玫瑰茄水提物对t-BHP诱导原代培养异育银鲫肝细胞损伤生化指标的影响

Effects of aqueous extract of Hibiseus sabdarifa L. on biological parameters in injuried primary cultured Carassius auratus gibel hepatocytes induced by t-BHP

以叔丁基氢过氧化物(t-BHP)诱导异育银鲫(Carassius auratus gibel)原代培养肝(细胞)损伤模型,采用不同的给药顺序,通过检测肝细胞培养上清液中谷丙转氨酶(ALT/GPT)、微量丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-PX)和超氧化物歧化酶(SOD)的含量,研究玫瑰茄水提取液(aqueous extract ofHibiseus sab-darifaL.)对急性肝细胞损伤的保护作用。结果表明:以浓度为1 mmol.L-1的t-BHP作用肝细胞2 h诱导肝损伤模型;玫瑰茄水提取液能通过提高上清中GSH-PX和SOD酶活力以及抑制脂质过氧化产物MDA的生成来减轻t-BHP对肝细胞的损伤,减少GPT的释放,使GPT活力水平的升高受到明显抑制(P<0.05或P<0.01),显示出对t-BHP造成的肝细胞急性损伤有一定的保护作用,该保护作用可能与其抗氧化,清除自由基能力有关;中药与损伤剂的给予顺序影响着玫瑰茄对肝细胞的保护作用,从对生化指标测定值的分析中可以看出,预防治疗组(DT)中玫瑰茄对损伤肝细胞的保护效果明显要优于预防组(D)和治疗组(T)。

Primary hepatocytes injury models in vitro were induced by t-BHP in Carassius auratus gibel and treated with aqueous extract of Hibiseus sabdarifa L.by different administration orders.The activities of GPT,MDA,SOD and GSH-PX in cell culture supernatants were measured to study on the protective effects of aqueous extract of Hibiseus sabdarifa L.on acute hepatic injury.The results demonstrated the model of acute liver damage was established by exposing to 1 mmol·L-1 t-BHP for 2 h.Aqueous extract of Hibiseus sabdarifa L.could reduce the injury of liver by increasing the activity of glutathione peroxidase（GSH-PX） and superoxide dismutase（SOD）,restraining the lipid peroxidation production-malondisldehyde（MDA） and inhibit alanine minotransferase（GPT） release（P〈0.05 or P〈0.01） in supernatant of cultured hepatocytes injured by t-BHP induction.The results suggested that aqueous extract of Hibiseus sabdarifa L.possessed direct protective effect on primary hepatocyte injury induced by t-BHP and this effect was probably associated with scavenging oxygen free radicals and anti-oxidative activity of CMPS.Meanwhile,the administration orders of aqueous extract of Hibiseus sabdarifa L.and t-BHP influenced the protection.The protective effects of aqueous extract of Hibiseus sabdarifa L.in defense-treatment group（DT） were significantly better than defense group（D） and treatment group（T） from the analysis of biochemical indicators.