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督脉隔药灸联合水凝胶多功能复合敷料对压力性损伤大鼠Nrf2/HO-1/NQO1信号通路的影响
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作者 刘红娜 奉水华 +1 位作者 易可兰 陈一青 《湖南中医药大学学报》 CAS 2024年第8期1401-1409,共9页
目的观察督脉隔药灸联合水凝胶多功能复合敷料对压力性损伤大鼠创面修复及核因子E2相关因子2(nuclear factor-erythroid 2 related factor 2,Nrf2)/血红素氧合酶1(heme oxygenase-1,HO-1)/NADPH醌氧化还原酶1(NADPH quinone oxidoreduct... 目的观察督脉隔药灸联合水凝胶多功能复合敷料对压力性损伤大鼠创面修复及核因子E2相关因子2(nuclear factor-erythroid 2 related factor 2,Nrf2)/血红素氧合酶1(heme oxygenase-1,HO-1)/NADPH醌氧化还原酶1(NADPH quinone oxidoreductase 1,NQO1)信号通路的影响。方法选取50只SPF级SD大鼠,随机分为假手术组、模型组、水凝胶敷料组、督脉隔药灸组、联合干预组,每组10只。除假手术组外,其余4组借助压力装置构建压力性损伤大鼠模型。分组干预并记录各组大鼠的压力性损伤修复情况及创面组织病理变化;借助ELISA检测各组大鼠的血清炎性因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素(interleukin,IL)-1β、IL-6以及氧化应激因子丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)水平;Western blot与RT-PCR检测各组大鼠创面肉芽组织Nrf2、HO-1、NQO1、基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)蛋白及mRNA的表达水平。结果HE染色结果显示:假手术组皮肤结构未被破坏;模型组创面肉芽组织可见明显的细胞坏死、变性及炎性细胞浸润;干预各组可见创面修复,表现为散在炎性细胞浸润,“气球样”坏死变性明显减少。Masson染色结果显示:假手术组创面皮肤组织胶原纤维较为整齐;模型组创面肉芽组织可见大面积的胶原纤维沉积、紊乱;干预各组可见不同程度的创面修复。与假手术组对比,模型组大鼠血清TNF-α、IL-1β、IL-6、MDA水平和创面肉芽组织Nrf2、HO-1、NQO1、MMP-9蛋白及mRNA的表达水平均升高(P<0.05),而创面修复率、血清SOD、GSH-Px水平均下降(P<0.05);与模型组比较,水凝胶敷料组、督脉隔药灸组、联合干预组的血清TNF-α、IL-1β、IL-6、MDA水平均下降(P<0.05),而创面修复率、血清SOD、GSH-Px水平和创面肉芽组织Nrf2、HO-1、NQO1、MMP-9蛋白及m RNA的表达水平均升高(P<0.05),且联合干预组较其他干预组更优(P<0.05)。结论督脉隔药灸可有效促进压力性损伤的创面修复,与水凝胶多功能复合敷料联合使用效果更佳,其机制可能与督脉隔药灸抑制创面炎性反应及氧化应激,并激活Nrf2/HO-1/NQO1信号通路相关。 展开更多
关键词 督脉 隔药灸 水凝胶多功能复合敷料 压力性损伤 nrf2/HO-1/nqo1信号通路 创面修复
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神经生长因子联合BMSCs-源外泌体通过Keap1/NQO1/Nrf2信号通路缓解脑出血大鼠神经损伤
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作者 李方 唐仕军 麦麦提依明·托合提 《医学分子生物学杂志》 CAS 2024年第4期341-346,共6页
目的探讨大鼠神经生长因子(rat nerve growth factor,RtNGF)联合骨髓间充质干细胞-源外泌体(BMSCs exosomes)缓解脑出血(intracerebral haemorrhage,ICH)大鼠神经损伤的疗效及其作用机制。方法制备BMSCs exosomes。60只大鼠随机分为假手... 目的探讨大鼠神经生长因子(rat nerve growth factor,RtNGF)联合骨髓间充质干细胞-源外泌体(BMSCs exosomes)缓解脑出血(intracerebral haemorrhage,ICH)大鼠神经损伤的疗效及其作用机制。方法制备BMSCs exosomes。60只大鼠随机分为假手术(Sham)组,ICH组,ICH+RtNGF组,ICH+BMSCs exosomes组,ICH+RtNGF+BMSCs exosomes组,每组12只。建立ICH大鼠模型,并给予RtNGF或BMSCs exosomes单独治疗或联合治疗。制备各分组大鼠脑组织石蜡组织切片,并对其进行HE染色。qPCR法测定各分组大鼠脑组织中Keap1/NQO1/Nrf2信号通路蛋白质因子mRNA的相对表达水平。免疫组化(IHC)法测定各分组大鼠脑组织中Keap1/NQO1/Nrf2信号通路蛋白质因子的表达水平。结果与Sham组相比,ICH组大鼠脑组织中存在多处明显的组织腔隙和血凝块。ICH+RtNGF组、ICH+BMSCs exosomes组和ICH+RtNGF+BMSCs exosomes组均有所改善,且ICH+RtNGF+BMSCs exosomes组缓解神经损伤效果最好。与Sham组相比,ICH组大鼠脑组织中Keap1,NQO1和Nrf2 mRNA表达水平升高(P<0.05);上述3种蛋白质IHC相对染色评分升高(P<0.05)。与ICH组相比,ICH+RtNGF组、ICH+BMSCs exosomes组和ICH+RtNGF+BMSCs exosomes组上述检测指标水平降低(P<0.05),且与ICH+RtNGF组或ICH+BMSCs exosomes组相比,ICH+RtNGF+BMSCs exosomes组上述检测指标水平更低(P<0.05)。结论RtNGF联合BMSCs exosomes治疗ICH大鼠,可通过Keap1/NQO1/Nrf2信号通路降低氧化应激缓解神经损伤。 展开更多
关键词 脑出血 大鼠神经生长因子 BMSCs-源外泌体 Keap1/nqo1/nrf2信号通路 神经损伤
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虫草素通过激活Nrf2/HO-1/NQO1通路缓解脑缺血再灌注大鼠脑组织损伤
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作者 吴双 代绪波 +2 位作者 崔珍 姜风英 庞素秋 《医学分子生物学杂志》 CAS 2024年第6期530-536,共7页
目的探讨虫草素(cordycepin,COR)在脑缺血再灌注(cerebral ischemia reperfusion,CI/R)大鼠脑组织损伤中的保护作用及机制。方法60只Wistar大鼠分为健康对照组、模型组、模型加药组。跳台试验和Y迷宫实验检测大鼠学习和记忆力;HE染色法... 目的探讨虫草素(cordycepin,COR)在脑缺血再灌注(cerebral ischemia reperfusion,CI/R)大鼠脑组织损伤中的保护作用及机制。方法60只Wistar大鼠分为健康对照组、模型组、模型加药组。跳台试验和Y迷宫实验检测大鼠学习和记忆力;HE染色法检测脑组织病理变化;干湿重法计算脑含水率和脑指数;TUNEL法观测脑组织细胞凋亡情况;ELISA测定大鼠血清中超氧化物歧化酶(superoxide dismutase。SOD)、丙二醛(malonic dialdehyde,MDA)、乳酸脱氢酶(lactate dehydrogenase,LDH)的含量;蛋白质印迹检测Bax/Bcl-2、cleaved cas9/cas9、cleaved cas3/cas3、Nrf2、HO-1和NQO1蛋白表达水平。结果与模型组比较,COR能剂量依赖地改善大脑组织损伤,抑制氧化应激,促进Nrf2/HO-1/NQO1通路激活。结论虫草素能够改善脑组织损伤,其作用机制与上调Nrf2通路有关。 展开更多
关键词 虫草素 脑缺血再灌注 凋亡 超氧化物歧化酶 nrf2/HO-1/nqo1通路
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Enhancement of porcine in vitro embryonic development through luteolin‑mediated activation of the Nrf2/Keap1 signaling pathway
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作者 Se-Been Jeon Pil-Soo Jeong +5 位作者 Min Ju Kim Hyo-Gu Kang Bong-Seok Song Sun-Uk Kim Seong-Keun Cho Bo-Woong Sim 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2024年第2期600-613,共14页
