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小儿慢性病贫血红系祖细胞与肿瘤坏死因子α、白介素6的关系研究
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作者 翟晓文 吴玥 陆凤娟 《中国小儿血液》 2005年第4期149-152,共4页
目的研究检测肿瘤坏死因子α(TNF-α)、IL-6(白介素-6)两种慢性病发生有关的细胞因子水平,以及红系造血祖细胞集落培养生长探讨它们在慢性病贫血(ACD)发病中的作用方法检测病例组为慢性病贫血组(ACD组)患儿,对照组为慢性病无贫血组(NA组... 目的研究检测肿瘤坏死因子α(TNF-α)、IL-6(白介素-6)两种慢性病发生有关的细胞因子水平,以及红系造血祖细胞集落培养生长探讨它们在慢性病贫血(ACD)发病中的作用方法检测病例组为慢性病贫血组(ACD组)患儿,对照组为慢性病无贫血组(NA组)和缺铁性贫血组(IDA组)患儿的血清肿瘤坏死因子α(TNF浕)、白介素-6(IL-6)水平,以及骨髓的红系祖细胞水平(BFU-E、CFU-E)。结果三组BFU-E有差异(F=3.56,P<0.05;三组CFU-E有显著差异(F=8.87,P<0.01)。ACD组与NA组相比,血清TNF-α前者高于后者(t=2.25,P<0.05),两组血清IL-6无差异(t=1.91,P>0.05)。在20例行骨髓培养的慢性病患儿中,血清TNFα与骨髓BFU-E之间无显著相关性(r=-0.37,P>0.05);血清TNF-α与CFU-E之间有负相关(r=-0.57,P<0.05);IL-6与BFU-E、CFU-E无相关性。结论ACD患儿骨髓红系祖细胞BFU-ECFU-E生成受抑制;血清TNF-α、IL-6的升高参与贫血发生;TNFα可能抑制慢性病患儿骨髓CFU-E形成而导致贫血。 展开更多
关键词 贫血 慢性病 儿童肿瘤坏死因子 白介素-6 肿瘤坏死因子α(TNF-α) 骨髓红系祖细胞 慢性病贫血 白介素6 肿瘤坏死因子α(TNFα) 血清TNF-Α 血清IL-6 CFU-E
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A rabbit model of pediatric nonalcoholic steatohepatitis: The role of adiponectin 被引量:10
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作者 Jun-Fen Fu Yan-Lan Fang Li Liang Chun-Lin Wang Fang Hong Guan-Ping Dong 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第8期912-918,共7页
AIM: To create a rabbit model of pediatric nonalcoholic steatohepatitis (NASH) and to evaluate the role of adiponectin in the process. METHODS: Thirty-two specific pathogen-free male New Zealand rabbits were divid... AIM: To create a rabbit model of pediatric nonalcoholic steatohepatitis (NASH) and to evaluate the role of adiponectin in the process. METHODS: Thirty-two specific pathogen-free male New Zealand rabbits were divided randomly into three groups: (1) the normal control group (n = 10) was fed with standard diet for 12 wk; (2) the model group A (n = 11); and (3) model group B (n = 11) were fed with a highfat diet (standard diet + 10% lard + 2% cholesterol) for 8 and 12 wk, respectively. Hepatic histological changes were observed and biochemical parameters as well as serum levels of adiponectin, interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-α were measured. RESULTS: Typical histological hepatic lesions of NASH were observed in both model groups described as liver steatosis, liver inflammatory infiltration, cytologic ballooning, perisinusoidal fibrosis and overall fibrosis. Compared with the normal control group, there were significant increases in model groups A and B in weight gain (1097.2 ± 72.3, 1360.5± 107.6 vs 928.0 ±58.1, P 〈 0.05, P 〈 0.01), liver weight (93.81±6.64, 104.6±4.42 vs 54.4±1.71, P 〈 0.01), Lg (ALT) (1.9±0.29, 1.84± 0.28 vs 1.60±0.17, P 〈 0.01), and Lg (TG) (1.03 ±0.24, 1.16 ±0.33 vs 0.00 ±0.16, P 〈 0.01). Weight gain was much more in model group B than in model group A (1360.5± 107.6 vs 1097.2 ±72.3, P 〈 0.05). But, there was no significant difference between the two groups concerning the other indexes. Pro-inflammatory cytokines (IL-6 and TNF-α) increased in model group B compared with that of control and model group A (IL-6:1.86±0.21 vs 1.41 ±0.33, 1.38± 0.42, P 〈 0.01; TNF-α: 1.18±0.07 vs 0.66 ±0.08, 0.86 ±0.43, P 〈 0.01, P 〈 0.05), whereas serum adiponectin and IL-10 decreased in model groups compared with that in the control (adiponectin: A: 21.87±4.84 and B: 21.48 ±4.60 vs 27.36 ±7.29, P 〈 0.05. IL-10: A: 1.72± 0.38 and B: 1.83 ±0.39 vs 2.26±0.24, P 〈 0.01). Lg (TC) and the degree of liver fatty infiltration was an independent determinant of serum adiponectin level analyzed by stepwise multiple regressions, resulting in 29.4% of variances. CONCLUSION: This rabbit model produces the key features of pediatric NASH and may provide a realistic model for future studies. Adiponectin level partially reflects the severity of liver steatosis, but not the degree of liver inflammation. 展开更多
关键词 Nonalcoholic steatohepatitis Pediatricanimal model ADIPONECTIN Interleukin 6 Tumornecrosis factor
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