Changes of leptin levels in serum and myocardium after myocardial ischemia/reperfusion injury / 中国应用生理学杂志

<p><b>AIM</b>To explore the effect of rat myocardial ischemia/reperfusion injury on leptin levels in serum and myocardium, and discuss the role of leptin in myocardial ischemia/reperfusion injury.</p><p><b>METHODS</b>A myocardial ischemia/reperfusion injury model of rats was established, serum lactate dehydrogenase (LDH) and leptin levels were detected, and histopathological changes and leptin expressions in myocardium were investigated by hematoxylin-eosin staining and immunohistochemistry, respectively.</p><p><b>RESULTS</b>Serum LDH of ischemia and reperfusion groups increased significantly (P < 0.05), suggesting the model was successfully established and a certain degree of local myocardial injury was induced. Serum leptin of ischemia group (6.34 +/- 2.49) ng/ml was significantly lower than control group (7.50 +/- 2.93 ng/ml, P <0.05). Leptin levels recovered gradually after reperfusion, reached (8.32 +/- 1.74)ng/ml at 2 h after reperfusion, which recovered to the level before injury (8.38 +/- 2.56) ng/ml, and showed a trend to increase as reperfusion time was elongated. Immunohistochemistry results showed that as compared with sham-operation group, myocardial leptin protein expressions of the other four groups were all significantly lower (P < 0.01), and decreased in order by 45 min ischemia/1 h reperfusion, 45 min ischemia/3 h reperfusion, 45 min ischemia and 45 min ischemia/2 h reperfusion.</p><p><b>CONCLUSION</b>Leptin level in the blood decreases significantly at the early 45 min after myocardial ischemia/reperfusion injury, and its expression in myocardium also decreases significantly. There may be a certain relationship between the pathological injury of myocardium and the changes of leptin.</p>

Leptin decreases post-septic pulmonary and intestinal FABP levels and its mechanism / 中国应用生理学杂志

<p><b>AIM</b>To detect the effect of sepsis on fatty acid binding proteins (FABP) levels and corresponding enzymes in lung and intestine of mice, and to explore the role for FABP in acute inflammation.</p><p><b>METHODS</b>A sepsis model of mice made with cecum deligation and perforation was established, and a radioimmunoassay for FABP and 96-well spectrophotometry assays for myeloperoxidase (MPO) and superoxide dismutase (SOD) which were related with clearance of free radicals,were used to detect their levels in lung and intestine homogenized fluids. Hematoxylin-eosin stain was used simultaneously to check the histopathologic chanes of both tissues.</p><p><b>RESULTS</b>Compared with sham group (108.11 +/- 94.03 and 67.22 +/- 19.47 ng/ml) 6 h and 12 h after sepsis, FABP levels in lung and intestine were significantly higher (204.98 +/- 70.72 and 154.29 +/- 60.14 ng/ml), respectively. Twelve hours after leptin (0.1 mg/kg i p) and indomethacin (2 mg/kg i p) injection, lung FABP level decreased and was lower than septic group (P < 0.05). Moreover, 12 h after sepsis intestinal FABP increased, but it decreased after leptin injection (419.80 +/- 80.06 vs 191.09 +/- 96.75 ng/ml), while indomethacin injection had no such effect. MPO and SOD activities in lung and intestine changed accordingly with time after sepsis, the effect of leptin and indomethacin injections on it had no significant correlation with FABP changes.</p><p><b>CONCLUSION</b>Leptin can protect vital organ functions such as lung and intestine after sepsis, as FABP levels, the cellular injury marker, were significantly lower than groups without injection. And this effect might have no correlation with the clearance factors of oxygenic free radicals such as MPO and SOD.</p>

Effect of intestinal ischemia/reperfusion injury on leptin and orexin-A levels / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the effect of intestinal ischemia/reperfusion (I/R) injury on leptin and orexin-A levels in peripheral blood and central secretory tissues, and investigate the roles of leptin and orexin-A in acute inflammatory responses.</p><p><b>METHODS</b>An intestinal I/R injury rat model was established, and the rats were grouped according to duration of the reperfusion time following a 60-min ischemia. Radioimmunoassay was used to examine the protein levels of leptin in the serum and adipose tissue, and the protein levels of orexin-A in the plasma and hypothalamus. Reverse transcriptase-polymerase chain reaction was also performed to detect the mRNA expressions of adipose leptin and hypothalamus orexin-A.</p><p><b>RESULTS</b>Compared with that before injury, serum leptin level of 60-min ischemia with 30-min reperfusion (I60'R30') group decreased significantly and that of I60'R360' increased significantly. Compared with the sham-operation group (sham) after injury, serum leptin level of I60'R360' group increased significantly, and adipose leptin protein levels of I60'R30' and I60'R90' groups decreased significantly, whereas that of I60'R360' group increased obviously. Compared with sham group after injury, adipose leptin mRNA expressions of I60'R30', I60'R240' and I60'R360' groups all increased significantly, while that of I60'R150' showed significant decrease. No significant changes were noted in the protein levels of orexin-A either in the plasma or hypothalamus after I/R injury. In comparison with sham group after injury, hypothalamus orexin-A mRNA expressions of I60'R30' and I60'R90' groups showed gradual but significant decrease, and till 150 min of reperfusion, the expression reached its lowest, followed then by slow recovery at 240 and 360 min, though still remaining significantly lower than that of sham group.</p><p><b>CONCLUSION</b>Leptin and orexin-A have a time-dependent response to intestinal I/R injury, but the former appears to exhibit a faster response, and they may play a certain role in the metabolic disorders of acute inflammation.</p>

Interleukin-1beta expression and phospholipase A(2) activation after intestinal ischemia/reperfusion injury / 生理学报

The experiments were carried out to explore the interactions between IL-1 beta gene expression, protein level and phospholipase A(2) PLA(2) inhibition after intestinal ischemia/reperfusion injury. Using a rat intestinal ischemia/reperfusion injury model, after collecting the serum, lung lavage, abdomen cavity lavage and important organ tissue samples from control, injury and PLA(2) inhibitor treated groups, IL-1 beta level was measured by radioimmunoassay, and the mRNA expression of IL-1 beta and type II PLA (2)was determined by RT-PCR. After 6 h of injury, the IL-1 beta level in serum was significantly higher than that in the control group; an increase in IL-1 beta was also observed in abdomen cavity lavage 1 or 3 h after injury. IL-1 beta was significantly increased in liver tissue after injury, but was not changed obviously in the lung, kidney and intestinal tissues. IL-1 beta in the lung lavage was significantly higher than that of control group. The mRNA expression of IL-1 beta in lung tissue was increased after injury, but type II PLA(2) mRNA expression was decreased. There were different changes in IL-1 beta level and gene expression after treatment with PLA(2) inhibitor chloroquine, cyclo-oxidase inhibitor indomethacin, or PAF receptor antagonist SR27417 respectively after injury. All these results indicate that after intestinal ischemia/reperfusion injury, the IL-1 beta level and mRNA gene expression are significantly increased, however, the relationship among IL-1 beta, PLA(2) activation and its metabolite release remains to be further elucidated.