Background Oxidative stress,caused by an imbalance in the production and elimination of intracellular reactive oxygen species(ROS),has been recognized for its detrimental effects on mammalian embryonic development.Lut... Background Oxidative stress,caused by an imbalance in the production and elimination of intracellular reactive oxygen species(ROS),has been recognized for its detrimental effects on mammalian embryonic development.Luteolin(Lut)has been documented for its protective effects against oxidative stress in various studies.However,its specific role in embryonic development remains unexplored.This study aims to investigate the influence of Lut on porcine embryonic development and to elucidate the underlying mechanism.Results After undergoing parthenogenetic activation(PA)or in vitro fertilization,embryos supplemented with 0.5μmol/L Lut displayed a significant enhancement in cleavage and blastocyst formation rates,with an increase in total cell numbers and a decrease in the apoptosis rate compared to the control.Measurements on D2 and D6 revealed that embryos with Lut supplementation had lower ROS levels and higher glutathione levels compared to the control.Moreover,Lut supplementation significantly augmented mitochondrial content and membrane potential.Intriguingly,activation of the Nrf2/Keap1 signaling pathway was observed in embryos supplemented with Lut,leading to the upregulation of antioxidant-related gene transcription levels.To further validate the relationship between the Nrf2/Keap1 signaling pathway and effects of Lut in porcine embryonic development,we cultured PA embryos in a medium supplemented with brusatol,with or without the inclusion of Lut.The positive effects of Lut on developmental competence were negated by brusatol treatment.Conclusions Our findings indicate that Lut-mediated activation of the Nrf2/Keap1 signaling pathway contributes to the enhanced production of porcine embryos with high developmental competence,and offers insight into the mechanisms regulating early embryonic development. 展开更多
关键词 LUTEOLIN Mitochondrial function nrf2/Keap1 signaling pathway Oxidative stress Porcine embryo development
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基于Nrf2/HO-1/NQO1信号通路探讨雷公藤内酯三醇对急性肝损伤大鼠的保护机制
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作者 吴雅君 《新中医》 CAS 2024年第19期199-203,共5页
目的:基于核因子E2相关因子2/血红素氧合酶/醌氧化还原酶1(Nrf2/HO-1/NQO1)信号通路探究雷公藤内酯三醇对四氯化碳(CCl4)诱导急性肝损伤大鼠的保护机制。方法:纳入40只SPF级雄性SD大鼠,适应性饲养7 d,而后随机分为4组(正常组、模型组及... 目的:基于核因子E2相关因子2/血红素氧合酶/醌氧化还原酶1(Nrf2/HO-1/NQO1)信号通路探究雷公藤内酯三醇对四氯化碳(CCl4)诱导急性肝损伤大鼠的保护机制。方法:纳入40只SPF级雄性SD大鼠,适应性饲养7 d,而后随机分为4组(正常组、模型组及低剂量组、高剂量组),每组10只。正常组及模型组每日尾静脉注射等体积无菌0.9%氯化钠溶液,低剂量组、高剂量组分别注射100 mg/kg、200 mg/kg雷公藤内酯三醇,均连续注射7 d,于第7天注射雷公藤内酯三醇(模型组为无菌生理盐水)3 h后,对模型组、低剂量组、高剂量组大鼠腹腔注射1 mL/kg CCl4以进行急性肝损伤模型诱导(正常组腹腔注射等体积的橄榄油溶液)。在注射CCl416 h后取大鼠血液及肝脏标本,采用HE组织化学染色法观察大鼠肝组织切片的病理学改变,并检测4组血清肝功能指标水平及肝组织Nrf2、HO-1、NQO1蛋白水平及mRNA表达量。结果:肝组织病理检查结果显示,正常组肝组织细胞排列整齐,组织结构及形态正常,细胞界限明显,胞质完整。模型组在注射CCl416 h后,肝组织出现肝细胞边界不清晰、细胞排列紊乱等肝细胞坏死特征,且可见炎症细胞浸润及肝细胞严重水肿呈气泡样变。相比于模型组,低剂量组、高剂量组的肝细胞水肿程度及肝细胞坏死特征较轻,且高剂量组轻于低剂量组。模型组、低剂量组及高剂量组的肝指数大于正常组,血清天冬氨酸转氨酶(AST)、甲氨酸转氨酶(ALT)水平高于正常组(P<0.05);模型组肝指数大于低剂量组及高剂量组,且低剂量组大于高剂量组(P<0.05);模型组AST、ALT水平高于低剂量组及高剂量组,且低剂量组高于高剂量组(P<0.05)。模型组、低剂量组及高剂量组的肝组织Nrf2、HO-1、NQO1蛋白水平及Nrf2、HO-1、NQO1 mRNA表达量高于正常组,且模型组高于低剂量组及高剂量组,低剂量组高于高剂量组(P<0.05)。结论:雷公藤内酯三醇可减轻CCl4诱导的大鼠急性肝损伤,其作用机制可能与其能激活Nrf2/HO-1/NQO1信号通路以抑制肝细胞氧化损伤有关。 展开更多
关键词 急性肝损伤 大鼠 雷公藤内酯三醇 nrf2/HO-1/nqo1信号通路 保护机制
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肺癌组织中Nrf2、Keap1和NQO1蛋白的表达 被引量:14
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作者 倪静 秦丽娟 +2 位作者 吴拥军 王静 吴逸明 《郑州大学学报(医学版)》 CAS 北大核心 2012年第4期456-459,共4页
目的:研究肺癌组织中Nrf2、Keap1和NQO1蛋白表达的情况。方法:采用免疫组化法检测67例肺癌患者的肺癌组织及癌旁正常组织中Nrf2、Keap1和NQO1蛋白的表达,并分析Keap1、Nrf2和NQO1蛋白的表达与肺癌临床病理特征的关系。结果:Keap1蛋白在... 目的:研究肺癌组织中Nrf2、Keap1和NQO1蛋白表达的情况。方法:采用免疫组化法检测67例肺癌患者的肺癌组织及癌旁正常组织中Nrf2、Keap1和NQO1蛋白的表达,并分析Keap1、Nrf2和NQO1蛋白的表达与肺癌临床病理特征的关系。结果:Keap1蛋白在肺Ⅰ、Ⅱ、Ⅲ期鳞癌和Ⅲ期、Ⅳ期腺癌中的表达高于癌旁正常组织(P<0.05);Nrf2蛋白在肺Ⅰ期鳞癌和Ⅱ、Ⅲ、Ⅳ期腺癌中的表达低于癌旁正常组织(P<0.05);NQO1蛋白在肺Ⅰ期鳞癌中的表达低于癌旁正常组织(P<0.05),在Ⅱ期腺癌中的表达高于癌旁正常组织(P<0.05)。3种蛋白的表达与肺癌患者的临床分期和是否侵及胸膜有关(P<0.05)。结论:肺癌组织中Keap1、Nrf2、NQO1蛋白表达异常,提示Keap1-Nrf2/ARE通路在肺癌的发生发展中可能发挥重要的作用。 展开更多
