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991.
Effects of diallyl trisulfide on induction of apoptotic death in murine leukemia WEHI‐3 cells in vitro and alterations of the immune responses in normal and leukemic mice in vivo
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Fang‐Ming Hung Hung‐Sheng Shang Nou‐Ying Tang Jen‐Jyh Lin Kung‐Wen Lu Jing‐Pin Lin Yang‐Ching Ko Chien‐Chih Yu Hai‐Lung Wang Jung‐Chi Liao Hsu‐Feng Lu Jing‐Gung Chung 《Environmental toxicology》2015,30(11):1343-1353
Diallyl trisulfide (DATS), a chemopreventive dietary constituent and extracted from garlic, has been shown to against cultured many types of human cancer cell liens but the fate of apoptosis in murine leukemia cells in vitro and immune responses in leukemic mice remain elusive. Herein, we clarified the actions of DATS on growth inhibition of murine leukemia WEHI‐3 cells in vitro and used WEHI‐3 cells to generate leukemic mice in vivo, following to investigate the effects of DATS in animal model. In in vitro study, DATS induced apoptosis of WEHI‐3 cells through the G0/G1 phase arrest and induction of caspase‐3 activation. In in vivo study DATS decreased the weight of spleen of leukemia mice but did not affect the spleen weight of normal mice. DATS promoted the immune responses such as promotions of the macrophage phagocytosis and NK cell activities in WEHI‐3 leukemic and normal mice. However, DATS only promotes NK cell activities in normal mice. DATS increases the surface markers of CD11b and Mac‐3 in leukemia mice but only promoted CD3 in normal mice. In conclusion, the present study indicates that DATS induces cell death through induction of apoptosis in mice leukemia WHEI‐3 cells. DATS also promotes immune responses in leukemia and normal mice in vivo. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1343–1353, 2015. 相似文献
992.
Pb2+ induced IL‐8 gene expression by extracellular signal‐regulated kinases and the transcription factor,activator protein 1, in human gastric carcinoma cells
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993.
Ma Hao Zhou Tao Li Xiang Maraganore Demetrius Heianza Yoriko Qi Lu 《Age (Dordrecht, Netherlands)》2022,44(3):1479-1488
GeroScience - We examined the interactions between educational attainment and genetic susceptibility on dementia risk among adults over 60 years old. A total of 174,161 participants were... 相似文献
994.
Guoliang Zhou Meisong Qin Xiaolin Zhang Jianting Yang Hao Yu 《Gastroenterologia y hepatologia》2021,44(1):1-12
BackgroundTopotecan is an anti-cancer chemotherapy drug with common side effects, including hepatotoxicity. In this study, we aim to investigate the mechanisms of topotecan-induced hepatocellular injury beyond conventional DNA damage.Materials and methodsMethyl Thiazolyl Tetrazolium (MTT) assay was used to detect the inhibitory effect of topotecan on cell proliferation. Western blot was used to detect protein expression. Flow cytometry assay was performed to determine apoptosis rate under topotecan treatment. ASCT2 overexpression was addressed using adenovirus vector. qRT-PCR and western blot assay were used to detect the expression of ASCT2. Glutamine uptake, intracellular glutathione (GSH) and reactive oxygen species (ROS) level were detected by glutamine detection kit, GSH detection kit and ROS detection kit respectively.ResultsMTT results showed that topotecan had an inhibitory effect on cell proliferation and induced apoptosis in both L02 and HepG2 cell lines. Topotecan inhibited the expression of glutamine transporter ASCT2 and the uptake of glutamine in both L02 and HepG2 cell lines. The uptake of glutamine and the GSH level was increased in both L02 and HepG2 cell lines after ASCT2 overexpression. The ROS level was inhibited by ASCT2 overexpression upon topotecan treatment in both L02 and HepG2 cell lines. Topotecan-induced hepatocellular apoptosis and proliferation inhibition were attenuated by ASCT2 overexpression in both L02 and HepG2 cell lines.ConclusionTopotecan-induced hepatocytes death is dependent on ASCT2 down-regulation, which causes oxidative stress via inhibiting GSH production. 相似文献
995.
