黄酮苷对赛洛西宾过氧化作用的拮抗效应

 目的 研究黄酮苷对赛洛西宾的过氧化作用的的拮抗效应。方法 将SD大鼠分为5个实验组，赛洛西宾低剂量组、赛洛西宾高剂量组、赛洛西宾低剂量+黄酮苷组、赛洛西宾高剂量+黄酮苷组、对照组。检测各组大鼠血清中的ALT、AST、BUN、MDA、SOD。结果 与空白对照组比较，赛洛西宾高剂量组超氧化物歧化酶(SOD)活力明显降低，丙二醛(MDA)含量明显增加，动物肝脏脏器系数明显增大，肝脏功能指标丙氨酸转氨酶(ALT)、心肌损伤特异性标志物天冬氨酸转氨酶（AST）和肾功能指标BUN活力水平增加；给予黄酮苷可减轻指标改变的程度。 结论 赛洛西宾可引起多脏器氧化损伤，而黄酮苷可减轻这种损害程度。

Flavone Glycoside Antagonizes Psilocybin-Induced Toxicity by Reducing Oxidative Stress in Rats Model

Objective To explore the effects of flavone glycoside on psilocybin-induced oxidative damage in rats.Methods Five group Sprague-Dawley rats(10 for each group) were received vehicle(Con),low dose of psilocybin(i.p.,0.5 μg/kg body weight)(LD),high dose of psilocybin(i.p.,1.5 μg/kg body weight)(HD),low dose of psilocybin(i.p.) plus flavone glycoside(i.p.100 mg/kg body weight)(LDR),and high dose of psilocybin(i.p.) plus flavone glycoside(i.p.)(HDR),respectively.Ratio of organ weight to body weight of each group was measured.Aspartate aminotransferase(AST) and alanine aminotransferase(ALT) in serum of each group was evaluated with automated biochemistry analyzer.Oxidative stress-associated biochemical profile such as superoxide dismutase(SOD) and malondialdehyde(MDA) was assessed using kits.Liver histology of each group was observed using immunohistochemistry method.Results Compared with control group,AST and ALT in HD group were significantly increased,suggested that high dose of psilocybin induced toxic damage.After high dose treatment with psilocybins,MDA and SOD of liver homogenesis were elevated but this enhancement was reduced in HDR group,indicated that flavone glycoside alleviated psilocybin-induced oxidative stress.Interestingly,this significant increase of SOD was not observed in the kidney and heart lysates,implying that injured sites may be organ-dependent.Furthermore,histological analysis showed that high dose psilocybin induced liver damage which was reversed by flavone glycoside.Conclusion Oxidative damage induced by psilocybin could be attenuated by flavone glycoside.Our present study provided a novel mechanism of psilocybin-induced toxicity evidence and its antidote strategy.