Nguyen Nhan Trung, Banskota Arjun H, Tezuka Yasuhiro, Le Tran Quan, Nobukawa Takahiro, Kurashige Youichi, Sasahara Masakiyo, Kadota Shigetoshi
Institute of Natural Medicine, Toyama Medical and Pharmaceutical University, Sugitani, Toyama, Japan.
Planta Med. 2004 Jan;70(1):29-33. doi: 10.1055/s-2004-815451.
The hepatoprotective effect of taxiresinol ( 1) and (7' R)-7'-hydroxylariciresinol ( 2), two tetrahydrofuran-type lignans isolated from the wood of Taxus yunnanensis, were investigated on D-galactosamine ( D-GalN)/lipopolysaccharide (LPS)-induced hepatic liver injury in mice. Pre-administration of 1 or 2 at doses of 50 and 10 mg/kg ( i. p.) at 12 and 1 h before D-GalN/LPS injection significantly inhibited hepatocyte DNA fragmentation and apoptotic body formation. Pre-treatment of these two lignans further suppressed hepatic necrosis which occur at later stage of D-GalN/LPS intoxication as demonstrated by the significant and dose-dependent reduction in serum glutamic pyruvic transaminase (sGPT) and serum glutamic oxaloacetic transaminase (sGOT) at 8 h after intoxication. The elevation of serum tumor necrosis factor-alpha (TNF- alpha) level by D-GalN/LPS toxication was significantly inhibited by 1 or 2 at doses of 50 and 10 mg/kg. Moreover, both of these lignans significantly protected hepatocytes from D-GalN/TNF- alpha-induced cell death in primary cultured mouse hepatocytes. These results suggested that 1 and 2 had protected the hepatocytes from apoptosis via an inhibition of TNF- alpha production by activated macrophages and a direct inhibition of apoptosis induced by TNF- alpha in D-GalN/LPS-treated mice.
从云南红豆杉木材中分离得到的两种四氢呋喃型木脂素,即紫杉叶素(1)和(7'R)-7'-羟基落叶松脂素(2),对D-半乳糖胺(D-GalN)/脂多糖(LPS)诱导的小鼠肝损伤的保肝作用进行了研究。在注射D-GalN/LPS前12小时和1小时,腹腔注射剂量为50和10mg/kg的1或2,可显著抑制肝细胞DNA片段化和凋亡小体形成。这两种木脂素的预处理进一步抑制了D-GalN/LPS中毒后期发生的肝坏死,中毒后8小时血清谷丙转氨酶(sGPT)和血清谷草转氨酶(sGOT)显著且呈剂量依赖性降低即证明了这一点。D-GalN/LPS中毒引起的血清肿瘤坏死因子-α(TNF-α)水平升高,在剂量为50和10mg/kg时被1或2显著抑制。此外,这两种木脂素在原代培养的小鼠肝细胞中均能显著保护肝细胞免受D-GalN/TNF-α诱导的细胞死亡。这些结果表明,在D-GalN/LPS处理的小鼠中,1和2通过抑制活化巨噬细胞产生TNF-α以及直接抑制TNF-α诱导的凋亡,从而保护肝细胞免受凋亡。