首页> 外文会议>2010 4th International Conference on Bioinformatics and Biomedical Engineering >Effects of Chronic Aluminum Exposure on the Collagen Metabolism of Bone and Cartilage in Rats: The Toxic Effects of Aluminum on Bone and Cartilage in Rats
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Effects of Chronic Aluminum Exposure on the Collagen Metabolism of Bone and Cartilage in Rats: The Toxic Effects of Aluminum on Bone and Cartilage in Rats

机译:慢性铝暴露对大鼠骨和软骨胶原代谢的影响:铝对大鼠骨和软骨的毒性作用

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The pathogenesis of collagen pathway on the metabolism disorder of bone and cartilage induced by chronic aluminum (Al) exposure was studied. One hundred Wistar rats were divided randomly into two groups. Experimental rats were given drinking water containing Al chloride (400 mg/L, Al3+), while control rats were given distilled water for up to 150 days. Ten rats were sacrificed in each group every 30 days. The weights of rats, the Al levels of serum, bone and cartilage and the serum levels of carboxyterminal propeptide of type I procollagen (PICP), C-telopeptide of type I collagen (CTX-Ⅰ), typeⅡ collagen and C-telopeptide of type Ⅱ collagen (CTX-Ⅱ) were detected. The Al-poisoning model was established successfully in rats. Al-treated rats showed lower body weight and higher Al accumulation compared with control rats. The serum levels of PICP and type Ⅱ collagen decreased gradually, and were significantly lower than those in the control group (P<0.05, P<0.01). The serum levels of CTX-Ⅰ and CTX-Ⅱ were higher in the Al-treated group than in the control group from day 90 and 60, respectively (P<0.01). The results indicate that chronic Al exposure can induce the dysequilibrium of bone formation and bone absorption. As a result, bone and cartilage metabolism disorder were induced.
机译:研究了胶原途径对慢性铝(Al)暴露引起的骨骼和软骨代谢紊乱的发病机理。将一百只Wistar大鼠随机分为两组。实验大鼠被给予含氯化铝的饮用水(400 mg / L,Al3 +),而对照大鼠被给予蒸馏水长达150天。每30天每组杀死10只大鼠。大鼠体重,I型胶原蛋白(PICP),I型胶原蛋白C-端肽(CTX-Ⅰ),II型胶原蛋白和C型端粒肽的血清铝,骨,软骨的Al含量和血清端羧基水平检测Ⅱ型胶原(CTX-Ⅱ)。在大鼠中成功建立了Al中毒模型。与对照大鼠相比,经铝处理的大鼠显示出较低的体重和较高的铝蓄积。 PICP和Ⅱ型胶原的血清水平逐渐下降,并明显低于对照组(P <0.05,P <0.01)。 Al治疗组从第90天和第60天开始的血清CTX-Ⅰ和CTX-Ⅱ水平分别高于对照组(P <0.01)。结果表明,长期暴露于铝会引起骨骼形成和骨骼吸收的不平衡。结果,诱发了骨骼和软骨代谢紊乱。

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