关键词 肺肿瘤 nrf2蛋白 Keap1蛋白 nqo1蛋白 Keap1-nrf2/ARE通路
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An exploration on the protective mechanism of Xuduan Zhongzi prescription against epididymis oxidative damage in oligoasthenospermia model rats based on Nrf2-NQO1/γ-GCS signaling pathway
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作者 Zi-Li Lin Yu Wang +3 位作者 Lu Chen Liu Chen Ya-Guang Zhang Quan-Sheng Wang 《Journal of Hainan Medical University》 2022年第11期13-17,共5页
Objective:To investigate the protective mechanism of Xuduan Zhongzi prescription against epididymal oxidative damage in oligoasthenospermia model rats.Methods:Forty SD rats were randomly divided into blank group,model... Objective:To investigate the protective mechanism of Xuduan Zhongzi prescription against epididymal oxidative damage in oligoasthenospermia model rats.Methods:Forty SD rats were randomly divided into blank group,model group,Xuduan Zhongzi prescription group(10g/kg)and L-carnitine group(0.1g/kg).Except blank group,all induced oligoasmospermia.The blank group and model group were given normal saline intragastric administration,the Xuduan Zhongzi prescription group was given Xuduan Zhongzi prescription solution intragastric administration,and the L-carnitine group was given L-carnitine intragastric administration.HE staining was used to observe the epididymis structure after 8 weeks.The concentration and activity rate of epididymis sperm were measured by sperm quality.MRNA and protein expression levels of Nrf2,NQO1 andγ-GCs in epididymis were detected by RT-qPCR and immunohistochemistry.Results:①HE staining:in the blank group,the epididymis tubes were arranged tightly and regularly,the tissue structure was complete,the epithelial cells were arranged orderly,and the lumen sperm were numerous and evenly distributed.The epididymis of model group showed structural atrophy,loose arrangement,enlarged mesenchyme,increased cell debris and significantly reduced sperm cells.Compared with the model group,the lumen lesions of epididymis in Xuduan Zhongzi prescription group and L-carnitine group were significantly improved,and the amount of normal sperm in lumen was increased and the distribution was uniform.②Results of sperm quality comparison among each group:sperm density and sperm motility rate:compared with blank group,sperm density and sperm motility rate in other groups were significantly decreased(P<0.05),and sperm density and sperm motility rate in model group were significantly decreased(P<0.05);Compared with model group,the sperm density and motility rate in Xuduan Zhongzi prescription group and L-carnitine group were significantly increased(P<0.05).③RT-qPCR and immunohistochemistry:Compared with the blank group,the mRNA and protein levels of Nrf2,NQO1 andγ-GCs in epididymal rats in model group were significantly decreased(P<0.05),while the mRNA and protein levels of Nrf2,NQO1 andγ-GCs were significantly increased in L-carnitine group and Continua seed formula group(P<0.05).Conclusion:Xuduan Zhongzi prescription can reduce oxidative stress damage and improve sperm quality of oligoasthenospermia.The mechanism may related to promoting the activation of Nrf2-NQO1/γ-GCS pathway in epididymis of oligoasthenospermia rats,and up-regulate the expressions of Nrf2,NQO1 andγ-GCS proteins. 展开更多
关键词 OLIGOASTHENOSPERMIA EPIDIDYMIS Oxidative damage nrf2-nqo1/γ-GCS signaling pathways Xuduan Zhongzi prescription
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Nrf2/NQO1信号通路在胃癌干细胞氧化应激反应中的作用机制 被引量:4
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作者 陈浩 许浪 《吉林大学学报(医学版)》 CAS CSCD 北大核心 2013年第3期463-466,共4页
目的:观察核因子E2相关因子2(Nrf2)、醌氧化还原酶(NQO1)在胃癌干细胞和正常胃黏膜组织中的表达,探讨Nrf2/NQO1信号通路在胃癌干细胞氧化应激反应中的作用机制。方法:采用肿瘤球悬浮分选法从60例胃癌组织标本中分选胃癌干细胞,干细胞随... 目的:观察核因子E2相关因子2(Nrf2)、醌氧化还原酶(NQO1)在胃癌干细胞和正常胃黏膜组织中的表达,探讨Nrf2/NQO1信号通路在胃癌干细胞氧化应激反应中的作用机制。方法:采用肿瘤球悬浮分选法从60例胃癌组织标本中分选胃癌干细胞,干细胞随机分为干细胞初分组和激活组。30例正常胃黏膜组织作为对照。采用Western blotting法检测各组Nrf2、NQO1蛋白表达水平和超氧化物歧化酶(SOD)、丙二醛(MDA)活性。结果:与正常对照组比较,干细胞初分组和激活组Nrf2、NQO1的表达水平升高(P<0.05),SOD活性显著降低,MDA活性则显著升高(P<0.05);与干细胞初分组比较,激活组Nrf2、NQO1的表达水平显著升高(P<0.05),SOD活性显著增强,MDA活性显著下降(P<0.05)。结论:激活Nrf2/NQO1通路可以调节胃黏膜组织中SOD和MDA的活性,增强细胞对氧化应激的耐受性,发挥保护细胞的作用。 展开更多
