大鼠急性脊髓损伤后肺水肿的机制及黄芪多糖对肺水肿的保护作用的初步研究
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摘要
观察大鼠急性脊髓损伤后不同时间节点肺组织的水肿情况及病理改变,探讨P物质及CD44含量的改变与肺水肿的关系。并探索中药黄芪对肺水肿的抑制作用,及对P物质和CD44的影响。实验采用C7段脊髓的大鼠Allen’s打击模型,打击力度为10×2.5g·cm,造成大鼠脊髓损伤。观察肺组织的病理改变和湿干重比。测定血清和肺泡灌洗液中P物质及CD44含量和蛋白浓度,计算肺通透指数。并设置对照组,观察不同浓度黄芪对大鼠脊髓损伤后肺组织的病理改变和肺湿干重比的影响,以及黄芪对P物质和CD44的影响。研究发现,大鼠急性脊髓损伤后肺部出现出血和水肿,伤后3d最为严重,伤后1周开始减轻。肺泡灌洗液及血清中P物质含量的变化与肺水肿轻重程度成正相关,血清CD44含量变化与肺水肿轻重程度呈负相关性。而不同浓度黄芪对急性脊髓损伤后大鼠肺水肿及血清和肺泡灌洗液P物质和CD44含量有影响。大鼠急性脊髓损伤后交感神经可能过度兴奋,刺激P物质的大量释放,参与急性脊髓损伤后肺水肿的形成过程。而肺损伤后肺泡上皮细胞受损,故肺泡细胞CD44表达下降,从而减弱对肺泡损伤修复能力及对炎症反应的控制。而黄芪多糖可有效减轻大鼠急性脊髓损伤后肺水肿的程度。
The purpose of this study was to observe the changes of the pulmonary edema and pulmonary histopathology at different time point in acute spinal cord injured rats, to investigate the relationship between pulmonary edema and the changes of substance P and CD44 in serum and bronchoalveolar lavage fluid(BALF). And to investigate the relationship between astragalin and pulmonary edema, substance P and CD44. The spinal cord injury(SCI) models were induced at the level of seven cervical vertebrae(C7) by dropping a weight of lOg from the height of 25mm(Allen's model). To observe the change of the pulmonary pathology and lung wet/dry weight ratios(W/D). The content of substance P and protein concentration in serum and BALF were measured. Then the lung permeability index(LPI) was calculated. To install control group to observe the effect of astragalin with different concentration on pulmonary pathology, lung wet/dry weight ratios, substance P and CD44. Pulmonary edema and hemorrhage were noted in SCI rats, which reach pea at 3d after injury, and relieve at 1 week. The degree of pulmonary edema was positive correlation with the change of substance P in serum and BALF, and was negative correlation with the change of CD44 in serum. Astragalin with defferent density affected the pulmonary pathology and edema and the change of substance P and CD44 in serum and BALF in SCI rats. In rats with spinal cord injury, sympathetic nerve may be over excitation, which may stimulate the release of substance P to take part in the development of neurogenic pulmonary edema. Furthermore, alveolar epithelial cell damaged after pulmonary injury, which decreased CD44 expression, so reconditioning ability decreased. Astragalin can lessen the degree of pulmonary edema in SCI rats.
The purpose of this study was to observe the changes of the pulmonary edema and pulmonary histopathology at different time point in acute spinal cord injured rats, to investigate the relationship between pulmonary edema and the changes of substance P and CD44 in serum and bronchoalveolar lavage fluid(BALF). And to investigate the relationship between astragalin and pulmonary edema, substance P and CD44. The spinal cord injury(SCI) models were induced at the level of seven cervical vertebrae(C7) by dropping a weight of lOg from the height of 25mm(Allen's model). To observe the change of the pulmonary pathology and lung wet/dry weight ratios(W/D). The content of substance P and protein concentration in serum and BALF were measured. Then the lung permeability index(LPI) was calculated. To install control group to observe the effect of astragalin with different concentration on pulmonary pathology, lung wet/dry weight ratios, substance P and CD44. Pulmonary edema and hemorrhage were noted in SCI rats, which reach pea at 3d after injury, and relieve at 1 week. The degree of pulmonary edema was positive correlation with the change of substance P in serum and BALF, and was negative correlation with the change of CD44 in serum. Astragalin with defferent density affected the pulmonary pathology and edema and the change of substance P and CD44 in serum and BALF in SCI rats. In rats with spinal cord injury, sympathetic nerve may be over excitation, which may stimulate the release of substance P to take part in the development of neurogenic pulmonary edema. Furthermore, alveolar epithelial cell damaged after pulmonary injury, which decreased CD44 expression, so reconditioning ability decreased. Astragalin can lessen the degree of pulmonary edema in SCI rats.
引文
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