CPVA微球表面接枝对羟基苯磺酸钠及其对茶碱的吸附研究

通过分子设计将2-氯乙基异氰酸酯(CIC)键合至聚乙烯醇微球(CPVA)表面制得CPVA-CIC,再将对羟基苯磺酸钠(HSS)固载于CPVA-CIC上制得功能微球CPVA-HSS。通过红外光谱(FI-TR)、扫描电子显微镜(SEM)及Zeta电位仪对功能微球进行表征,并考察主要因素对接枝微球固载量的影响,探索功能微球CPVA-HSS对茶碱分子的吸附性能及吸附机理。结果表明,通过CIC改性,阴离子单体HSS成功固载于基质CPVA表面,形成功能微球CPVA-HSS。CPVA-HSS对茶碱吸附5 h达到平衡,凭借其强的静电相互作用,pH5时在水溶液中吸附容量可达60 mg/g,随着温度的降低吸附量升高,而随介质盐度的增大吸附容量降低。功能微球的重复使用性较好。

碱催化p-QMs的1,6-共轭加成合成二芳基甲基(硫)醚

在摩尔分数为20%的氢氧化钠的催化作用下,实现了对亚甲基苯醌(p-QMs)与醇(或硫酚)的溶剂解反应,即p-QMs的1,6-共轭加成反应,以37%~95%的产率制备了一系列二芳基甲基(硫)醚类化合物。结果表明,该反应具有操作简便、反应条件温和高效、官能团耐受性良好等特点;该方法易于放大,能以80%的产率得到二芳基甲基乙基醚,为后期的潜在应用与转化提供了可能。

Alcohol dehydrogenase coexisted solid-state electrochemiluminescence biosensor for detection of p53 gene

An alcohol dehydrogenase （ADH）-coexisted solidstate electrochemiluminescence （ECL） biosensor for sensitive detection of the p53 gene was developed. The electrode modified by multiwalled carbon nanotubes, Ru（bpy）]2＋3 and polypyrrole （ MWNTs-Ru （bpy） ]2＋3 -PPy ） was prepared to adsorb the ssDNA by electrostatic interactions. Then, the ssDNA recognized the gold nanoparticles （AuNPs）-labeled p53 gene and produced the AuNPs-dsDNA electrode with the AuNPs layer. The AuNPs layer adsorbed the ADH molecules for producing the ECL signal. Thus, the biosensor was based on coupling enzyme substrate reaction with solid-state ECL detection, and it displayed good sensitivity and specificity. The detection limit of the wild type p53 sequence （wtp53） is as low as 0. 1 pmol/L and the discrimination is up to 57. 1% between the wtp53 and the muted type p53 sequence （mtp53）. The amenability of this method to the analyses of p53 from normal and cancer cell lysates is demonstrated. The signal of wtp53 in the MGC-803 gastric cancer cell lysates turns out to be about 61.8% that of the wtp53 in the GES-1 normal gastric mucosal cell lysates, and the concentration of the wtp53 is found to decrease about 59 times. The method is highly complementary to enzyme-linked immunosorbent assay （ELISA）, and it holds promise for the diagnosis and management of cancer.

基于AHP法结合正交试验法优选参麻益智方水提工艺

目的优选参麻益智方最佳水提工艺。方法以溶剂倍数(A)、煎煮时间(B)、煎煮次数(C)为考察因素,以天麻素转移率、对羟基苯甲醇转移率、阿魏酸转移率和出膏率作为评价指标,多指标层次分析法(AHP)结合单因素试验和正交试验优化水提工艺。结果通过层次分析法确认各指标权重系数,通过综合评分优选出最佳水提工艺为加水提取3次,第1次10倍量水2 h,第2次8倍量水1 h,第3次8倍量水1 h。此工艺条件下的天麻素转移率为108.10%,对羟基苯甲醇转移率为39.12%,阿魏酸转移率为74.45%,出膏率为20.21%,综合评分97.68分。结论该工艺简单、稳定、提取率高,适用于工业化大生产,同时为参麻益智方的开发利用提供了试验依据。

Genetic polymorphisms in cytochrome P4502E1, alcohol and aldehyde dehydrogenases and the risk of esophageal squamous cell carcinoma in Gansu Chinese males