关键词 nrf2 nqo1信号通路 氧化应激 胃癌干细胞 超氧化物歧化酶 丙二醛
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人参皂苷对糖尿病肾病大鼠体内ColⅣ、Nrf2和NQO1表达的影响 被引量:4
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作者 吴胜斌 王应灯 《河北医药》 CAS 2021年第15期2245-2249,共5页
目的研究人参皂苷对糖尿病肾病大鼠体内Ⅳ型胶原蛋白(ColⅣ)、Nrf2和醌氧化还原酶1(NQO1)表达的影响。方法30只雄性SD大鼠随机分为正常对照组(NC组),糖尿病肾病模型组(DN组),糖尿病肾病模型加人参皂苷治疗组(MG组),每组10只。对3组大鼠... 目的研究人参皂苷对糖尿病肾病大鼠体内Ⅳ型胶原蛋白(ColⅣ)、Nrf2和醌氧化还原酶1(NQO1)表达的影响。方法30只雄性SD大鼠随机分为正常对照组(NC组),糖尿病肾病模型组(DN组),糖尿病肾病模型加人参皂苷治疗组(MG组),每组10只。对3组大鼠的体重、血糖和生化指标分别进行记录;HE染色观察大鼠肾组织形态;Western blot检测大鼠ColⅣ、Nrf2和NQO1蛋白并比较,用RT-PCR法检测mRNA的相对表达量。结果实验前3组大鼠体重差异无统计学意义(P>0.05),实验后与NC组大鼠的体重和血糖比较,DN组大鼠显著降低,血糖值显著升高(P<0.05);与DN组大鼠比较,GM组大鼠的体重和血糖值明显得到改善(P<0.05)。DN组生化指标的浓度明显高于NC组,而Ins明显降低(P<0.05);和DN组生化指标比较,GM组的浓度明显降低,Ins明显升高(P<0.05);与NC组大鼠的肾组织形态比较显示,DN组大鼠的情况明显较差,并且肾小球系膜细胞与高度增生出现;GM组大鼠的肾组织形态比DN组大鼠有明显的改善。蛋白和mRNA比较显示,DN组大鼠ColⅣmRNA和蛋白的表达均比NC组显著增高(P<0.05),Nrf2、NQO1表达明显减少,MG组和DN组大鼠比较,经过人参皂苷治疗后,其ColⅣ表达量明显降低,Nrf2、NQO1表达量显著升高(P<0.05)。结论人参皂苷可以抑制大鼠体内ColⅣ的表达,提高Nrf2和NQO1蛋白的表达,从而改善糖尿病肾病大鼠血糖及肾功能水平。 展开更多
关键词 人参皂苷 糖尿病肾病 ColⅣ nrf2 nqo1 影响
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蒿鳖养阴软坚方通过激活Nrf2/NQO1信号通路抑制肝纤维化发生 被引量:7
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作者 刘悦 李杉杉 +1 位作者 唐诗慧 方步武 《天津医科大学学报》 2018年第1期20-24,共5页
目的:探讨蒿鳖养阴软坚方通过激活Nrf2/NQO1信号通路对四氯化碳复合因素所致大鼠肝纤维化的抑制作用。方法:选用健康Wistar大鼠作为研究对象,将大鼠随机分为正常组、模型组、低剂量组、中剂量组、高剂量组和秋水仙碱组。除正常组大鼠外... 目的:探讨蒿鳖养阴软坚方通过激活Nrf2/NQO1信号通路对四氯化碳复合因素所致大鼠肝纤维化的抑制作用。方法:选用健康Wistar大鼠作为研究对象,将大鼠随机分为正常组、模型组、低剂量组、中剂量组、高剂量组和秋水仙碱组。除正常组大鼠外,其余大鼠均给予自制高脂饲料饲养,每周两次皮下注射40%CC14花生油混合溶液,隔日灌胃给予30%乙醇,各给药组每日灌胃给药的同时给予正常组和模型组以等容积的蒸馏水,直至造模时间(共6周)结束后,乌拉坦麻醉大鼠并收集肝组织标本,比色法检测肝组织中羟脯氨酸(Hyp)的含量,免疫组织化学法检测各组大鼠肝组织中Nrf2和NQO1的分布情况,Western blot法检测各组大鼠肝组织中Nrf2和NQO1的表达水平。结果:与正常组相比,模型组Hyp含量明显升高(P<0.05);各给药组的Hyp含量显著低于模型组,且肝组织中Nrf2和NQO1的表达水平显著升高(P<0.05)。结论:蒿鳖养阴软坚方可以通过激活Nrf2/NQO1通路,上调Nrf2和NQO1的表达,降低肝组织中Hyp的含量,从而发挥抑制由四氯化碳复合因素所致大鼠肝纤维化的作用。 展开更多
关键词 肝纤维化 四氯化碳 蒿鳖养阴软坚方 羟脯氨酸 nrf2 nqo1
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川芎嗪对顺铂耳毒性大鼠耳蜗组织Nrf2/NQO1信号通路相关蛋白表达影响 被引量:1
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作者 金婧 马贤德 +5 位作者 舒福 张琦 曲中源 马梽轩 冷辉 石磊 《辽宁中医药大学学报》 CAS 2023年第2期28-32,共5页
目的探讨川芎嗪(即四甲基吡嗪,tetramethylpyrazine,TMP)对顺铂耳毒性大鼠的作用机制,以及血清中谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)含量变化、耳蜗组织中肌腱膜纤维肉瘤癌基因(musculoaponeurotic fibrosarcoma,Maf)... 目的探讨川芎嗪(即四甲基吡嗪,tetramethylpyrazine,TMP)对顺铂耳毒性大鼠的作用机制,以及血清中谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)含量变化、耳蜗组织中肌腱膜纤维肉瘤癌基因(musculoaponeurotic fibrosarcoma,Maf)、血红素氧合酶1(HO-1)和还原型辅酶/醌氧化还原酶(NQO1)蛋白表达对其的影响。方法采用腹腔注射顺铂(4 mg/kg)诱导顺铂耳毒性大鼠模型。将大鼠随机分为空白对照组、空白+TMP组、模型对照组(M组)、模型+TMP组。通过比较大鼠听性脑干反应(auditory brainstem response,ABR)听力阈值的变化、基底膜铺片技术观察内耳毛细胞纤毛形态变化(硝酸银染色),评估TMP对顺铂耳毒性大鼠耳蜗毛细胞结构的影响。比色法测定大鼠血清中GSH-Px含量变化。Western blot检测法检测各组大鼠耳蜗组织中Maf、HO-1和NQO1的表达变化。结果与空白组相比,模型组大鼠血清中抗氧化酶GSH-Px活性显著下降(P<0.05),耳蜗组织中Maf、NQO1和HO-1基因表达均呈上升趋势;与模型对照组比较,模型+TMP组能够显著提高药物性耳聋大鼠血清中抗氧化酶GSH-Px(P<0.05)活性,增加耳蜗组织中Maf,NQO1和HO-1的蛋白的相对表达(P<0.05)。结论TMP对药物性耳聋大鼠病理损伤具有恢复作用,其机制可能与血清中GSH-Px含量变化和Nrf2/NQO1信号通路相关蛋白的表达有关。 展开更多
关键词 川芎嗪 氧化应激 药物性耳聋 nrf2/nqo1
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电项针干预对急性脑出血大鼠Nrf2、NQO1表达和神经功能的影响 被引量:2
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作者 张晓辉 沈诗彦 +2 位作者 柳依江 邵文娜 崔海 《中国中医急症》 2021年第5期766-769,共4页
目的观察电项针干预对急性脑出血(ICH)大鼠脑组织中转录因子E2相关因子(Nrf2)、NAD(P)H醌氧化还原酶(NQO1)的表达和神经功能评分的影响,探讨电项针干预脑出血大鼠抗氧化应激损伤的机制。方法随机将24只SD大鼠分为空白对照组、假手术组、... 目的观察电项针干预对急性脑出血(ICH)大鼠脑组织中转录因子E2相关因子(Nrf2)、NAD(P)H醌氧化还原酶(NQO1)的表达和神经功能评分的影响,探讨电项针干预脑出血大鼠抗氧化应激损伤的机制。方法随机将24只SD大鼠分为空白对照组、假手术组、ICH模型组、ICH电项针组。ICH电项针组在造模后干预治疗5 d。各组分别在造模后1、3、5 d进行平衡木行走试验,同时在造模后5 d选取病变周围脑组织,检测Nrf2、NQO1 mRNA和蛋白的表达水平。结果大鼠脑组织Nrf2、NQO1 mRNA和蛋白的表达情况:与空白对照组比较,ICH模型组和ICH电项针组的表达量均升高(P<0.01或P<0.05);与假手术组相比,ICH模型组、ICH电项针组Nrf2、NQO1 mRNA和蛋白的表达均升高(P<0.01);与ICH模型组比较,ICH电项针组Nrf2、NQO1mRNA和蛋白的表达增高(P<0.05)。平衡木行走试验:造模后,假手术组和空白对照组评分差异无统计学意义(P>0.05);与假手术组相比,ICH模型组和ICH电项针组干预1 d后评分均增高;与模型组比较,电项针组干预3、5 d后评分有下降趋势(P<0.01)。结论电项针干预脑出血大鼠能促进脑组织损伤周围区Nrf2、NQO1的表达,抑制氧化应激反应,改善神经功能缺损。 展开更多
