灵芝多糖对小鼠肿瘤的抑制作用及免疫指标的观察

目的:观察灵芝多糖的抑瘤作用及对小鼠免疫系统的影响。方法:MTT法测定灵芝多糖的细胞毒作用。小鼠荷瘤建立动物模型,观察灵芝多糖对荷瘤小鼠的存活期、抑瘤率和免疫系统的影响。结果:灵芝多糖对肿瘤细胞无直接杀伤作用(P<0.005),体内可延长荷瘤小鼠的存活期;治疗组小鼠的NK细胞活性、淋巴细胞转化率、血清中TNF蛳α均有显著提高。结论:灵芝多糖抗肿瘤作用是通过机体的免疫系统介导的。     

赤灵芝对小鼠非特异性免疫功能的影响

目的 :探讨百色灵芝对正常小鼠和免疫抑制小鼠非特异性免疫功能的影响。方法 :用不同剂量赤灵芝液给正常小鼠和环磷酰胺免疫抑制小鼠灌胃 ,检测小鼠免疫器官重量和巨噬细胞吞噬功能。结果 :赤灵芝水煎剂对正常小鼠非特异性免疫功能无显著影响 ,但能显著增加环磷酰胺免疫抑制小鼠的胸腺和脾脏重量及胸腺指数和脾指数 ,增加巨噬细胞吞噬功能。结论 :赤灵芝对正常小鼠免疫功能无显著影响 ,对环磷酰胺免疫抑制小鼠的非特异性免疫功能具有正调节作用。     

灵芝孢子粉提取物降血糖作用及机制的实验研究

用Ｓｔｚ复制大鼠糖尿病模型观察了灵芝孢子粉乙醇提取物的水溶部分（Ｇｌｓｅ）的降糖作用及其对胰岛素离体生物活力和内分泌激素Ｉｎｓ、ＧＨ、Ｃｏｒ的影响。实验结果表明Ｇｌｓｅ（相当生药６２５０ｍｇ／ｋｇ）对糖尿病大鼠有明显的降低血糖作用，增强耐糖效应，对Ｓｔｚ损伤有一定的对抗作用，促进糖尿病大鼠的Ｉｎｓ分泌，维持ＧＨ、Ｃｏｒ的正常水平。含药血清对胰岛素离体生物活力无明显影响     

富锗灵芝菌丝体氨基酸及超氧化物歧化酶含量的测定

目的:测定富锗灵芝菌丝体氨基酸及超氧化物歧化酶(SOD)的含量,探讨培养基中GeO2的最适加量。方法:高效液相色谱仪分析氨基酸,氯化硝基四氮唑蓝(NBT)光化还原法测定SOD的含量。结果:培养基中添加400 mg.L-1的GeO2,灵芝菌丝体中氨基酸含量比对照提高54.34%,SOD提高16.73%。结论:为富锗灵芝菌丝体的应用奠定基础。     

灵芝孢子粉与环磷酰胺联合使用抑瘤作用的实验研究

目的　探讨灵芝孢子粉与环磷酰胺合用对小鼠移植性动物肿瘤的抑制作用。方法　按药物体内抑瘤作用常规筛选方法进行,试验动物用NIH小鼠。瘤株为小鼠肝癌 (Hepatoma)。小鼠随机分成 4组,每组 10只。阴性对照组以 0. 5%羧甲基纤维素钠 20ml·kg-1 /d灌胃。第一实验组以环磷酰胺(CTX)20mg·kg-1 /d灌胃。第二实验组:灵芝孢子粉 4g·kg-1 /d灌胃。第三实验组:灵芝孢子粉 4g·kg-1 /d+环磷酰胺20mg·kg-1 /d灌胃,各组均于接种后 24小时开始灌胃给药,连续 10天。均于末次给药后 24小时处死,计算抑瘤率。结果　各组抑瘤率分别是:第一实验组 (CTX)为 63. 5% ~66. 1%,第二实验组为 63. 0% ~64.7%,第三实验组为 77. 8% ~79. 1%。各实验组的抑瘤作用与阴性对照组比较,差异均有非常显著性意义(P<0. 001)。孢子粉与CTX联合用药组与单用灵芝孢子粉组或单用CTX组比较,前者的抑瘤率均明显高于后两者单独用药的抑瘤率(P<0. 05)。结论　灵芝孢子粉与CTX两者联合使用具有协同抑瘤作用,灵芝孢子粉可减轻CTX的副作用。     

