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用含氟饮水给SD大鼠染氟，同时服用SOD诱生剂——绞股蓝复方制剂，通过组织氟、尿氟、血清SOD的测定以及骨组织的光镜观察及体视学分析，探讨氟中毒所致骨组织的损伤是否与脂质过氧化损伤有关，并观察绞股蓝复方制剂对氟中毒所致骨损伤有否保护作用。染氟4月后，未经处理的染氟大鼠血清SOD显著降低，尿氟、骨氟明显升高；6月后，染氟对照大鼠出现骨髓胜狭窄，骨小梁面积密度增大等骨质硬化表现，部分动物有骨赘形成。股用绞股蓝复方制剂的染氟大鼠血清SOD保持正常，尿氟明显升高，但无骨氟蓄积，骨质硬化等损伤不明显。结果表明：慢性氟中毒时骨组织损伤可能与脂质过氧化损伤有关。绞股蓝复方制剂能诱使体内SOD合成，保持体内正常SOD水平，对氟中毒时通过自由基对骨细胞的脂质过氧化损伤有一定保护作用。
Fluoride-containing drinking water was used to dye fluoride-exposed SD rats. At the same time, SOD inducing agent-Gynostemma pentaphyllum was used to treat fluoride poisoning. Tissue fluoride, urinary fluoride and serum SOD were measured, as well as light microscopy and stereological analysis of bone tissue The damage caused by bone tissue is related to lipid peroxidation injury, and to observe whether Gynostemma Compound Fluoride-induced bone damage caused by the protective effect. In April, the serum SOD of untreated fluoride-exposed rats decreased significantly, and urinary fluoride and bone fluoride increased significantly. After 6 months, the rats in the fluorosis control group showed bone marrow stenosis and increased trabecular area density Bone sclerosis performance, some animals have osteophyte formation. The gypenositis in the compound Gynostemma pentaphylla compound-treated rats remained normal and the urinary fluoride increased obviously, but the injury such as no bone fluorosis and bone sclerosis was not obvious. The results showed that bone injury induced by chronic fluorosis may be related to lipid peroxidation. Gynostemma pentaphylla compound preparation can induce the synthesis of SOD in vivo and maintain the normal level of SOD in vivo, which can protect the osteoblasts against lipid peroxidation through free radicals during fluorosis.