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41.
M Maneesh H Jayalekshmi Sanjiba Dutta Amit Chakrabarti D M Vasudevan 《Indian journal of clinical biochemistry : IJCB》2005,20(2):62-67
The study was undertaken to evaluate the possible involvement of oxidative stress in the pathogenesis of ethanol induced testicular
atrophy in rats. Adult male rats were orally administered ethanol at a dose of 1.6 g/kg body weight/day for four weeks. Twenty-four
hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and weighed. Apoptosis
was studied by using the Feulgen reaction on 5 μ thin paraffin sections of testis. Testicular homogenate was prepared and
centrifuged. The supernatant was used for the estimation of extent of lipid peroxidation and antioxidant defense status. There
was significant reduction in body weight: and in testicular weight and diameter in ethanol treated rats. Extent of germ cell
apoptosis was significantly high in ethanol treated rats. Ethanol treated rats showed significantly high tissue TBARS level
and glutathione S-transferase activity; and low tissue ascorbic acid, reduced glutathione, superoxide dismutase, catalase,
glutathione peroxidase and glutathione reductase activities. Chronic ethanol administration resulted in high oxidative stress
in the testes either due to increased extent of lipid peroxidation or due to decreased antioxidant defenses, and thereby induces
germ cell apoptosis leading to testicular atrophy. 相似文献
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43.
目的:究动脉粥样硬化对SMC凋亡及凋亡相关基因表达的影响,探讨凋亡的分子机制及晚期AS斑块破裂之原因。方法:采用高维生素D3 高脂肪高胆固醇饲料喂养法建立大鼠AS的模型;运用DNA琼脂糖凝胶电泳法鉴定基因组DNA的断裂情况;使用Northern Blot检测P53、c-myc及bcl-2基因的表达活性。结果:a.AS斑块中SMC的DNA片断在电泳中呈特征性梯状分布;b.AS斑块中P53及C-myc基因转录明显增强;c.AS斑块中SMC的bcl-2mRNA含量显著下降。提示1.AS斑块中存在凋亡的SMC,P53及C-myc表达的增强和bcl-2的表达下调介导了这一过程;2.SMC的凋亡可能是晚期AS斑块玻裂的重要原因。 相似文献
44.
对近年来大量的文献研究,运动训练是人体的重要的应激源,在运动应激下会诱发骨骼肌细胞的凋亡,并且随着运动形式与强度等改变而改变。骨骼肌中的细胞凋亡与运动能力的下降有着密切的联系,这有可能是诱发运动性疲劳的机制之一。因此,研究运动训练与细胞凋亡的关系及运动导致骨骼肌细胞凋亡的机制意义重大。运动可以诱导骨骼肌细胞凋亡,细胞凋亡发生的比率和程度与运动形式、运动强度和运动持续时间密切有关。这些问题的研究对于预防和处理运动导致的骨骼肌损伤以及缓解运动性疲劳、提高运动成绩提供了理论指导。 相似文献
45.
BackgroundButyrate is a histone deacetylase inhibitor that induces apoptosis and inhibits cell proliferation of colorectal cancer cells. To improve its anticancer activity, butyrate has been evaluated mixed with drugs and different molecules. Plant antimicrobial peptides are attractive anticancer alternative molecules because they show selective cytotoxic activity against different cancer cell lines. In this work, we explore if the plant defensin γ-thionin (Capsicum chinense) can improve butyrate activity on Caco-2 cell line and we also determined the mechanism of death activated.ResultsThe combined treatment of γ-thionin (3.5 µM) and butyrate (50 mM) showed higher cytotoxicity on Caco-2 cells with respect to single treatments. Also, the combined treatment reduced cell proliferation and exhibited a higher rate of apoptosis than single treatments. Combined treatment induced caspases 8 and 9 activation to an extent comparable with that of butyrate while γ-thionin did not activate caspases. Additionally, reactive oxygen species generation preceded the onset of apoptosis, and superoxide anion production was higher in cells treated with the combined treatment.ConclusionsThe γ-thionin from Habanero chili pepper improved the butyrate cytotoxicity on Caco-2 cells. This effect occurred through apoptosis induction associated with reactive oxygen species production. Therefore, the combination of butyrate with cytotoxic antimicrobial peptides could be an attractive strategy for cancer therapy.How to cite: Velázquez-Hernández ME, Ochoa-Zarzosa A, López-Meza JE, Defensin γ-thionin from Capsicum chinense improves butyrate cytotoxicity on human colon adenocarcinoma cell line Caco-2. Electron J Biotechnol 2021;52. https://doi.org/10.1016/j.ejbt.2021.04.009 相似文献
46.