AIM:To evaluate the association between genetic polymorphisms in CYP2E1, ALDH2 and ADH1B and the risk of esophageal squamous cell carcinoma (ESCC) in a high risk area of Gansu Province, in Chinese males. METHODS: A case-control study was conducted to investigate the genetic polymorphisms of these enzymes (CYP2E1 *c1/*c2, ALDH2 *1/*2 and ADH1B *1/*1 genotypes). A total of 80 esophageal cancer cases and 480 controls were recruited. RESULTS: Compared with controls, cases had a greater prevalence of heavier alcohol consumption (53.8% vs 16.2%) and a higher proportion of alcohol drinkers with > 30 drink-years (28.8% vs 13.5%). Heavier alcohol consumption and alcohol drinking with > 30 drink- years increased the risk of ESCC, with ORs (95% CI) of 3.20 (1.32-9.65) and 1.68 (0.96-3.21). CYP2E1 (*c1/*c1), ALDH2 (*1/*2) and ADH1B (*1/*1) genotype frequencies were higher among patients with squamous cell carcinomas, at a level close to statistical significance (P = 0.014; P = 0.094; P = 0.0001 respectively). There were synergistic interactions among alcohol drinking and ALDH2, ADH1B and CYP2E1 genotypes. The risk of the ESCC in moderate-to-heavy drinkers with an inactive ALDH2 encoded by ALDH2 *1/*2 as well as ADH1B encoded by ADH1B *1/*1 and CYP2E1 encoded by CYP2E1 *c1/*c1 was higher than that in the never/rare-to-light drinkers with an active ALDH2 (*1/*1 genotype) as well as ADH1B (*1/*2 + *2/*2) and CYP2E1 (*c1/*c2 + *c2/*c2) genotypes, with a statistically significant difference; ORs (95% CI) of 8.58 (3.28-22.68), 27.12 (8.52-70.19) and 7.64 (2.82-11.31) respectively. The risk of the ESCC in moderate-to-heavy drinkers with ALDH2 (*1/*2) combined the ADH1B (*1/*1) genotype or ALDH2 (*1/*2) combined the CYP2E1 (*c1/*c1) genotype leads to synergistic interactions, higher than drinkers with ALDH2 (*1/*1) + ADH1B (*1/*2 + *2/*2), ALDH2 (*1/*1) + CYP2E1 (*c1/*c2 + *c2/*c2) respectively , ORs (95% CI) of 7.46 (3.28-18.32) and 6.82 (1.44-9.76) respectively. Individuals with the ADH1B combined the CYP2E1 genotype showed no synergistic interaction. CONCLUSION: In our study, we found that alcohol consumption and polymorphisms in the CYP2E1, ADH1B and ALDH2 genes are important risk factors for ESCC, and that there was a synergistic interaction among polymorphisms in the CYP2E1, ALDH2 and ADH1B genes and heavy alcohol drinking, in Chinese males living in Gansu Province, China.

Exposure to ambient air particulate matter and non-alcoholic fatty liver disease

The present study was designed to alert the public opinion and policy makers on the supposed enhancing effects of exposure to ambient air particulate matter with aerodynamic diameters < 2.5 mm (PM 2.5 ) on non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease in Western countries. For far too long literature data have been fixated on pulmonary diseases and/or cardiovascular disease, as consequence of particulate exposure, ignoring the link between the explosion of obesity with related syndromes such as NAFLD and air pollution, the worst characteristics of nowadays civilization. In order to delineate a clear picture of this major health problem, further studies should investigate whether and at what extent cigarette smoking and exposure to ambient air PM 2.5 impact the natural history of patients with obesity-related NAFLD,i.e. , development of non alcoholic steatohepatitis, disease characterized by a worse prognosis due its progression towards fibrosis and hepatocarcinoma.

Protective effects of puerarin on alcohol-induced oxidative injury in PC12 cells

OBJECTIVE The aim of this study was to investigate the protective effect of puerarin on alcoholtoxicity in rat pheochromocytoma cell line(PC12). METHODS The PC12 cells were incubated with different concentrations of puerarin in advance. The protective effects of the puerarin on alcohol induced PC12 cel impairment were evaluated according to the fol owing approach: the viability of PC12 cel was determined by MTT assay and the impairment level was evaluated by analysis the leakage content of the lactate dehydrogenase(LDH). The cel apoptosis degree and the pro-apoptotic p53 protein expression were measured by flow cytometry. RESULTS Alcohol significantly impaired PC12 cel viability(P<0.05),and increased LDH leakage(P<0.05),induced cell apoptosis and upregulated expression of p53(P<0.05).While Puerarin significantly reversed these changes(P<0.05). CONCLUSION Puerarin might exert protection effect against ethanol-induced neurotoxicity via inhibition the expression of p53 protein.

