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以Ｆｅ２＋－Ｈ２Ｏ２和ＮＡＤＰＨ－Ｆｅ２＋作为氧自由基生成系统造成大鼠肝线粒体脂质过氧化，研究了黄芩甙对脂质过氧化产物丙二醛（ＭＤＡ）生成的抑制作用；以乙酰氨基酚和四氯化碳分别诱导肝脂质过氧化损伤，测定血清丙氨酸转氨酶（ｓＡＬＴ）活性、肝中超氧化物歧化酶（ＳＯＤ）活性、肝中丙二醛（ＭＤＡ）和谷胱甘肽（ＧＳＨ）含量，研究了黄芩甙对这些指标的影响．结果表明黄芩甙对大鼠肝线粒体脂质过氧化产物ＭＤＡ的生成有抑制作用，对乙酰氨基酚和四氯化碳引起的肝脂质过氧化损伤有保护作用．
The mitochondrial lipid peroxidation of rat liver was induced by Fe2 + -H2O2 and NADPH-Fe2 + as oxygen free radical generating system. The inhibitory effect of baicalin on malondialdehyde (MDA) production was studied. Acetaminophen and Carbon tetrachloride induced hepatic lipid peroxidation injury respectively. Serum alanine aminotransferase (sALT) activity, hepatic superoxide dismutase (SOD) activity, malondialdehyde (MDA) and glutathione ) Content, the impact of baicalin on these indicators. The results showed that baicalin on rat liver mitochondrial lipid peroxidation product MDA inhibition, paracetamol and carbon tetrachloride-induced hepatic lipid peroxidation injury has a protective effect.