Chronic ethanol exposure is associated with a local increase in TNF-alpha and decreased proliferation in the rat distraction gap.
Chronic ethanol exposure is associated with a local increase in TNF-alpha and decreased proliferation in the rat distraction gap.
复制标题
慢性乙醇暴露与 TNF-α 局部增加和大鼠牵引间隙增殖减少有关。
DOI：
10.1016/s1043-4666(03)00225-4
复制
发表时间：
2003
期刊：
影响因子：
3.8
通讯作者：
LumpkinJr,CharlesK
中科院分区：
文献类型：
--
作者：
Perrien,DanielS;Liu,Zhendong;Wahl,ElizabethC;Bunn,RobertC;Skinner,RobertA;Aronson,James;Fowlkes,John;Badger,ThomasM;LumpkinJr,CharlesK
长期饮酒是骨质疏松症的危险因素，并抑制骨修复和再生。我们研究了慢性乙醇暴露诱导肿瘤坏死因子-α和/或白介素1β的表达，并在牵张成骨过程中抑制增殖的假说。分别用免疫组织化学和RTPCR法检测成年雄性大鼠牵张间隙和对侧股骨骨髓中肿瘤坏死因子α和白介素1β的表达。在骨髓中，乙醇显著增加肿瘤坏死因子-α和IL-1β的表达(p<；0.04)。在DO间隙，乙醇暴露使纤维带间区和初级基质前线的肿瘤坏死因子-α表达增加，而IL-1β的表达在这两个区域均无明显影响。增殖细胞核抗原阳性细胞和肿瘤坏死因子阳性细胞在PMF中的百分比呈负相关(p<；0.015，R2=0.655)。乙醇与MC3T3E1细胞孵育24或48h后，其肿瘤坏死因子α的转录水平呈时间和剂量依赖性增加2~4倍，表明乙醇可直接诱导成骨样细胞中肿瘤坏死因子α的表达。这些结果支持这样的假设，即乙醇对骨形成的抑制可能部分是通过成骨过程中局部肿瘤坏死因子-α的增加来调节的。
Chronic alcohol consumption is a risk factor for osteoporosis and inhibits osseous repair and regeneration. We investigated the hypothesis that chronic ethanol exposure induces the expression of TNF-α and/or IL-1β and inhibits proliferation during distraction osteogenesis (DO). Following six weeks of liquid diet infusion (±ethanol) and 14 days of DO, the expression of TNF-α and IL-1β in the distraction gap and contralateral femoral marrow of adult male rats was examined by immunohistochemistry and RT-PCR, respectively. In the bone marrow, the expression of both TNF-α and IL-1β mRNA was significantly increased by ethanol (p<0.04 for both). In the DO gap, ethanol exposure increased the expression of TNF-α in both the fibrous interzone and primary matrix front (PMF), while IL-1β expression was not significantly affected in either region. A negative correlation was found between the percentage of PCNA+ and TNF+ cells in the PMF (p<0.015, R2=0.655). Incubation of MC3T3-E1 cells with ethanol for 24 or 48 h produced a time and dose dependent two- to fourfold increase in TNF-α transcripts as measured by RT-PCR, demonstrating that ethanol can directly induce TNF-α expression in osteoblast-like cells. These results support the hypothesis that attenuation of bone formation by ethanol may be mediated, in part, by local increases in TNF-α during osteogenesis.