Gentiopicroside alleviates alcoholic fatty liver through suppression of P2X7r-Caspapse-1 pathway

Aim To investigate the protective effects of gentiopicroside （GPS） on acute alcohol-induced fatty liver.Methods Mice were treated with ethanol （5 g · kg^-11 of body weight） by gavage every 12 h for a total of three do- ses to induce acute fatty liver. GPS （40 or 80 mg · kg^-1 ） was garaged with ethanol simultaneously for three doses. Administration of GPS significantly prevented the increases of serum ALT and AST caused by ethanol, as well as se- rum and hepatic TG. Results GPS could significantly prevent ethanol-induced hepatic steatosis and necrosis by H＆E and Oil Red O staining. GPS also significantly inhibited lipogenic genes including sterol regulatory element binding transcription factor 1 （ SREBP-1 ）, fatty acid synthase （FASN） and acetyl-CoA carboxylase （ACC） in eth- anol-treated mice. Additionally, GPS possessed the ability to prevent ethanol-induced acute liver steatosis, possibly through inducing the phosphorylation of AMP-activated protein kinase （AMPK） and liver kinase B1 （LKB1）. Af- ter treatment with GPS, peroxisome proliferator-activated receptor eL （PPARoL） protein expression in mouse liver was recovered as that level of normal mice. Ethanol treatment evoked P2X7r and caspase-1 protein expression, while GPS significantly suppressed those protein expressions. GPS may be developed as a potential therapeutic can- didate for ethanol-induced hepatic steatosis and inflammation.

柯里拉京调控AMPK-自噬信号改善高脂高果糖饮食诱导的小鼠非酒精性脂肪肝病

目的探究柯里拉京通过调控AMPK-自噬信号对高脂高果糖饮食诱导的小鼠非酒精性脂肪肝病的影响。方法健康雄性8周龄C57BL/6J小鼠随机分为对照组、模型组和柯里拉京给药组,其中模型组和柯里拉京给药组小鼠于8周龄开始给予高脂高果糖饮食饲养4周,柯里拉京给药组小鼠同时腹腔注射柯里拉京20 mg·kg-1,隔天给药1次,连续给药4周,对照组和模型组给予等剂量生理盐水。造模和给药结束后小鼠处死并记录其肝质量,HE染色、油红O染色、Masson染色观察肝组织病理学特征,试剂盒检测血清和肝脏组织中生化指标,Western blot检测肝脏自噬和p-AMPK水平。结果实验结果发现,模型组小鼠肝质量增加,血清中AST、ALT明显升高,肝脏中出现了大量的脂肪空泡和严重的脂质沉积并有轻度的胶原纤维增生,肝脏中TG水平明显升高,柯里拉京干预后小鼠肝质量降低,肝脏病理改变得到明显改善,TG水平降低;Western blot结果发现,模型组肝脏中Atg7和Atg5等自噬相关蛋白水平明显降低,p-AMPK水平也明显降低,柯里拉京干预后明显升高p-AMPK,并上调自噬水平。结论柯里拉京可以改善高脂高果糖饮食诱导的小鼠非酒精性脂肪肝病,其机制可能是通过促进AMPK磷酸化进而上调自噬水平。

灰树花发酵过程天麻成分变化的HPLC检测方法研究

建立HPLC方法对天麻醇提取物成分及灰树花发酵液进行分析。色谱柱为Agilent TC-C18(4.6mm×250mm,5μm),流动相为A:0.1%磷酸水和B:乙腈,以梯度洗脱:0min^35min,B:3%~30%(V/V);35min^45min,B:30%~70%(V/V)。流速1mL/min,柱温30℃,检测波长221nm。在此条件下,天麻提取液及灰树花发酵液中3种已确定的天麻成分具有良好的分离度,且线性关系良好;精密度高(RSD<5%);回收率在96%~102%之间,同时检测到经过6d发酵后发酵液中天麻素、对羟基苯甲醇和对羟基苯甲醛质量浓度与发酵第0d相比分别下降了46.38%、11.85%和36.75%。该方法可以用于灰树花发酵过程中天麻成分变化情况的跟踪检测,为进一步探明天麻成分与灰树花代谢相互作用打下基础,同时也初步探明了灰树花对于天麻成分的利用情况。