Neeta Singh 《Indian journal of clinical biochemistry : IJCB》2007,22(2):6-16
Apoptosis a physiological mechanism that eliminates excessive, damaged or unwanted cells, is a highly regulated pathway important
for maintaining homeostasis in multicellular organisms. It can be initiated through various signals via the extrinsic pathway
which involves death receptors, or via the intrinsic pathway which is initiated by intracellular damage and involves the mitochondria
and release of cytochrome c from it to further activate caspases. The Bcl-2 family of proteins is situated upstream to the
irreversible damage of cellular constituents and is an important checkpoint in the fate of a cell. The pro-apoptotic members,
BH3 only members include BID, BAD and BIM. They directly or indirectly activate multidomain BAX/BAK that constitute the requisite
gateway to the intrinsic pathway which operates at the mitochondrial surface and endoplasmic reticulum. In contrast, antiapoptotic
members such as Bcl-2, Bcl-XL bind and sequester activation. Downstream of mitochondria, the apoptosome involvement is seen
to generate caspase activity. Post mitochondria regulation involves IAPs, and their inhibitors. The pathogenesis of several
diseases such as cancer, neurodegenerative disorders, autoimmune disorders, heart disease, infectious diseases including AIDS
is closely related to aberrant apoptosis. Consequently interest has emerged in employing various the rapeutic approaches such
as gene therapy, antisense therapy, recombinant biologicals, organic and combinatorial chemistry, to specifically target apoptosis
signaling pathways such as death receptors FAS/TRAIL, Bcl-2, p53, IAPs, SMAC and caspases, etc. and are now advancing from
preclinical to clinical phase. 相似文献
47.
Yang CHEN Qian LI Sisi REN Ting CHEN Bingtao ZHAI Jiangxue CHENG Xiaoyan SHI Liang SONG Yu FAN Dongyan GUO 《Journal of Zhejiang University. Science. B》2022,23(8):682
ObjectiveTo determine the potential molecular mechanisms underlying the therapeutic effect of curcumin on hepatocellular carcinoma (HCC) by network pharmacology and experimental in vitro validation.MethodsThe predictive targets of curcumin or HCC were collected from several databases. the identified overlapping targets were crossed with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) platform. Two of the candidate pathways were selected to conduct an experimental verification. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium (MTT) assay was used to determine the effect of curcumin on the viability of HepG2 and LO2 cells. The apoptosis and autophagy of HepG2 cells were respectively detected by flow cytometry and transmission electron microscopy. Besides, western blot and real-time polymerase chain reaction (PCR) were employed to verify the p53 apoptotic pathway and adenosine 5''-monophosphate (AMP)-activated protein kinase (AMPK) autophagy pathway. HepG2 cells were pretreated with pifithrin-α (PFT-α) and GSK690693 for further investigation.ResultsThe 167 pathways analyzed by KEGG included apoptosis, autophagy, p53, and AMPK pathways. The GO enrichment analysis demonstrated that curcumin was involved in cellular response to drug, regulation of apoptotic pathway, and so on. The in vitro experiments also confirmed that curcumin can inhibit the growth of HepG2 cells by promoting the apoptosis of p53 pathway and autophagy through the AMPK pathway. Furthermore, the protein and messenger RNA (mRNA) of the two pathways were downregulated in the inhibitor-pretreated group compared with the experimental group. The damage-regulated autophagy modulator (DRAM) in the PFT-α-pretreated group was downregulated, and p62 in the GSK690693-pretreated group was upregulated.ConclusionsCurcumin can treat HCC through the p53 apoptotic pathway and the AMPK/Unc-51-like kinase 1 (ULK1) autophagy pathway, in which the mutual transformation of autophagy and apoptosis may occur through DRAM and p62. 相似文献
48.
