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目的 :从急性反应相蛋白 (AP)方面研究毒素清对肺炎老龄大鼠组织损伤的防护机制 ,为其防治老龄肺炎提供依据。方法 :老龄大鼠 (2 0～ 2 2月龄 )分为正常组、模型组、毒素清高剂量组、毒素清低剂量组织和头孢氨苄组。以肺脏病理和外周白细胞数量改变做对照 ,观察血清C -反应蛋白 (CRP)和铜蓝蛋白 (CP)含量。结果 :模型组血清CRP和CP含量高于正常组。毒素清高剂量组和头孢氨苄组血清CRP与CP含量低于模型组 ,毒素清低剂量组和模型组CRP与CP含量无明显差异。结论 :肺炎双球菌肺炎老龄大鼠肺组织损伤的病理机制与CRP和CP有关。毒素清能有效降低CRP和CP含量以保护肺组织以免损伤。
OBJECTIVE: To study the protective mechanism of Toxin on the tissue injury of aged aged rats with pneumonia from the acute phase reaction protein (AP), and provide the basis for its prevention and treatment of aged pneumonia. Methods: The aged rats (20 ~ 22 months old) were divided into normal group, model group, high dose toxin group, low dose toxin group and cefalexin group. The changes of lung pathology and peripheral white blood cells were used as controls to observe the levels of serum C - reactive protein (CRP) and ceruloplasmin (CP). Results: The levels of serum CRP and CP in model group were higher than those in normal group. The levels of CRP and CP in serum of high dose dexamethasone group and cefalexin group were lower than that of model group, and there was no significant difference of CRP and CP content between low dose dexamethasone group and model group. Conclusion: The pathological mechanism of lung injury in aged pneumonia pneumonia rats is related to CRP and CP. Toxin Qing can effectively reduce the content of CRP and CP to protect the lung tissue from damage.