Hu Nan Zhang Jing Wang Jing Wang Pei Wang Jing Qiang Yongqian Li Zicheng Wu Tianming Wang Xing Wang Yahong Li Jiao Liu Xiaoping Zhang Jirong Feng Xiuyuan Ju Bomiao Hao Zhiming Pu Dan Lu Xiaohong Wang Qiang He Lan 《Clinical rheumatology》2022,41(3):819-829
Clinical Rheumatology - Biomarkers of bone and cartilage metabolism were proposed as early diagnosis indicators for knee osteoarthritis (OA), however, which were influenced by disease stage, age,... 相似文献
996.
Li Jia Xue Zhixin Wu Zhenbiao Bi Liqi Liu Huaxiang Wu Lijun Liu Shengyun Huang Xiangyang Wang Yong Zhang Yan Qi Wufang He Lan Dai Lie Sun Lingyun Li Xiaomei Shuai Zongwen Zhao Yi Wang Yanyan Xu Jian Zhang Hao Yu Hao Chen Xiaoxiang Bao Chunde 《Clinical rheumatology》2022,41(10):3005-3016
Clinical Rheumatology - To assess the clinical equivalence of TQ-Z2301, a biosimilar of adalimumab, to the reference adalimumab in the treatment of Chinese patients with active ankylosing... 相似文献
997.
Clinical Rheumatology - 相似文献
998.
Wu Dan Chen Mengya Chen Shile Zhang Shimin Chen Yongheng Zhao Qian Xue Ke Xue Feng Chen Xiaosong Zhou Min Li Hao Zheng Jie Le Yunchen Cao Hua 《Clinical rheumatology》2022,41(10):3107-3117
Clinical Rheumatology - Extrahepatic tryptophan (Trp)-kynurenine (Kyn) metabolism via indoleamine 2,3-dioxygenase 1 (IDO1) induction was found to be associated with intrinsic immune regulation.... 相似文献
999.
Qiu Zhen Ming Hao Zhang Yi Yu Yanli Lei Shaoqing Xia Zhong-yuan 《Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy》2022,36(2):229-243
Cardiovascular Drugs and Therapy - Histone deacetylase 3 (HDAC3) and silent information regulator 1 (SIRT1) are histone deacetylases that regulate important metabolic pathways and play important... 相似文献
1000.
目的:探讨乌司他丁保护百草枯中毒大鼠肺免受损伤的作用及其机制。方法:Wistar大鼠108只,随机分为对照组、百草枯组和乌司他丁组。百草枯组和乌司他丁组给予百草枯灌胃染毒,对照组给予无菌生理盐水灌胃,乌司他丁组同时给予乌司他丁治疗。1、3、7、14、21、28 d测血清中的MDA、SOD、IL-6、IL-10和TNF-α水平,以及肺组织中的p38 MAPK、MMP-2和TIMP-1表达水平。结果:1、3、7 d百草枯组和乌司他丁组的SOD均较对照组下降(P0.01),乌司他丁组SOD明显高于百草枯组(P0.05)。1、3、7 d百草枯组和乌司他丁组的MDA、IL-6、IL-10及TNF-α均较对照组增高(P0.01),乌司他丁组各指标明显低于百草枯组(P0.05)。1、3、7、14、21、28d百草枯组和乌司他丁组肺组织中的p38 MAPK及TIMP-1均较对照组增高(P0.01),乌司他丁组各指标明显低于百草枯组(P0.05)。1、3、7、14、21 d百草枯组和乌司他丁组肺组织中的MMP-2均较对照组增高(P0.01),乌司他丁组MMP-2明显低于百草枯组(P0.05)。结论:乌司他丁通过抑制p38 MAPK信号通路及抗炎、抗氧化作用保护百草枯中毒大鼠肺免受损伤的作用。 相似文献