酒精性肝损伤大鼠细胞色素P450 CYP2E1和细胞色素P450 CYP3A的代谢活性

目的观察酒精性肝损伤对大鼠细胞色素P450CYP3A(CYP3A)和细胞色素P450CYP2E1(CYP2E1)代谢活性的影响。方法采用ig给予白酒制备大鼠酒精性肝损伤模型,检测血清中谷丙转氨酶(GPT)和谷草转氨酶(GOT)活性,采用HE染色法光镜下观测酒精对肝脏损伤程度。大鼠ip给予CYP3A探针药物咪达唑仑10mg·kg-1或ig给予CYP2E1探针药物氯唑沙宗50mg·kg-1后,采用高效液相色谱法测定不同时间点大鼠血浆中咪达唑仑和氯唑沙宗的血药浓度,并应用3P87软件计算其药代动力学参数,以考察CYP2E1和CYP3A的代谢活性的变化。大鼠ig给予氯唑沙宗80mg·kg-1后,热板方法测定大鼠添足次数和添足反射潜伏期。结果酒精性肝损伤可致大鼠肝小叶结构不清,肝索排列紊乱,肝细胞体积增大,呈弥漫性中度水变性,肝窦受压,大部分肝细胞胞浆内见大小不等的脂肪空泡;与正常对照组相比,酒精性肝损伤组大鼠GPT和GOT活性分别增加了16.0%和20.0%(P<0.05,P<0.01)。酒精性肝损伤致大鼠CYP2E1对探针药物氯唑沙宗的代谢活性增强,AUC,t1/2和cmax分别降低了38.0%,30.5%和35.0%(P<0.05);酒精肝损伤组大鼠氯唑沙宗镇痛效果明显降低;酒精性肝损伤致大鼠CYP3A对探针药物咪达唑仑的代谢活性增强,AUC,t1/2和cmax分别降低了122.6%,54.9%和56.9%(P<0.01,P<0.05)。结论酒精性肝损伤可使大鼠CYP2E1和CYP3A代谢活性增强。

应用HPLC-DAD/MS技术评价中药天麻的质量

分析比较不同产地及不同炮制方法的天麻药材质量。天麻药材指纹图谱HPLC-DAD分析条件如下:Zorbax XDB C18色谱柱;流动相为乙腈-0.1%醋酸水梯度洗脱,检测波长为270 nm。MS分析条件:采用ESI电离源,负离子检测模式。天麻药材含量测定HPLC条件:流动相为乙腈-0.1%醋酸水等度洗脱,其余均同天麻药材指纹图谱的液相分析条件。结果表明,不同产地天麻药材具有相似的指纹图谱,原药材直接冻干的炮制方法较其他方法具有较高的相似度;指认了天麻药材指纹图谱中8个主要的色谱峰;指纹图谱相似度的分析结果与主要成分定量分析的结果基本一致。本文所建立的HPLC-DAD/MS分析方法能够对天麻药材进行全面的质量评价。

电针丰隆穴对非酒精性脂肪肝病大鼠肝脏p-PERK、p-IRE1α及炎性因子的影响

目的:探讨电针丰隆穴对非酒精性脂肪肝病大鼠肝脏p-PERK、p-IRE1α及炎性因子表达的影响。方法:SD大鼠按随机数字表法分为普食组、高脂对照组、手针"丰隆"组、电针"丰隆"组、电针"足三里"5组各12只,高脂饲料造模,取相应穴位给予毫针针刺、电针干预4周,HE染色观察肝脏病理形态变化,检测大鼠血清FFA、TG含量与肝组织TNF-α、IL-6 mRNA及p-PERK、pIRE1α蛋白表达。结果:HE染色示高脂对照组大鼠肝细胞排列紊乱,胞浆疏松,细胞内见大量大泡型脂肪空泡,干预后各组大鼠肝细胞脂肪变性减轻,两电针组效果更明显;各干预组血清FFA、TG含量及肝脏TNF-α、IL-6 mRNA与p-PERK、p-IRE1α蛋白表达明显低于高脂对照组,且电针"丰隆"组表达低于手针"丰隆"组;电针"丰隆"组与电针"足三里"组比较,FFA含量及TNF-α、IL-6mRNA与p-PERK蛋白表达降低。结论:电针能下调p-PERK、p-IRE1α蛋白和TNF-α、IL-6 mRNA的表达水平,调节脂质代谢,改善内质网应激与炎症反应状态,且电针"丰隆"穴效果更优。