灵芝深层发酵产生超氧化物歧化酶的初步研究

灵芝富含各种对人体有益的营养成分，其主要活性成分除高分子多糖和灵芝酸外，多肽、蛋白质甚至其中的酶对其功效也有着重要影响。本研究旨在探讨灵芝深层发酵液中SOD的存在情况和含量特性，为其在保健营养品中的应用提供科学依据。     

超高压撞击流技术制备破壁灵芝孢子的数值模拟

通过有限元方法分析灵芝孢子的撞击过程.按照灵芝孢子的结构,建立了计算模型,得到结构在高速撞击时的应力分布.结果显示:高速射流引起撞击粉碎时,孢壁的破坏不仅和冲击速度有关,还和接触角有关.冲击速度越大,孢壁中产生应力值越大,越易破碎.当接触角分别为10°和80°时,孢壁破坏程度最大.研究结果可为工艺参数的优化提供重要依据.     

The role of polysaccharide peptide of Ganoderma lucidum as a potent antioxidant against atherosclerosis in high risk and stable angina patients

ObjectivesAntioxidants can reduce oxidative radicals that affect the early phase of atherogenesis, that is endothelial dysfunction. Polysaccharide Peptide (PsP) derived from Ganoderma lucidum has an active substance in the form of β-glucan. Previous studies have proven the PsP of Ganoderma lucidum as an effective antioxidant in atherosclerotic rats and shows no toxicity in animal model. This study aims to prove the effect of PsP as potent antioxidant in high risk and stable angina patients.MethodThis is a clinical trial conducted to 37 high risk and 34 stable angina patients, which were determined based on ESC Stable CAD Guidelines and Framingham risk score, with pre and post test design without control group. The parameters are superoxide dimustase (SOD) and malondialdehyde (MDA) concentration, circulating endothelial cell (CEC) and endothelial progenitor cell (EPC) counts. The patients were given PsP 750 mg/day in 3 divided dose for 90 days. Paired t-test was performed for normally distributed data, and Wilcoxon test for not normally distributed data, and significant level of p ≤ 0,05.ResultsSOD level in high risk patients slightly increased but not statistically significant with p = 0,22. Level of SOD in stable angina group significantly increased with p = 0,001. MDA concentration significantly reduced in high risk and stable angina patients with p = 0.000. CEC significantly reduced both in high risk and stable angina patients, with p = 0.000 in both groups. EPC count significantly reduced in high risk and stable angina with p = 0.000.ConclusionPsP of Ganoderma lucidum is a potent antioxidant against pathogenesis of atherosclerosis in stable angina and high risk patients     

A new lanostane-type triterpene from the fruiting bodies of Ganoderma lucidum

A new lanostane-type triterpene, named ganoderic acid LM 2 ( 5 ), was isolated from the fruiting bodies of Ganoderma lucidum . Its structure was characterized as (23S) 7 g , -dihydroxy-3, 11, 15-trioxo-5 f -lanosta-8, 24-dien-26-oic acid by 1D- and 2D-NMR spectra. In addition, a known triterpene, ganoderic acid l ( 4 ), was obtained. Both of them exhibited potent enhancement of ConA-induced mice splenocytes proliferation in vitro .     

高剂量灵芝孢子粉干预戊四氮致痫模型大鼠海马及皮质区神经细胞Bcl-2、Bax的表达

采用中药灵芝孢子粉低、中、高剂量（150, 300, 450 mg/kg）干预戊四氮致癫痫模型28 d，并设空白对照组。经免疫组织化学染色和TUNEL检测后发现，与模型相比，灵芝孢子粉高剂量组大鼠海马和皮质区神经细胞TUNEL阳性细胞数及Bax阳性细胞数均减少，而Bcl-2阳性表达细胞数增加。Morris水迷宫实验检测结果显示，灵芝孢子粉高剂量组大鼠逃避潜伏期缩短，跨过原平台次数增加。说明高剂量灵芝孢子粉上调癫痫模型大鼠海马和皮质区神经细胞Bcl-2蛋白的表达，抑制Bax免疫反应及癫痫所致的神经细胞凋亡，明显改善其学习记忆功能。