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以Ｄ－半乳糖复制小鼠衰老模型，观察内毒素导致脏器ＳＯＤ和ＬＰＯ含量的变化和中药复方毒素清对其保护作用，并与青年小鼠和氢化可的松对照。结果表明，青年内毒素组血清、心、肝、肺和衰老模型组血清、心、肝、肺、肾ＳＯＤ含量明显低于青年组（Ｐ＜０．０５～０．０１），衰老内毒素组血清、肝、肺ＳＯＤ低于衰老模型组（Ｐ＜０．０５）；与衰老内毒素组比较，毒素清高剂量组血清、肝、肺、肾和低剂量组的肝及氢化可的松组肺ＳＯＤ含量均明显升高（Ｐ＜０．０５）。衰老内毒素组肾、肝、肺ＭＤＡ含量较衰老模型组有升高趋势，高低剂量组肺、肝和氢化可的松组肺ＭＤＡ含量明显低下（Ｐ＜０．０１），其中肝的ＭＤＡ水平接近模型组和青年组（Ｐ＞０．０５）。提示内毒素降低衰老小鼠肝、肺等ＳＯＤ含量和增加ＬＰＯ水平，减弱机体抗自由基能力和增强脂质过氧化损伤；毒素清能够显著降低肝、肺等ＬＰＯ含量和提高ＳＯＤ水平，增强脏器组织抗自由基能力和抑制脂质过氧化反应，从而防止组织细胞的损伤。
D-galactose was used to replicate the mouse model of aging, and the changes of SOD and LPO content in organs were observed by endotoxin. The protective effect of traditional Chinese medicine compound toxin was also observed. Compared with young mice and hydrocortisone, The results showed that the content of SOD in serum, heart, liver, lung and kidney of serum, heart, liver, lung and kidney of endotoxin group was significantly lower than that of young group (P <0.05 ~ 0.01) Serum, liver and lung SOD levels were lower than those in the aging model group (P <0.05). Compared with the senescent endotoxin group, serum levels of the liver, lungs, kidney and low dose liver and hydrocortisone group SOD levels were significantly increased (P <0.05). The contents of MDA in kidney, liver and lung of aging endotoxin group were higher than those in aging model group. The levels of MDA in lung, liver and hydrocortisone group were significantly lower (P <0.01) Close to model group and youth group (P> 0.05). It is suggested that endotoxin can reduce the content of SOD and increase the level of LPO in the liver and lung of aging mice, weaken the body’s anti-free radical capacity and increase the lipid peroxidation injury. Toxin-Qing can significantly reduce the content of LPO in liver and lung, increase the level of SOD, Tissue anti-free radical capacity and inhibition of lipid peroxidation, thereby preventing damage to tissue cells.