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脂多糖(LPS)能诱导 D-氨基半乳糖致敏小鼠坏死性肝炎.LPS 的毒性是因其作用于靶细胞引起内源性递质释放而触发的.一氧化氮(NO)作为一种信使或调质,它既有利于机体的自身免疫防御能力,又具有潜在的毒性.NO 的作用和信使功能主要受一氧化氮合酶(NOS)调控.LPS 作用于小鼠枯否细胞和巨噬细胞而产生大量的 NO 是其诱导病理性肝损伤的重要递质.三七是一种名贵中药材用于止血、强心和消炎等.人参皂甙 Rg1是从三七中分离提取的一种主要活性成分.现报道人参皂甙 Rg1对 LPS 诱导 D-氨基半乳糖致敏小鼠坏死性肝炎和血清一氧化氮、一氧化氮合酶及谷丙转氨酶活性影响.
Lipopolysaccharide (LPS) induces necrotizing hepatitis induced by D-galactose in mice. The toxicity of LPS is triggered by its action on the release of endogenous transmitters from target cells. Nitric oxide (NO) as a Messenger or conditioning, which is not only beneficial to the body’s autoimmune defense capability, but also potentially toxic. The role of NO and messenger function is mainly regulated by nitric oxide synthase (NOS). LPS acts on mouse Kupffer cells and giant The phagocytes produce a large amount of NO is an important transmitter that induces pathological liver injury. Panax notoginseng is a valuable Chinese herbal medicine for hemostasis, cardiac arrest, and anti-inflammation, etc. Ginsenoside Rg1 is a kind of isolated and extracted from Panax pseudoginseng. The main active ingredients. Now reported that ginsenoside Rg1 on LPS induced D-galactose-sensitized mice necrotizing hepatitis and serum nitric oxide, nitric oxide synthase and alanine aminotransferase activity.