[Intervention Effect and Mechanism of Regulating MiR-155 on Young Rats with Dysfunction of Blood Coagulation].

OBJECTIVE: To investigate the intervention effect and mechanism of regulating miR-155 on young rats with dysfunction of blood coagulation. METHODS: Twenty-six healthy and clean SD male rats were selected to establish the coagulopathy models. Twenty-four rats successfully established models and were randomly divided into three groups: model group, up-regulated miR-155 group and down-regulated miR-155 group, with 8 rats in each group. The expression of miR-155 was detected by real-time fluorescence quantitative polymerase chain reaction. The changes of coagulation factors and coagulation indicators were observed. Liver pathological tissues were observed by HE staining. The expressions of HMGB1-RAGE/TLRs-NF-κB signaling pathway related proteins were detected by Western blot. RESULTS: Compared with model group, the expressions of HMGB1, RAGE, TLR2, TLR4 and NF-κB were significantly increased in up-regulated miR-155 group (all P < 0.05), while decreased in down-regulated miR-155 group (all P < 0.05). Compared with model group, the expressions of coagulation factor Ⅱ, Ⅶ, Ⅸ, and Ⅹ were significantly decreased in up-regulated miR-155 group (all P < 0.05), while increased in down-regulated miR-155 group (P < 0.05). There was no significant difference in the expression of coagulation factor Ⅺ among the three groups (P >0.05). Compared with model group, the levels of prothrombin time (PT) and activated partial thromboplastin time (APTT) were lower and fibrinogen (FIB) was higher in up-regulated miR-155 group (all P < 0.05), while in the down-regulated miR-155 group they were opposite. CONCLUSION: Down-regulation of miR-155 can effectively improve coagulation factors and coagulation indexes and inhibit inflammation in young rats with dysfunction of blood coagulopathy, and the mechanism may be related to HMGB1-RAGE/TLRs-NF-κB signaling pathway.

[Serum levels of insulin-like growth factor-1 in neonates with hyperbilirubinemia].

OBJECTIVE: Insulin-like grouth factor-1 (IGF-1) is polypetide hormone that has demonstrated effects on neural cells. Up to now, there is few reports about the relation between serum IGF-1 and brain damage in neonates with hyperbilirubinemia. This study explored the potential role of serum IGF-1 in neonatal hyperbilirubinemia. METHODS: Serum levels of IGF-1 were measured using ECLIA in 57 term neonates with hyperbilirubinemia and 25 normal term neonates. Meanwhile, total serum bilirubin (TSB), unconjugated bilirubin (USB) and serum albumin (ALB) contents were measured by the automatic biochemistry analyzer and the ratio of USB/ALB (B/A) was calculated. The hyperbilirubinemia group was classified into three subgroups based on serum TSB levels: mild (221-256 micromol/L), moderate (257-342 micromol/L) and severe (>342 micromol/L). Serum TSB levels in the 25 normal neonates were less than 85 micromol/L (control group). NBNA was performed on the day of serum sample collection. RESULTS: Serum IGF-1 levels in the mild, moderate and severe hyperbilirubinemia groups (39.38+/- 8.42, 30.77+/- 4.65 and 26.34+/- 2.05 ng/L, respectively) were obviously lower than those in the control group (50.16+/- 15.73 ng/L) (P< 0.01). There were significant differences among the three hyperbilirubinemia subgroups in serum IGF-1 levels (P< 0.01). Mean NBNA scores in the mild, moderate and severe hyperbilirubinemia groups (35.01+/- 2.26, 32.45+/- 2.74 and 26.77+/- 5.02, respectively) were significantly lower than those in the control group (38.24+/- 0.78) (P< 0.01). Significant differences in the NBNA scores were noted among the three hyperbilirubinemia subgroups (P< 0.01). Serum IGF-1 levels were positively correlated to NBNA scores (r=0.603, P< 0.01) and negatively correlated to the ratio of B/A (r=-0.483, P< 0.01). CONCLUSIONS: Serum IGF-1 levels decreased obviously in neonates with hyperbilirubinemia and correlated to the severity of disease. IGF-1 might be associated with bilirubin-induced brain damage.