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1.
Chongqing Medicine ; (36): 2024-2027, 2015.
Article in Chinese | WPRIM | ID: wpr-463454

ABSTRACT

Objective To observe the effect of nerve growth factor(NGF) on CCL4‐induced hepatic fibrosis in mice .Methods The hepatic fibrosis model was induced by subcutaneous injection of CCL 4 in mice .Thirty female Kunming mice were equally and randomly divided into three groups :fibrosis model group (A) ,NGF intervention group (B) and normal saline control group (C) .At 8 weeks following the initiation of experiment ,the samples were collected to measure ALT ,AST ,TBIL ,ALB by the fully automativ biochemical analyzer ,an the liver fibrosis indices (HA ,LN ,PC Ⅲ ) by radioimmunoassay .The Ishaki scoring system was adopted to assess the severity of hepatic inflammation and fibrosis degree .Results Serum levels of ALT ,AST ,HA and LN in the group A and B were significantly higher than those in the group C (F= 111 .45 ,658 .80 ,157 .43 ,167 .99 ;P< 0 .05) ,the levels of ALT 、AST and LN in the group B were significantly lower than those in the group A (P< 0 .05) .The HE staining ,reticular fiber staining and Masson staining showed that the liver fibrosis degree and the liver tissue inflammation in the group A were most obvious ,the liver tissue inflamation in the group B were significantly alleviated as compared with the group A .No fibrous septum was formed and the fiber tissues were fine and short .No obvious inflammatory cells infiltration and fibers formation were found in the liver tissue of the group C .The scores of liver inflamation grade and fibrosis staging in the group C were higher than those in the group B and C ,moreover the scores of liver inflammation grade and fibsosis had statstical differences among 3 groups (P < 0 .05) .Conclusion NGF can block hepatic fibrosis induced by CCL4 and relieve the liver inflammation .

2.
Chinese Journal of Infectious Diseases ; (12): 238-241, 2009.
Article in Chinese | WPRIM | ID: wpr-393022

ABSTRACT

Objective To detect the levels of tumor necrosis factor (TNF)-a,interleukin (IL)-1β,IL-2,1L-6,IL-8,1L-10,IL-12 and interferon (IFN)-α in the serum and cerebrospinal fluid of the patients with epidemic encephalitis B,and to investigate the roles in pathogenesis of epidemic encephalitis B.Methods Approximately of 2 mL serum and 2 mL cerebrospinal fluid from 24 patients with epidemic encephalitis B during acute phase were collected,and 2 mL serum from 20 healthy controls were collected.The levels of eytokines in serum and cerebrospinal fluid were detected by enzyme linked immunosorbent assay (ELISA).Means of multi-sample were compared by analysis of variance and means of two-sample were compared by t test.Results The levels of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-α in eerebrospinal fluid were (24.5±6.6),(7.8±2.4),(16.0±5.7),(17.6±4.8),(130.2±33.6) and (45.2±10.8) ng/L,respectively,and in serum were (25.3±11.2),(7.1±3.2),(14.5±6.2),(16.0±6.5),(82.0±27.8) and (42.5±16.2) ng/L,respectively.The levels of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-α in serum and cerebrospinal fluid from patients with epidemic encephalitis B were all higher than those in serum of healthy controls [(12.7±7.9),(2.6±1.0),(6.2±2.2),(9.6±3.3),(71.4±12.8) and (30.0±14.0) ng/L;F value was 14.10,29.46,23.38,14.78,32.59,7.52;all P<0.01];while the levels of IL-2 and IL-12 were not increased significantly.The levels of IL-1β,IL-6,IL-8,IL-10,IL-12 and IFN-α in cerebrospinal fluid were higher than those in serum,while the levels of TNF-± and IL-2 in cerebrospinal fluid were lower than those in serum.The levels of IL-6 and IL-8 in cerebrospinal fluid from patients with severe type of epidemic encephalitis B were (18.8±5.4) ng/L and (20.7±2.7) ng/L,and were higher than those with common type [(12.1±3.0) and (13.3±3.3) ng/L;t=3.50,t=5.96;P<0.05],while the levels of IL-2 in serum and in cerebrospinal fluid from patients with severe type were lower than those with common type. Conclusions Oversecretions of TNF-α,IL-1β,IL-6,IL-8,IL-10 and IFN-a are involved in the inflammatory damage of epidemic encephalitis B,while under-secretions of IL 2 and ILl2 may be involved in cellular immune responses.

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