关键词 脑出血 电项针 nrf2 nqo1 神经功能 大鼠
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黄芪多糖介导Nrf2-HO-1/NQO1信号通路促进大鼠难愈创面的愈合 被引量:3
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作者 徐燕婷 李哲明 范丽娜 《中国现代医生》 2023年第21期39-43,49,共6页
目的 研究黄芪多糖对创面难愈合大鼠创面的促愈合作用及对核因子E2相关因子2(nuclearfactor-erythroid2related factor 2,Nrf2)-血红素氧合酶1(heme oxygenase-1,HO-1)/NADPH醌氧化还原酶1(NADPH quinone oxidoreductase1,NQO1)信号通... 目的 研究黄芪多糖对创面难愈合大鼠创面的促愈合作用及对核因子E2相关因子2(nuclearfactor-erythroid2related factor 2,Nrf2)-血红素氧合酶1(heme oxygenase-1,HO-1)/NADPH醌氧化还原酶1(NADPH quinone oxidoreductase1,NQO1)信号通路表达的影响。方法 18只SD大鼠用于构建慢性难愈合创面模型,造模成功后随机分为模型组、黄芪多糖组、京万红软膏组,另6只大鼠纳入空白对照组,药物涂抹创面21d,期间分析大鼠创面愈合情况。苏木精-伊红染色观察各组大鼠创面组织病理变化情况,全自动生化仪检测血清中超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、丙二醛(malondialdehyde,MDA)水平;酶联免疫吸附测定(enzyme linked immunosorbent assay,ELISA)检测血清中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素(interleukin,IL)-1β、IL-6水平;蛋白质免疫印迹(Western blot)检测大鼠创面组织中Nrf2、HO-1、NQO1蛋白表达水平。结果 与空白对照组比较,模型组大鼠的创面组织病理改变明显,血清SOD、GSH-Px活性下降,而MDA、TNF-α、IL-1β及IL-6水平上升(P<0.01),Nrf2、NQO1、HO-1蛋白表达水平升高(P<0.05)。与模型组相比,黄芪多糖组和京万红软膏组大鼠治疗第7、14、21d的创面愈合率均显著提高,创面组织病理改变均明显减轻,血清SOD与GSH-Px活性均提高,而MDA、TNF-α、IL-1β及IL-6水平均下降(P<0.01),Nrf2、NQO1、HO-1蛋白表达水平均升高(P<0.05)。结论 黄芪多糖可通过抑制氧化应激及炎症反应促进大鼠难愈创面的愈合,并进一步激活组织Nrf2-HO-1/NQO1信号通路表达。 展开更多
关键词 黄芪多糖 氧化应激 炎症 nrf2-HO-1/nqo1信号通路
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AMPK/NRF2/NQO1信号通路与SD大鼠酒精性心肌病的相关性研究
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作者 宋艳莉 李雪峰 +2 位作者 尹昌浩 杨超 张佳梁 《牡丹江医学院学报》 2023年第4期1-5,39,共6页
目的明确单磷酸腺苷依赖的蛋白激酶/核因子E2相关因子2/还原型烟酰胺腺嘌呤二核苷酸磷酸脱氢酶醌1(Adenosine monophosphate dependent protein kinase/nuclear factor E2-related factor 2/NADPH dehydrogenase quinone 1,AMPK/NRF2/NQ... 目的明确单磷酸腺苷依赖的蛋白激酶/核因子E2相关因子2/还原型烟酰胺腺嘌呤二核苷酸磷酸脱氢酶醌1(Adenosine monophosphate dependent protein kinase/nuclear factor E2-related factor 2/NADPH dehydrogenase quinone 1,AMPK/NRF2/NQO1)信号通路与SD大鼠的酒精性心肌病(alcoholic myocardiopathy,ACM)的关系。方法选用健康的8周龄SD大鼠构建ACM模型,采用随机数字表法分成2组,全价颗粒饲料+饮水组(对照组n=24只),全价颗粒饲料+饮酒组(实验组n=24只)。实验组大鼠于每日10:00、17:00给予定量[20 g/(kg·d)]20%浓度酒精喂养(灌胃);正常对照组同时给予等量蒸馏水(灌胃)。从造模开始,实验组以20%酒精浓度持续喂养12周。记录大鼠一般情况。分别于第4周、第8周、第12周实施超声心动图与病理分析。马松染色(Masson)检测大鼠心肌纤维化,免疫组化及RT-qpcr法检测大鼠心肌组织中AMPK、NRF2、NQO1蛋白及基因的表达,分析其关系,从蛋白及基因水平探讨ACM的发病机制。结果心脏彩超:实验组大鼠与对照组相比左室射血分数(left ventricular ejection fraction,LVEF)左室短轴缩短率(left ventricular fractional shortening,LVFS)均下降(P<0.05);病理:对照组HE染色无异常,实验组心肌细胞出现充血水肿等变性;Masson染色:与对照组相比,实验组大鼠心肌纤维化加重;免疫组化:与对照组相比,实验组大鼠心肌AMPK、NRF2、NQO1蛋白表达减弱,染色变浅;RT-qpcr:与对照组相比,实验组大鼠心肌AMPK、NRF2、NQO1基因表达减弱(P<0.05)。结论大鼠心肌纤维化及损伤程度与饮酒时间及浓度积累呈正相关,随着饮酒时间的延长,酒精在体内蓄积,心肌纤维化及损伤程度更严重,抑制AMPK/NRF2/NQO1信号通路可能是分子机制。 展开更多
关键词 酒精性心肌病 心功能 心肌纤维化 AMPK/nrf2/nqo1信号通路
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温肾醒脑方干预对血管性痴呆大鼠Nrf2-HO-1/NQO1信号通路的影响 被引量:2
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作者 胡久略 赵淼 +5 位作者 商健 陈丽平 臧文华 王三沆 张瓅方 侯紫君 《南阳理工学院学报》 2020年第4期106-112,共7页
目的:观察温肾醒脑方对VD大鼠Nrf2-HO-1/NQO1信号通路的影响,探讨其对VD大鼠脑保护作用机制。方法:将60只大鼠分为正常组、模型组、脑复康组(0.6 g·kg^-1)和温肾醒脑方组(2 g·kg^-1),每组15只,构建肾虚痰瘀型VD大鼠模型,给予... 目的:观察温肾醒脑方对VD大鼠Nrf2-HO-1/NQO1信号通路的影响,探讨其对VD大鼠脑保护作用机制。方法:将60只大鼠分为正常组、模型组、脑复康组(0.6 g·kg^-1)和温肾醒脑方组(2 g·kg^-1),每组15只,构建肾虚痰瘀型VD大鼠模型,给予相应药物灌胃治疗后,HE染色法观察脑组织海马形态学变化,运用ELISA检测血清和脑组织SOD、MDA、IL-1β、TNF-α、AchE、ChAT等,RT-PCR和免疫组化法检测Nrf2、HO-1、NQO1的mRNA和蛋白表达。结果:与正常组相比较,模型组海马区组织结构高度疏松,神经元高度水肿,结构模糊,神经元变性,胞核呈深染、固缩、溶解;血清MDA、IL-1β和TNF-α显著升高(P<0.05或P<0.01),SOD显著降低(P<0.01);脑组织MDA和AchE均显著升高(P<0.05或P<0.01),SOD和ChAT显著降低(P<0.05或P<0.01);海马区Nrf2、HO-1、NQO1的mRNA和蛋白表达均显著降低(P<0.01)。与模型组相比较,温肾醒脑方组和脑复康组海马区病理形态较模型组有所改善,神经元病理变化较轻,软化灶减少,神经元肿胀、空泡变性程度、核固缩、核溶解程度不同程度的减轻;血清MDA、IL-1β和TNF-α显著降低(P<0.05或P<0.01),SOD显著升高(P<0.05);脑组织MDA和AchE均显著降低(P<0.05或P<0.01),SOD和ChAT显著升高(P<0.05或P<0.01);海马区Nrf2、HO-1、NQO1的mRNA和蛋白表达均显著升高(P<0.05或P<0.01),且温肾醒脑方组更为明显。结论:温肾醒脑方能够改善脑组织病理形态结构,其机制可能是通过激活Nrf2-HO-1/NQO1信号通路调控下游相关因子的表达,调节血清和脑组织氧自由基和炎性因子代谢,抑制氧化应激及炎性反应损伤,发挥神经保护作用。 展开更多
关键词 温肾醒脑方 血管性痴呆 nrf2-HO-1/nqo1 氧化应激 炎性反应
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Water Extract of Rice False Smut Balls Activates Nrf2/HO-1 and Apoptosis Pathways,Causing Liver Injury