HPLC法测定鲜天麻中多指标成分的含量

建立了高效液相色谱测定鲜天麻中天麻素、对羟基苯甲醇、对羟基苯甲醛、腺苷、巴利森苷A、4,4'-二羟基二苄基醚6种成分含量的方法。采用Agilent 1120高效液相系统,YMC-PEAK ODS-A column(250 mm×4.6 mm,5μm)色谱柱,流动相为0.1%甲酸水溶液(A)-甲醇溶液(B),梯度洗脱:0~5 min,5%B;5~65 min,5%~40%B;65~80 min,40%~100%B;分析时间80 mins;流速1 m L/min;柱温25℃;进样量50μL。其中天麻素、对羟基苯甲醇、对羟基苯甲醛、腺苷、巴利森苷A、4,4'-二羟基二苄基醚6种成分在线性范围内均具有良好的线性关系(R≥0.999 2);平均回收率在94.20%~99.68%,相对标准偏差小于1.96%。在不同品种的鲜天麻中,6种成分的量存在差异,红天麻各成分含量稍高于乌天麻。同一品种天麻中,巴利森苷类成分含量较高,腺苷和4,4'-二羟基二苄基醚含量均较低,且鲜天麻中提取的天麻素等6种成分在8 h内稳定。该方法分离效果与重复性好、快速、简便,能够为客观、全面地研究天麻药材提供参考。

HPLC测定天麻成分对甲氧基苄醇在大鼠血液中的药代动力学参数

目的采用高效液相色谱法（HPLC）测定天麻成分对甲氧基苄醇在大鼠血液中的药代动力学参数。方法采用灌胃和静脉注射2种方式给药,HPLC测定不同时间大鼠血液中天麻成分对甲氧基苄醇的浓度,DAS3.0软件计算药代动力学参数。结果大鼠血液中对甲氧基苄醇在0.63-321.17μg/mL浓度范围内线性关系良好,r^2=0.994 5;日内、日间精密度、绝对回收率和稳定性均在规定范围内。结论本方法操作简便,能较准确地测出天麻成分对甲氧基苄醇在大鼠血液中的药代动力学参数。

细胞色素P450Ⅱ E1-基因多态性在酒精性肝病发病中的意义

目的 :探讨细胞色素 P45 0 E1的基因型与酒精性肝病的相关性。方法 :采用 PCR- RFLP分析方法对 1 0 0例酒精性肝病患者 ,1 5 0例非酒精性肝病患者 ,2 5例酗酒无肝病者和 5 0例正常对照者进行 CYP45 0 E1多态性分析。结果 :CYP45 0 El分成 A型为 C1基因野生纯和子 ,B型为( C1 /C2 )基因的杂合子 ,C型为 C2基因的突变型纯合子。酒精性肝病中 A、B、C型分别 3%、93%、4%;酗酒无肝病组 A型为 1 0 0 %;非酒精性肝病中 A、B型分别 74%、2 6%;健康志愿者 A、B型分别 72 %、2 8%。酒精性肝病与酗酒无肝病组、非酒精性肝病及健康志愿者比较 ,有统计学意义。乙肝引起肝癌与酒精相关性肝癌的 A型明显减少 ,而 B型则明显增多 ,有统计学意义。结论

