Biliverdin Protects the Isolated Rat Lungs from Ischemia-reperfusion Injury via Antioxidative, Anti-inflammatory and Anti-apoptotic Effects / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Biliverdin (BV) has a protective role against ischemia-reperfusion injury (IRI). However, the protective role and potential mechanisms of BV on lung IRI (LIRI) remain to be elucidated. Thus, we aimed to investigate the protective role and potential mechanisms of BV on LIRI.</p><p><b>METHODS</b>Lungs were isolated from Sprague-Dawley rats to establish an ex vivo LIRI model. After an initial 15 min stabilization period, the isolated lungs were subjected to ischemia for 60 min, followed by 90 min of reperfusion with or without BV treatment.</p><p><b>RESULTS</b>Lungs in the I/R group exhibited significant decrease in tidal volume (1.44 ± 0.23 ml/min in I/R group vs. 2.41 ± 0.31 ml/min in sham group; P< 0.001), lung compliance (0.27 ± 0.06 ml/cmH2O in I/R group vs. 0.44 ± 0.09 ml/cmH2O in sham group; P< 0.001; 1 cmH2O=0.098 kPa), and oxygen partial pressure (PaO2) levels (64.12 ± 12 mmHg in I/R group vs. 114 ± 8.0 mmHg in sham group; P< 0.001; 1 mmHg = 0.133 kPa). In contrast, these parameters in the BV group (2.27 ± 0.37 ml/min of tidal volume, 0.41 ± 0.10 ml/cmH2O of compliance, and 98.7 ± 9.7 mmHg of PaO2) were significantly higher compared with the I/R group (P = 0.004, P< 0.001, and P< 0.001, respectively). Compared to the I/R group, the contents of superoxide dismutase were significantly higher (47.07 ± 7.91 U/mg protein vs. 33.84 ± 10.15 U/mg protein; P = 0.005) while the wet/dry weight ratio (P < 0.01), methane dicarboxylic aldehyde (1.92 ± 0.25 nmol/mg protein vs. 2.67 ± 0.46 nmol/mg protein; P< 0.001), and adenosine triphosphate contents (297.05 ± 47.45 nmol/mg protein vs. 208.09 ± 29.11 nmol/mg protein; P = 0.005) were markedly lower in BV-treated lungs. Histological analysis revealed that BV alleviated LIRI. Furthermore, the expression of inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-β) was downregulated and the expression of cyclooxygenase-2, inducible nitric oxide synthase, and Jun N-terminal kinase was significantly reduced in BV group (all P< 0.01 compared to I/R group). Finally, the apoptosis index in the BV group was significantly decreased (P < 0.01 compared to I/R group).</p><p><b>CONCLUSION</b>BV protects lung IRI through its antioxidative, anti-inflammatory, and anti-apoptotic effects.</p>

Protective effect of heme oxygenase-1 on lung injury induced by erythrocyte instillation in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Intratracheal instillation of blood induces self-repaired acute lung injury. However, the mechanism of repair has been unclear. Heme-oxygenase (HO)-1, which catalyzes heme breakdown, acts as an inducible defense against oxidative stress and plays an important role in inflammation. The objective of this study was to test the role of HO-1 in lung injury caused by intratracheal instillation of red cells.</p><p><b>METHODS</b>Forty healthy, male Sprague-Dawley rats were randomly divided into five groups: normal group, saline group, erythrocyte group, erythrocyte+zinc-protoporphyrin (ZnPP, HO-1 inhibitor) group and saline+ZnPP group. At 2 days after intratracheal instillation of red cells, lung tissues and lavage samples were isolated for biochemical determinations and histological measurements.</p><p><b>RESULTS</b>Histological analysis revealed that administration of ZnPP worsened the acute lung injury induced by instilled erythrocytes. HO-1 was over-expressed in the erythrocyte group and in the erythrocyte + ZnPP group. Compared with the erythrocyte + ZnPP group, the levels of total protein, lactate dehydrogenase and tumor necrosis factor-alpha in the lavage were lower (P < 0.01), while the level of interleukin-10 was higher in the erythrocyte group (P < 0.01).</p><p><b>CONCLUSION</b>HO-1 protects against erythrocyte-induced inflammatory injury in lung.</p>

Effects of two fluid resuscitations on the bacterial translocation and inflammatory response of small intestine in rats with hemorrhagic shock / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the effects of two fluid resuscitations on the bacterial translocation and the inflammatory factors of small intestine in rats with hemorrhagic shock.</p><p><b>METHODS</b>Fifty SD healthy male rats were randomly divided into 5 groups (n equal to 10 per group): Group A (Sham group), Group B (Ringer's solution for 1 h), Group C (Ringer's solution for 24 h), Group D (hydroxyethyl starch for 1 h) and Group E ((hydroxyethyl starch for 24 h). A model of rats with hemorrhagic shock was established. The bacterial translocation in liver, content of tumor necrosis factor-alpha (TNF-alpha) and changes of myeloperoxidase enzyme (MPO) activities in small intestine were pathologically investigated after these two fluid resuscitations, respectively.</p><p><b>RESULTS</b>The bacterial translocation and the expression of TNF-alpha in the small intestine were detected at 1 h and 24 h after fluid resuscitation. There were significant increase in the number of translocated bacteria, TNF-alpha and MPO activities in Group C compared with Group B, significant decrease in Group E compared with Group D and in Group B compared with Group D. The number of translocated bacteria and TNF-alpha expression significantly decreased in Group E as compared with Group C.</p><p><b>CONCLUSIONS</b>The bacterial translocation and the expression of TNF-alpha in the small intestine exist 24 h after fluid resuscitation. 6% hydroxyethyl starch can improve the intestinal mucosa barrier function better than the Ringer's solution.</p>