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作者 ZHANG Guomei LI Han +4 位作者 LIU Shanshan ZHOU Xuming LU Mingyang TANG Liang SUN Lihua 《Rice science》 SCIE CSCD 2023年第5期473-485,I0025-I0028,共17页
Ustiloxins are vital cyclopeptide mycotoxins originally isolated from rice false smut balls that form in rice spikelets infected by the fungal pathogen Ustilaginoidea virens.The toxicity of the water extract of rice f... Ustiloxins are vital cyclopeptide mycotoxins originally isolated from rice false smut balls that form in rice spikelets infected by the fungal pathogen Ustilaginoidea virens.The toxicity of the water extract of rice false smut balls(RBWE) remains to be investigated.Studies have shown that RBWE may be toxic to animals,but toxicological evidence is still lacking.In this study,we found that the IC50 values of RBWE to BNL CL.2 cells at 24 and 48 h were 40.02 and 30.11 μg/m L,respectively,with positive correlations with dose toxicity and time toxicity.After treatment with RBWE,the number of BNL CL.2 cells decreased significantly,and the morphology of BNL CL.2 cells showed atrophy and wall detachment.RBWE induced DNA presynthesis phase arrest of BNL CL.2 cells,increased the proportion of apoptotic cells and inhibited cell proliferation.RBWE up-regulated reactive oxygen species(ROS) levels and lowered mitochondrial membrane potentials.Additionally,Western blot and q RT-PCR results suggested that RBWE exerted the above effects by promoting the Nrf2/HO-1 and caspase-induced apoptosis pathways in vitro and in vivo.The contents of alanine aminotransferase,aspartate aminotransferase,alkaline phosphatase,and total bile acids in the serum of mice from Institute of Cancer were significantly up-regulated by RBWE.At the same time,RBWE can lead to increases in ROS and malondialdehyde contents,decreases in contents of oxidized glutathione,glutathione and reduced glutathione,as well as decrease in catalase and superoxide dismutase activities in mouse liver tissues,demonstrating that oxidative stress occurred in mice.Moreover,liver damage was further detected by haematoxylin-eosin staining and electron microscopy to verify the damage to the mice caused by RBWE.In general,RBWE may cause hepatotoxicity in vivo and in vitro via the apoptosis pathway,which provides a reference for hepatotoxicity and its mechanism of action. 展开更多
关键词 water extract rice false smut ball ustiloxin liver injury nrf2/HO-1 pathway apoptosis pathway
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Scutellarin alleviates complete freund’s adjuvant-induced rheumatoid arthritis in mice by regulating the Keap1/Nrf2/HO-1 pathway
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作者 JIAN LI QINGQING WANG XIAOYING ZHANG 《BIOCELL》 SCIE 2023年第6期1307-1316,共10页
Scutellarin(SCU)is a herbal flavonoid glucuronide with multiple pharmacological activities,including antioxidant,anti-inflammation,vascular relaxation,anti-platelet,and myocardial protection.However,the effect of SCU... Scutellarin(SCU)is a herbal flavonoid glucuronide with multiple pharmacological activities,including antioxidant,anti-inflammation,vascular relaxation,anti-platelet,and myocardial protection.However,the effect of SCU on complete Freund’s adjuvant(CFA)-induced rheumatoid arthritis(RA)had not been studied.In this study,we investigated the beneficial effects of SCU in the CFA-induced RA mice model and the anti-arthritic activity was evaluated by paw edema.Enzyme-linked immunosorbent assay(ELISA)was carried out to evaluate the plasma levels of immunoglobulin(Ig)G,IgE,tumor necrosis factor(TNF)-α,interleukin(IL)-1β,IL-6,receptor activator of nuclear factor-κB ligand(RANKL),and osteoprotegerin(OPG).Histological slides were prepared from the harvested paws of mice to determine the pathological changes in the joints.The proportions of T helper type 1(Th1)and T helper type 2(Th2)cells of CD4+T lymphocyte subsets were analyzed by flow cytometry.The expression of Kelch-like ECHassociated protein 1(Keap1),nuclear factor erythroid 2-related factor 2(Nrf2),and