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目的:探讨痰热清注射液阻抑内毒素血症炎症反应和发热反应的效应机制。方法:SD大鼠和LCR小鼠各72只,雌雄各半,随机分为正常组、模型对照组、甲基强的松龙组、清开灵注射液组、痰热清注射液小剂量组、痰热清注射液大剂量组,每组12只。注射大肠杆菌内毒素(LPs,Ecoli055B5)制作内毒素血症病理模型。观察注射给药对中枢发热介质PGE2和cAMP,血清炎性细胞因子肿瘤坏死因子α(TNFα)、白细胞介素1β(IL1β)和白细胞介素6(IL6),以及脾淋巴细胞CD4CD8的影响。结果:内毒素导致模型鼠血清TNFα、IL1β和IL6表达水平及脾淋巴细胞CD4CD8的显著升高,下丘脑前列腺素E2(PGE2)和cAMP含量极显著增加。痰热清和清开灵对炎性细胞因子反应作用显著;三种药物均对脾淋巴细胞超敏反应有不同程度的阻抑作用;痰热清和清开灵能够有效地阻抑内毒素血症时下丘脑PGE2和cAMF,含量的升高,甲基强的松龙未显示该作用。结论:痰热清能够有效阻抑内毒素血症状态下的炎症反应及下丘脑PGE2和cAMP的含量升高,可能是其良好抗炎作用和解热效应的生物学基础。
Objective: To investigate the mechanism of Tanreqing injection in suppressing inflammatory reaction and fever reaction of endotoxemia. METHODS: Seventy-two male SD rats and female LCR mice were randomly divided into normal group, model control group, methylprednisolone group, Qingkailing injection group and Tanreqing injection small dose group. Large doses of Tanreqing Injection, 12 in each group. Escherichia coli endotoxin (LPs, Ecoli055B5) was injected to make a pathological model of endotoxemia. Observed the effect of injection on PGE2 and cAMP, the inflammatory cytokines tumor necrosis factor-α (TNFα), interleukin-1β (IL1β) and interleukin-6 (IL6), and the spleen lymphocyte CD4CD8. RESULTS: Endotoxin induced the expression of TNFα, IL1β and IL6 in the serum of the model mice and the CD4CD8 of spleen lymphocytes significantly increased, and the hypothalamic prostaglandin E2 (PGE2) and cAMP content increased significantly. Tanreqing and Qingkailing had significant effects on inflammatory cytokines; all three drugs had different degrees of inhibitory effect on hypersensitivity of spleen lymphocytes; Tanreqing and Qingkailing could effectively block endotoxemia. Thalamic brain PGE2 and cAMF levels increased, methylprednisolone did not show this effect. Conclusion: Qinreqing can effectively inhibit the inflammatory reaction in endotoxemia state and increase the content of PGE2 and cAMP in hypothalamus, which may be the biological basis of its good anti-inflammatory effect and antipyretic effect.