Optimal time for mesenchymal stem cell transplantation in rats with myocardial infarction 总被引:1,自引:0,他引:1
Jiang CY Gui C He AN Hu XY Chen J Jiang Y Wang JA 《Journal of Zhejiang University. Science. B》2008,9(8):630-637
Background:Bone marrow mesenehymal stem cell(MSC)transplantation is a promising strategy in the treatment of myocardial infarction(MI).However,the time for transplanting cells remains controversial.The aim of this study was to find an optimal time point for cell transplantation.Methods:MSCs were isolated and cultured from Sprague-Dawley(SD) rats.MI model was set up in SD rats by permanent ligation of left anterior descending coronary artery.MSCs were directly injected into the infarct berder zone at 1 h,1 week and 2 weeks after MI,respectively.Sham-operated and MI centrel groups received equal volume of phosphate buffered saline(PBS).At 4 weeks after MI,cardiac function Was assessed by echocardiography;vessel density Was analyzed on hematoxylin-eosin stained slides by light microscopy;the apoptosis of cardiomyocytes Was evaluated by terminal deoxynucleotidy1 transferase-mediated dUTP nick end-labeling(TUNEL) assay;the expressions of proteins were analyzed by Western blot.Results:MSC transplantation improved cardiac function.reduced the apoptosis of cardiomyocytes and increased vessel density.These benefits were more obvious in l-week group than in 1-h and 2-week groups.There are more obvious increases in the ratio of bc1-2/bax and the expression of vascular endothelial growth factor(VEGF)and more obvious decreases in the expression of cleaved-caspase-3 in 1-week group than those in other two groups.Conclusion:MSC transplantation was beneficial for the recovery of cardiac function.MSC transplantation at l week post-MI exerted the best effects on increases of cardiac function,anti-apoptosis and angiogenesis. 相似文献
49.
目的:探讨肺康饮含药血清对人肺癌细胞(NC-H446)的作用。方法:采用血清药理学方法,以细胞增殖抑制率及凋亡率为观察指标,对实验结果进行分析。结果:肺康饮含药血清培养24h、48h,均对NC-H446细胞株增殖具有抑制作用,且对NC-H446细胞株增殖的抑制作用具有一定的量效及时效关系,实验组与对照组间差异有统计学意义(P<0.01)。各实验组含药血清均可诱导NC-H446细胞株发生凋亡,且该作用具有一定的量效及时效关系,实验组与对照组间差异有统计学意义(P<0.01)。结论:肺康饮含药血清可明显抑制NC-H446细胞株的增殖,抑制作用具有一定的量效及时效关系。肺康饮含药血清也可诱导NC-H446细胞株发生凋亡,作用具有一定的量效及时效关系。 相似文献
50.
Wang Guan Hao Mingyue Liu Qiong Jiang Yanlong Huang Haibin Yang Guilian Wang Chunfeng 《Journal of Zhejiang University. Science. B》2021,22(5):348-365
This study probed the protective effect of recombinant Lactobacillus plantarum against hydrogen peroxide(H_2O_2)-induced oxidative stress in human umbilical vein endothelial cells(HUVECs). We constructed a new functional L. plantarum(NC8-p SIP409-alr-angiotensin-converting enzyme inhibitory peptide(ACEIP)) with a double-gene-labeled non-resistant screen as an expression vector. A 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2 H-tetrazolium bromide(MTT) colorimetric assay was carried out to determine the cell viability of HUVEC cells following pretreatment with NC8-p SIP409-alr-ACEIP. Flow cytometry(FCM) was used to determine the apoptosis rate of HUVEC cells. Cysteinyl aspartate specific proteinase(caspase)-3/8/9 activity was also assayed and western blotting was used to determine protein expression of B-cell lymphoma 2(Bcl-2), Bcl-2-associated X protein(Bax), inducible nitric oxide synthase(i NOS), nicotinamide adenine dinucleotide phosphate oxidase 2(gp91 phox), angiotensin II(Ang II), and angiotensin-converting enzyme 2(ACE2), as well as corresponding indicators of oxidative stress, such as reactive oxygen species(ROS), mitochondrial membrane potential(MMP), malondialdehyde(MDA),and superoxide dismutase(SOD). NC8-p SIP409-alr-ACEIP attenuated H_2O_2-induced cell death, as determined by the MTT assay. NC8-p SIP409-alr-ACEIP reduced apoptosis of HUVEC cells by FCM. In addition, compared to the positive control, the oxidative stress index of the H_2O_2-induced HUVEC(Hy-HUVEC), which was pretreated by NC8-p SIP409-alr-ACEIP, i NOS,gp91 phox, MDA, and ROS, was decreased obviously; SOD expression level was increased; caspase-3 or-9 was decreased, but caspase-8 did not change; Bcl-2/Bax ratio was increased; permeability changes of mitochondria were inhibited; and loss of transmembrane potential was prevented. Expression of the hypertension-related protein(Ang II protein) in HUVEC cells protected by NC8-p SIP409-alr-ACEIP decreased and expression of ACE2 protein increased. These plantarum results suggested that NC8-p SIP409-alr-ACEIP protects against H_2O_2-induced injury in HUVEC cells. The mechanism for this effect is related to enhancement of antioxidant capacity and apoptosis. 相似文献