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灵芝多糖对四氧嘧啶诱导的胰岛损伤的体内外保护作用

In vitro and in vivo protective effect of Ganoderma lucidum polysaccharides on alloxan-induced pancreatic islets damage.

作者信息

Zhang Hui-Na, He Jing-Hua, Yuan Lan, Lin Zhi-Bin

机构信息

Department of Pharmacology, School of Basic Medical Sciences, Peking University Health Science Center, 38 Xueyuan Road, Beijing 100083, PR China.

出版信息

Life Sci. 2003 Sep 19;73(18):2307-19. doi: 10.1016/s0024-3205(03)00594-0.

Abstract

This study was undertaken to investigate the protective effect against alloxan-induced pancreatic islets damage by Ganoderma lucidum Polysaccharides (Gl-PS) isolated from the fruiting body of Ganoderma lucidum (Leyss. ex Fr.) Karst. In vitro, alloxan caused dose-dependent toxicity on the isolated pancreatic islets. Pre-treatment of islets with Gl-PS for 12 h and 24 h significantly reversed alloxan-induced islets viability loss. Gl-PS was also found to inhibit the free radicals production induced by alloxan in the isolated pancreatic islets using confocal microscopy. Gl-PS dose-dependently increased serum insulin and reduced serum glucose levels when pretreated intragastrically for 10 days in alloxan-induced diabetic mice. It was found that the pancreas homogenates had higher lipid peroxidation products in alloxan-treated mice than in the Gl-PS-treated animals. Aldehyde fuchsin staining revealed that alloxan caused nearly all the beta cells disappearing from the pancreatic islets, while Gl-PS partly protected the beta cells from necrosis. Alloxan (60 mg/kg) induced NF-kappa B activation in the pancreas at 30 min after injection, pretreatment with Gl-PS inhibited alloxan-induced activation of NF-kappa B. These results suggest that Gl-PS was useful in protecting against alloxan-induced pancreatic islets damage in vitro and in vivo; one of the mechanisms is through its scavenging ability to protect the pancreatic islets from free radicals-damage induced by alloxan.

摘要

本研究旨在探讨从灵芝(Leyss. ex Fr.)Karst.子实体中分离得到的灵芝多糖(Gl-PS)对四氧嘧啶诱导的胰岛损伤的保护作用。在体外,四氧嘧啶对分离的胰岛具有剂量依赖性毒性。用Gl-PS预处理胰岛12小时和24小时可显著逆转四氧嘧啶诱导的胰岛活力丧失。使用共聚焦显微镜还发现,Gl-PS可抑制四氧嘧啶在分离的胰岛中诱导的自由基产生。在四氧嘧啶诱导的糖尿病小鼠中,经胃内预处理10天,Gl-PS可剂量依赖性地增加血清胰岛素水平并降低血糖水平。结果发现,四氧嘧啶处理的小鼠胰腺匀浆中的脂质过氧化产物高于Gl-PS处理的动物。醛复红染色显示,四氧嘧啶导致几乎所有胰岛β细胞消失,而Gl-PS可部分保护β细胞免于坏死。四氧嘧啶(60mg/kg)在注射后30分钟诱导胰腺中NF-κB活化,用Gl-PS预处理可抑制四氧嘧啶诱导的NF-κB活化。这些结果表明,Gl-PS在体外和体内均有助于保护免受四氧嘧啶诱导的胰岛损伤;其中一种机制是通过其清除能力保护胰岛免受四氧嘧啶诱导的自由基损伤。

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