中药降脂颗粒对非酒精性脂肪肝大鼠肝脏瘦素受体mRNA及P-JAK2/P-STAT3的影响

目的:观察降脂颗粒对非酒精性脂肪肝大鼠的治疗作用及其对血清瘦素、肝组织瘦素受体mRNA、P-JAK2/P-STAT3蛋白含量表达的影响.方法:将60只SD♂大鼠,随机分为空白组(正常饮食)和造模组(高脂饮食).待造模成功后将造模组大鼠随机分为模型对照组、降脂颗粒低、中、高剂量组和东宝甘泰组.治疗4 wk后行肝组织生化和病理学检测,并同时应用ELISA试剂盒检测血清瘦素,RT-PCR法检测肝组织瘦素受体mRNA表达,应用Western blot检测肝组织P-JAK2和P-STAT3蛋白的表达.结果:低、中、高剂量组降脂颗粒能明显降低非酒精性脂肪肝大鼠模型肝脂(TG和TC)水平,改善脂肪变性,降低肝脏炎症反应,并能明显降低血清瘦素高水平状态(193.02±23.8ng/ L,163.97±31.38ng/L,147.83±17.59ng/L vs 317.22±39.26ng/L,P<0.01),改善瘦素抵抗,同时增加瘦素受体mRNA的表达(1.87±0.06,2.20±0.04,2.78±0.04 vs 1.50±0.05,P<0.01),增加肝组织P-JAK2和P-STAT3蛋白的含量(119.88±2.98,123.45±0.68,124.34±3.42 vs 113.15±1.27,P<0.01;94.15±0.78,100.18±3.33,101.94±2.20 vs 89.06±0.69,P<0.01).结论:降脂颗粒对非酒精性脂肪肝大鼠肝脏脂质和炎症有较好的治疗作用,其可能机制是改善瘦素抵抗,增加肝脏瘦素受体mRNA表达及P-JAK2,P-STAT3蛋白含量.

H9P2W15V3／C催化绿色合成对羟基苯甲酸丁酯

以活性碳为载体,通过浸渍法制备了H9P2W15V3/C催化剂,对催化剂进行Uv-Vis、FT-IR表征。以对羟基苯甲酸丁酯的合成反应为探针,考察了催化剂的催化性能。研究了磷钨钒杂多酸负载量、催化剂用量、醇酸比、反应时间和反应温度对反应的影响。通过单因素实验和正交实验确定了反应的最佳条件:杂多酸负载量为30%,催化剂用量8.7%(按反应体系总质量计算),醇酸摩尔比2∶1,反应时间3h,反应温度125℃,酯化率可达91.30%。催化重复使用5次,酯化率仍可达76.42%。

葛根素注射液对急性酒精中毒大鼠β-内啡肽、丙二醛、P-选择素影响的实验研究

目的研究急性酒精中毒时大鼠β-内啡肽(β-EP)、丙二醛(MDA)、P-选择素(P-selectin)的变化及葛根素注射液的作用。方法将大鼠分为对照组、酒精中毒组、葛根素组、纳络酮组、葛根素+纳络酮组;观察大鼠睡眠潜伏时间,测定各组血浆β-EP、血清MDA、P-selectin水平。结果与对照组比较,酒精中毒组大鼠β-EP、MDA、P-selectin水平显著升高(P<0.01);葛根素组较酒精中毒组大鼠睡眠的潜伏时间延长(P<0.05),β-EP、MDA、P-selectin水平显著降低;葛根素与纳洛酮降低β-EP、MDA作用无显著差异,纳洛酮对P-selectin无影响。结论急性酒精中毒可使β-EP释放增加,MDA、P-selectin升高。葛根素注射液通过抑制β-EP、自由基的释放、血小板积聚,对急性酒精中毒大鼠起保护作用。

益生菌发酵对姜制天麻活性成分及其抗氧化活性的影响

该文采用产乳酸芽孢杆菌Bacillus sp.DU-106和植物乳杆菌Lactobacillus plantarum复合菌种发酵姜制天麻,对比发酵前后主要活性成分含量变化,并利用体外抗氧化实验和秀丽隐杆线虫模型进一步探讨益生菌发酵姜制天麻抗氧化活性的变化。实验结果显示,经发酵能够显著的提高发酵姜天麻(Fermented Gastrodia elata with ginger,FGEG)的对羟基苯甲醇和总酚含量(P<0.05),分别为5.78 mg/g和10.15 mg/g,两种物质相较于未发酵对照组分别增加了2.54倍和1.74倍。在秀丽隐杆线虫实验中,FGEG能够显著延长正常生长条件下和急性应激条件下线虫的寿命(P<0.01),同时降低线虫体内活性氧自由基含量和提高线虫体内过氧化氢酶活性、谷胱甘肽的含量,并呈现一定剂量依赖效应。同时,FGEG能够显著降低线虫体内MDA的含量和脂褐素相对含量(P<0.001),与空白组相比分别降低了87.21%和82.53%。与未发酵对照组相比,FGEG的体内体外抗氧化活性显著提高(P<0.05)。综上,经发酵后天麻对羟基苯甲醇和总酚含量显著提高,FGEG相较于未发酵样品抗氧化活性显著提升,为FGEG的开发和利用提供理论支撑。