heme oxygenase-1(HO-1)was analyzed using real-time quantitative PCR(RT-qPCR)and western blotting assays.The present study demonstrated that SCU prevented CFA-induced RA,and inhibited the expression of inflammation factors,IgG,IgE,TNF-α,IL-1β,and IL-6.While SCU also reduced the RANKL level,it increased OPG expression in RA mice.The Th1/Th2 ratio was significantly lower in mice treated with SCU.Additionally,HO-1 expression was reduced while the expression of Keap1 and Nrf2 was elevated following SCU treatment.Results provide preliminary evidence to employ SCU in arthritis treatment which might be related to the regulation of Th1/Th2 balance and the Keap1/Nrf2/HO-1 pathway. 展开更多
关键词 SCUTELLARIN Rheumatoid arthritis Th1/Th2 balance Keap1/nrf2/HO-1 pathway Immunosuppression
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Mechanism of hesperidin improving myocardial ischemia/reperfusion injury in type 2 diabetic rats through SIRT1/Nrf2/HO-1 signaling pathway
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作者 Zhen-Wang Ma De-You Jiang +3 位作者 Bing-Cheng Hu Xing-Xing Yuan Shao-Jie Cai Jing Guo 《Journal of Hainan Medical University》 2022年第8期5-10,共6页
Objective:To observe the protective effect of hesperidin on myocardial ischemia/reperfusion injury in type 2 diabetes mellitus and its effect on SIRT1/Nrf2/HO-1 signaling pathway.Methods:50 Sprague-Dawley(SD)rats were... Objective:To observe the protective effect of hesperidin on myocardial ischemia/reperfusion injury in type 2 diabetes mellitus and its effect on SIRT1/Nrf2/HO-1 signaling pathway.Methods:50 Sprague-Dawley(SD)rats were randomly assigned to the normal control group(NC),model group,ischemia-reperfusion group(IR),hesperidin group,SIRT1 inhibitor group and hesperidin plus SIRT1 inhibitor group.In addition to NC,the rats in the remaining groups were replicated by intraperitoneal of high-fat diet combined with injection of streptozotocin for type 2 diabetic rats.After then,the myocardial ischemia/reperfusion injury(MIRI)rat model was established by LAd for 30 minutes with 2 hours reperfusion.He staining was used to observe the pathological changes of myocardial tissue,and the levels of serum LDH,CK-MB and SOD,GSH and MDA in myocardial tissue were detected by kit methods,and the expression abundance of related proteins in 4-HNE and SIRT1/Nrf2/HO-1 signal pathway were detected by immunohistochemistry and Western blot;Results:Hesperidin could significantly inhibit cardiomyocyte necrosis and inflammatory cell infiltration,reduce LDH activity,CK-MB and MDA level,and increase SOD activity,GSH and 4-HNE level,the differences were statistically significant when compared with IR group(P<0.01).In addition,compared with the ischemia-reperfusion group,the expressions of SIRT1,Nrf2 and HO-1 proteins in hesperidin group were significantly up-regulated,the differences were statistically significant(P<0.01);Conclusion:Hesperidin inhibits oxidative stress by activating SIRT1/Nrf2/HO-1 signaling pathway,and play a protective effect of myocardial ischemia reperfusion injury in diabetic rats. 展开更多
关键词 HESPERIDIN Type 2 diabetes mellitus Ischemia/reperfusion Myocardial injury SIRT1/nrf2/HO-1 signaling pathway
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Effect of pestle intervention in type 2 diabetic peripheral neuropathy on Keap1/Nrf2/ARE pathway and the relationship with oxidative stress
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作者 Fang Wang Hui Yang +4 位作者 Shun-Qi Liao Yao Wang Han Wang Xi-Mei Weng Ya-Ling Huang 《Journal of Hainan Medical University》 2022年第6期24-28,共5页
