, with HS induction). Before the study, the BL strain was identified by genomic DNA analysis. Experimental HS was induced by placing rats in a hot and humid chamber for 60 min until meeting the diagnostic criterion of HS onset. Body weight, core body temperature, survival rate, biochemical markers, inflammatory cytokines, and histopathology were investigated to evaluate the preventive effects of BL on HS. D-Lactate, I-FABP, endotoxin, and tight-junction proteins were investigated, and the fluorescein isothiocyanate-dextran (FD-4) test administered, to assess the degree of intestinal injury and integrity. Gut microbiota of rats in each group were analyzed by 16S rRNA sequencing. The results showed that pre-administration with BL significantly attenuated hyperthermia, reduced HS-induced death, alleviated multiple-organ injury, and decreased the levels of serum inflammatory cytokines. Furthermore, BL sustained the intestinal barrier integrity of HS rats by alleviating intestinal injury and improving tight junctions. We also found that BL significantly increased the ratios of two probiotic bacteria, Lactobacillus and Lactococcus. In addition, Romboutsia, a candidate biomarker for HS diagnosis, was unexpectedly detected. In summary, BL pre-administration for 7 days has preventative effects on HS that may be mediated by sustaining intestinal barrier function and modulating gut microbiota.
Objectives: The objectives were to investigate the potential beneficial effects and molecular mechanisms of heparin and low-molecular-weight heparin (LMWH) on acute lung injury (ALI).Methods: Forty-eight rabbits were randomized into four groups: normal control group (Group A), lipopolysaccharide (LPS) group (Group B), LPS + heparin group (Group C), and LPS + LMWH group (Group D). The rabbit ALI model was established by intravenous (IV) injection with LPS. Alveolar-arterial O 2 difference (P A-a O 2 ), serum tumor necrosis factor a (TNF-a), circulating p38 mitogen-activated protein kinase (p38 MAPK) levels, lung nuclear factor (NF)-jB levels, and lung dry ⁄ wet (D ⁄ W) ratio were measured, and the lung injury scores were calculated.Results: Lipopolysaccharide caused significant increases in P A-a O 2 , serum TNF-a, expression of p38 MAPK in polymorphonuclear neutrophils (PMNs), the lung injury scores, and nuclear factor-jB (NF-jB) activity in the lung tissue and caused a decrease in lung D ⁄ W ratio. A positive linear correlation was found between p38 MAPK and TNF-a at 1, 2, 4, and 6 hours (r = 0.68, 0.92, 0.93, and 0.93, respectively) and between NF-jB and p38 MAPK and TNF-a at 6 hours (r = 0.94 and 0.83, respectively). IV heparin or LMWH given after LPS treatment attenuated these changes in inflammatory response, oxygenation, p38 MAPK expression, and NF-jB activation. Conclusions:The anti-inflammatory mechanisms of heparin in ALI may be inhibiting p38 MAPK and NF-jB activities, and then TNF-a overexpression, thus alleviating the inflammatory reaction. ACADEMIC EMERGENCY MEDICINE 2008; 15:656-663 ª 2008 by the Society for Academic Emergency MedicineKeywords: acute lung injury (ALI), acute respiratory distress syndrome (ARDS), tumor necrosis factor a (TNF-a); p38 mitogen-activated protein kinase (p38 MAPK); nuclear factor-jB (NF-jB); heparin; low-molecular-weight heparin (LMWH). R ecent studies have demonstrated that in the early stage of acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), a hypercoagulable state coexists with an inflammatory reaction. These two states interact and interpromote, potentially aggravating the condition of the patient.1,2 In recent years, some researchers and clinicians therefore began using heparin for anticoagulation therapy as part of the treatment for ALI or ARDS. They found that apart from the anticoagulatory effect, heparin also had an anti-inflammatory action.3 More recent studies have shown that the inflammatory reaction in ALI and ARDS was closely associated with the signal transduction pathway of p38 mitogen-activated protein kinase (p38 MAPK) and activation of nuclear factor-jB (NF-jB), 4 but whether this pathway and NF-jB activation are related to the anti-inflammatory effect of heparin has not been reported. The purpose of this study was to evaluate the relationships between signal transduction pathways (p38 MAPK and NF-jB activation) and the potential anti-inflammatory action of unfractionated and low-molecular-weight heparin (LMWH) in an anim...
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