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How to Return the Death Programs of Cancer Cells to Work again and Cure Cancer within a Short Time?
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作者 Mahmoud Saad Mohamed El-Khodary Sahar Ezeldien Hasan +4 位作者 Wael A. Hassan Maather M. El-Lamie Ismail A. M. Eissa Waleed F. Khalil Salah M. Aly 《CellBio》 2019年第2期17-39,共23页
Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swi... Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swiss albino mice which were inoculated intraperitoneally and subcutaneously with Ehrlich Ascites Carcinoma cells;1 × (106) cell/mouse. The activity of the cell death programs of the tumor was detected by measuring the volume of Ascites fluid, counting the number of dead cancer cells, measuring the size of the tumor, detecting the positive reaction of caspase enzyme in cancer cells and presence of macrophages and apoptotic bodies in tumor tissue. The experimental formula succeeded in removing the blockers of the cell death program in cancer cells returning the cell death program to work again. 展开更多
关键词 CANCER Therapeutic Strategy Accumulation DETOXIFICATION Enzymes Free RADICALS Antioxidants H2O2 GLUTATHIONE NF-kB SULFORAPHANE Flavonoid cur cumin
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姜黄素对缺氧诱导的人原发性肝癌细胞HepG2上皮细胞间充质转化的影响 被引量:8
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作者 常远鸿 江梅 +1 位作者 刘凯歌 李徐奇 《中国中西医结合杂志》 CAS CSCD 北大核心 2013年第8期1102-1106,共5页
目的探讨姜黄素对缺氧诱导下人原发性肝癌细胞HepG2上皮细胞间充质转化的影响及其可能机制。方法将HepG2细胞分3组:正常对照组、氯化钴(CoCl2)组和CoCl2加10μmol/L姜黄素组。采用MTT法检测细胞增殖能力,划痕实验检测细胞迁移能力,Real-... 目的探讨姜黄素对缺氧诱导下人原发性肝癌细胞HepG2上皮细胞间充质转化的影响及其可能机制。方法将HepG2细胞分3组:正常对照组、氯化钴(CoCl2)组和CoCl2加10μmol/L姜黄素组。采用MTT法检测细胞增殖能力,划痕实验检测细胞迁移能力,Real-timeRT-PCR检测缺氧诱导因子-1α(hy-poxia-induciblefactor-1α,HIF-1α)mRNA表达,Westernblot检测HIF-1α蛋白、E-钙黏蛋白(epithelial-cadher-in,E-cadherin)、波形蛋白(Vimentin)表达。结果 HepG2细胞被CoCl2诱导缺氧后,细胞增殖及迁移能力增强,HIF-1α蛋白表达上调,上皮标志蛋白E-cadherin表达下降而间质标志蛋白Vimentin表达上调,与正常对照组比较,差异均有统计学意义(P<0.05)。姜黄素干预缺氧HepG2细胞后,其增殖与迁移能力被明显抑制,同时HIF-1α蛋白表达下降,E-cadherin蛋白表达上调,Vimentin蛋白表达下降,与CoCl2组比较,差异均有统计学意义(P<0.05)。3组HIF-1αmRNA表达比较,差异无统计学意义(P>0.05)。结论缺氧诱导肝癌细胞HepG2增殖和迁移能力的增强可被姜黄素逆转,可能与姜黄素抑制缺氧诱导的HIF-1α蛋白上调和上皮细胞间充质转化有关。 展开更多
关键词 肝癌细胞 侵袭 缺氧 上皮细胞间充质转化 姜黄素
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姜黄素对百草枯致肺纤维化的干预治疗临床研究 被引量:6
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作者 蒋丽 张彧 《医学综述》 2015年第5期883-885,共3页
目的通过监测姜黄素干预下百草枯中毒(PQP)患者血清基质金属蛋白酶(MMP)9、组织金属蛋白酶抑制物(TIMP)1及肺部影像学的变化,探讨姜黄素对PQP患者肺纤维化的干预作用。方法选择2008年5月至2010年3月大连医科大学附属第一医院急诊科收治... 目的通过监测姜黄素干预下百草枯中毒(PQP)患者血清基质金属蛋白酶(MMP)9、组织金属蛋白酶抑制物(TIMP)1及肺部影像学的变化,探讨姜黄素对PQP患者肺纤维化的干预作用。方法选择2008年5月至2010年3月大连医科大学附属第一医院急诊科收治的PQP患者共61例,依据随机量表法分为姜黄素干预组(31例)和非姜黄素组(30例)。姜黄素干预组给姜黄素1000 mg/(kg·d),每日2次口服,两组其他治疗方案相同,采用双抗体夹心酶联免疫吸附法测定患者入院后第1、3、5、7、11天血清MMP-9、TIMP-1水平;并监测肺CT对PQP患者肺纤维化进展程度进行评估。结果姜黄素干预组与非姜黄素组在病死率方面的差异无统计学意义,但是姜黄素干预组的生存时间与对照组的差异有统计学意义(P<0.05)。非姜黄素干预组MMP-9、TIMP-1与姜黄素干预组比较各时点间的差异均有统计学意义(均P<0.05)。姜黄素干预组血清MMP-9、TIMP-1水平均显著低于同期非姜黄素组(P<0.05)。PQP患者肺CT检查,姜黄素干预组组肺纤维化程度较非姜黄素组显著减轻。结论 MMP-9及TIMP-1可能参与PQP肺纤维化的启动及进展过程,可作为临床生化指标联合CT等其他检查对肺纤维化的程度及预后做出评估。对PQP患者早期进行姜黄素干预治疗可降低血循环中MMP-9及TIMP-1水平,减轻肺纤维化程度,延缓病情发展,延长生存时间,但不能降低患者病死率。 展开更多
关键词 百草枯中毒 基质金属蛋白酶9 组织金属蛋白酶抑制物1 姜黄素 肺纤维化
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Quranic Verse No. 8 of Surat Al-Jumu’ah Leads us to Describe Cancer and Determine Its True Cause (Part-III) 被引量:1
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作者 Mahmoud Saad Mohamed El-Khodary 《CellBio》 2018年第3期35-49,共15页
Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and A... Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and Activation of nuclear factor kappa B stage and the shutting down of programs of cell death stage) to become a cancerous cell. The success of the therapeutic strategy to treat cancer depends on making either one or both programs of cell death run again. Shutting down one stage completely will be sufficient to stop the transformation of the natural cell into a cancerous cell, which eliminates the production of hydrogen peroxide, thus the activity of the NF-Kb will be inhibited. However, shutting down all stages is the most comprehensive therapeutic strategy and guarantees treatment success. 展开更多
关键词 CANCER Therapeutic Strategy Accumulation DETOXIFICATION Enzymes Free Radicals Antioxidants H2O2 Glutathione NF-Kb SULFORAPHANE Flavonoid cur cumin
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