Objective:To investigate the effect of pestle needle treatment on Nrf2 pathway and the relationship with oxidative stress in diabetic peripheral neuropathy.Methods:Patients with DPN who met the inclusion criteria were... Objective:To investigate the effect of pestle needle treatment on Nrf2 pathway and the relationship with oxidative stress in diabetic peripheral neuropathy.Methods:Patients with DPN who met the inclusion criteria were randomly divided into control and test groups with 30 patients in each group in a 1:1 allocation ratio.Both groups were given basic treatment,and the pestle group was treated with needle pestle therapy 5 times a week for a total of 4 weeks of intervention.Serum SOD and GSH PX levels were examined by colorimetry before and after intervention;Serum Keap1/Nrf2/ARE signaling pathway related factors expression levels were measured by ELISA;Keap1 and Nrf2 mRNA expression was determined by RT-PCR.Results:Compared with the control group,SOD and GSH-Px in the test group were significantly increased,Keap1 expression was decreased,Nrf2 expression was increased,Keap1 mRNA expression was significantly decreased,and Nrf2 mRNA expression was significantly increased.Conclusions:the pestle needle may enhance the body's antioxidant capacity by modulating the Keap1/Nrf2/ARE signaling pathway to enhance the production of its downstream antioxidant enzymes SOD and GSH Px,thereby protecting and repairing the damaged peripheral nerves in DPN patients. 展开更多
关键词 Diabetic peripheral neuropathy Pestle needle Oxidative stress Keap1/nrf2/ARE signaling pathway
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Effects of nuciferine on Nrf2/HO-1 signaling pathway in adipose tissue of obesity model rats
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作者 Zhi-Xia Yang Jia-Bao Liao 《Food Therapy and Health Care》 2022年第1期1-5,共5页
Objective:This study aimed to explore the therapeutic effect of nuciferine on high-fat diet-induced obesity in rats and the influence of nuciferine on nuclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase-1... Objective:This study aimed to explore the therapeutic effect of nuciferine on high-fat diet-induced obesity in rats and the influence of nuciferine on nuclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)signaling pathway in the adipose tissue.Methods:A total of 40 male Sprague Dawley(SD)rats were evenly divided into the normal,model,positive control,and nuciferine groups,using the random number table method.Except for the normal group,rats in the other groups were fed with high-fat diet for 12 weeks to establish the obesity model.During the model establishment,rats in the positive control group received atorvastatin calcium 2 mg/kg,rats in the nuciferine group received nuciferine 20 mg/kg,and rats in the normal and model groups received normal saline 2 mL,daily through intragastric administration for 12 consecutive weeks.After model establishment and administration,the body weight,Lee’s index,and blood lipids of rats in each group were measured,and hematoxylin and eosin(HE)staining was performed on the liver and adipose tissues to evaluate the therapeutic effect of nuciferine on obesity rat model.Additionally,the levels of superoxide dismutase(SOD),malondialdehyde(MDA),and glutathione peroxidase(GSH-Px)in the serum of rats in each group were determined,and the gene expressions of Nrf2 and HO-1 in the adipose tissue of rats in each group were detected through quantitative polymerase chain reaction(qPCR)to investigate the mechanism of action of nuciferine in the treatment of obesity.Results:After 12 weeks of model establishment and administration,we observed that compared with the model group,nuciferine could significantly reduce the body weight,Lee’s index,and serum triglyceride(TG),total cholesterol(TC),and low-density lipoprotein cholesterol(LDL-C)levels and increase the serum high-density lipoprotein cholesterol(HDL-C)level in obesity rat model(P<0.05 or P<0.01).HE staining revealed that nuciferine could significantly alleviate liver steatosis in obesity rat model and improve the cell morphology in epididymal adipose tissue.Moreover,nuciferine could elevate serum SOD and GSH-Px activities in obesity rat model and lower the serum MDA level(P<0.05 or P<0.01).The qPCR indicated that nuciferine could upregulate the gene expression of Nrf2 and HO-1 in the adipose tissue of obesity rat model(P<0.05 or P<0.01). 展开更多
关键词 OBESITY NUCIFERINE ANTIOXIDANT nrf2/HO-1 signaling pathway
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