• 关键词：慢性铝暴露  大鼠  骨与软骨损伤  胶原途径  动态分析

• 基金项目：黑龙江省自然科学基金(No.C200935)

• 李心慰
• 东北农业大学动物医学院, 哈尔滨 150030

• 张立超
• 东北农业大学动物医学院, 哈尔滨 150030

• 胡崇伟
• 东北农业大学动物医学院, 哈尔滨 150030

• 顾庆云
• 东北农业大学动物医学院, 哈尔滨 150030

• 李艳飞
• 东北农业大学动物医学院, 哈尔滨 150030

• 摘要：为了探讨慢性铝暴露致大鼠骨与软骨损伤胶原途径的机制及胶原代谢水平,实验将100只4周龄清洁级Wistar大鼠随机均分成染铝组(430mg·L^-1Al³⁺)与对照组(蒸馏水),通过饮水染铝,每隔30d处死染铝大鼠和对照大鼠各10只,设立5个观测点,最长染铝时间为150d.同时,用电子秤每30d称大鼠体重1次;用火焰原子吸收分光光度法测定血清、骨与软骨中铝含量;用固相夹心ELISA法检测血清中Ⅰ型前胶原羧基末端前肽(PICP)、Ⅰ型胶原C末端肽(CTX-Ⅰ)、Ⅱ型胶原(collagenⅡ)和Ⅱ型胶原C末端肽(CTX-Ⅱ)含量.结果表明,大鼠铝中毒模型复制成功;随着铝暴露时间的延长,染铝组大鼠体重在染铝60d后显著低于对照组(p<0.01);染铝组血清、骨与软骨中铝含量逐渐升高,显著高于对照组(p<0.01);PICP、Ⅱ型胶原合成量呈逐渐下降趋势,且显著低于对照组(p<0.05,p<0.01);CTX-Ⅰ和CTX-Ⅱ含量持续维持在高水平,分别在铝暴露90d、60d后显著高于对照组(p<0.01).说明长时间铝暴露可致铝在骨与软骨中蓄积,并使骨与软骨中结构性胶原减少,引发骨与软骨损伤.

• Abstract：The pathogenesis of collagen pathway and the metabolic level of collagen on bone and cartilage injuries induced by chronic aluminium exposure were studied. One hundred clean grade Wistar rats(four-week-old)were randomly divided into an aluminium exposure group (430 mg·L^-1,Al³⁺) and a control group (distilled water). Ten rats in each group were sacrificed every 30 days and the longest experimental period was 150 days. The weights of the rats were measured on an electronic scale every 30 days. The contents of aluminium in serum,bone and cartilage were detected by flame atomic absorption spectrometry,and the contents of carboxyterminal propeptide of type Iprocollagen (PICP),C-telopeptide of type Icollagen (CTX-Ⅰ),collagen Ⅱ and C-telopeptide of type Ⅱ collagen(CTX-Ⅱ)in serum were detected by solid phase sandwich ELISA. The results showed that an aluminium-intoxicated model was established successfully in rats. With the increase of aluminium exposure time,the weights of rats in aluminium exposure groups were significantly lower than those in control groups(p <0.01)after 60 days of aluminium exposure. The contents of aluminium in serum,bone and cartilage in aluminium exposure groups increased gradually,and were significantly higher than those in control groups (p <0.01). The contents of PICP and collagen Ⅱ in serum decreased gradually,and were significantly lower than those in control groups(p <0.05,p <0.01),and the contents of CTX-Ⅰand CTX-Ⅱin serum remained at high levels,which were higher than those in control groups after 90 and 60 days of aluminium exposure respectively (p<0.01). The results indicated that long-term aluminium exposure could induce accumulation of aluminium and decrease of structural collagen in bone and cartilage,which may result in bone and cartilage injuries.

• Key words：chronic aluminium intoxication  rats  bone and cartilage injuries  collagen pathway  dynamic analysis

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