concanavalin-a and Hypoxia

We studied the relationship between hypoxia and microRNA-210 (miR-210) levels, the miR-210 levels in patients with hepatitis B and the roles of miR-210 in liver inflammation. We used the concanavalin A (Con A) murine hepatitis model and inflammation, hypoxia and miR-210 levels were examined. In these patients, we studied serum miR-210 levels and clinical indexes related to hepatitis in 90 patients with different stages of chronic hepatitis B and 30 controls. Two functional assays of miR-210 in vitro under hypoxic condition were conducted. The animal experiments indicated that the liver and serum miR-210 levels significantly increased with liver hypoxia and inflammation. In humans, serum miR-210 levels enhanced with hepatitis severity and were related to serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) and prothrombin activity (PTA) levels. The miR-210 functional assays showed that miR-210 elevation might be related to the decreases in HepG2.2.15 cell dehydrogenase activity and HBV replication under hypoxic conditions. Because the liver inflammation causes liver hypoxia which also results in liver and serum miR-210 level elevation, the serum miR-210 level may serve as a molecular biomarker for the severity of hepatitis and increases in liver miR-210 that we see may be a response of hepatocytes to hypoxia during hepatitis progression.

Topics: Adult; Alanine Transaminase; Animals; Aspartate Aminotransferases; Bilirubin; Biomarkers; Cell Line, Tumor; Chemical and Drug Induced Liver Injury; Concanavalin A; Disease Models, Animal; Disease Progression; Female; Hepatitis B virus; Hepatitis B, Chronic; Humans; Hypoxia; Liver; Male; Mice; Mice, Inbred BALB C; MicroRNAs; Middle Aged; Prothrombin; Specific Pathogen-Free Organisms; Virus Replication

To observe the effects of acute hypoxia and adenosine on splenic T lymphocyte proliferation.. Wistar rats were divided into control and hypoxic group, and the latter were exposed to hypoxia (5000 m simulated high altitude, 23 h/d). Three days later, spleen cells were collected and stimulated by 5.0 microg/ml and 2.5 microg/ml concanavalin A (ConA) to determine the splenocyte proliferation. The proliferation was also observed after addition of different amount of adenosine to culture medium.. Acute hypoxia and adenosine had marked inhibitory effect on mitogenic response to Con A in splenic T cells, and the inhibitory effect induced by adenosine displayed concentration-dependent.. Acute hypoxia may impair the T cell function and adenosine could be involved in this process.

Topics: Adenosine; Animals; Cell Proliferation; Concanavalin A; Culture Media; Hypoxia; Male; Rats; Rats, Wistar; Spleen; T-Lymphocytes

Hypoxemia depresses cell-mediated immune functions in males, whereas proestrous females do not show such a depression. We hypothesized that elevated systemic estradiol levels in proestrous females prevent hypoxemia-induced immune depression. To study this hypothesis, male C3H/HeN mice were pretreated with 17 beta-estradiol (E(2), 40 microg/kg body wt sc) or vehicle for 3 days before induction of hypoxemia and again immediately before induction of hypoxia. The mice were subjected to hypoxemia (95% N(2)-5% O(2)) or sham hypoxemia (room air) for 60 min, and plasma and spleen cells were collected 2 h later. In vehicle-treated mice, splenocyte proliferation and interleukin-2 and interleukin-3 production were depressed after hypoxemia. E(2)-pretreated animals, however, displayed no such depression in splenic T cell parameters after hypoxemia. Splenic macrophage cytokine production was also depressed in vehicle-treated mice subjected to hypoxia, whereas it was normal in E(2)-pretreated mice. In summary, these findings indicate that administration of E(2) before hypoxemia prevented the depression of cell-mediated immune functions. Thus administration of 17 beta-estradiol in high-risk patients before major surgery might decrease hypoxemia-induced immune depression under those conditions.

Topics: Animals; Cells, Cultured; Concanavalin A; Dinoprostone; Estradiol; Female; Hypoxia; Immune System; Interleukins; Lipopolysaccharides; Male; Mice; Mice, Inbred C3H; Random Allocation; Spleen