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21.
粉防己碱促进增生性瘢痕成纤维细胞凋亡的实验研究 总被引:5,自引:0,他引:5
钟晓春 《杭州师范学院学报(自然科学版)》2005,4(6):426-427
目的观察粉防己碱对培养的人增生性瘢痕成纤维细胞凋亡的影响。方法取材自人体增生性瘢痕,提取出成纤维细胞进行培养,设实验组和对照组,实验组加入粉防己碱,用Tunnel法检测细胞的凋亡,比较两组间的细胞凋亡率。结果使用粉防己碱后,成纤维细胞的凋亡率显著增加,与对照组比较,差异有非常显著意义(P<0.01)。结论通过促进瘢痕组织成纤维细胞的凋亡,粉防己碱可能具有防治瘢痕的作用,值得进一步探讨。 相似文献
22.
采用MTT法检测纤毛婆婆纳(Veronica ciliata Fisch.)乙酸乙酯提取物(ethyl acetate extract,VEAE)对五种不同癌细胞(A549,Hela,U20S,MCF-7和SMMC-7721)的增殖抑制作用,筛选出对VEAE最敏感的细胞,并进一步运用DAPI染色、Annexin V/PI双染及荧光定量PCR(qRT-PCR)来探究其作用机制.MTT结果显示,VEAE对五种癌细胞的增殖均有抑制作用,并呈现时间和剂量的依赖效应,其中对MCF-7细胞的抑制作用最为显著,处理48h后其IC50达到最低,为63.42±0.19μg/mL;DAPI染色和Annexin V/PI双染结果发现,VEAE处理MCF-7细胞后,细胞皱缩变圆,凋亡细胞的数量增加,从对照组的5.00%上升到47.45%;qRT-PCR结果表明;VEAE处理MCF-7细胞后,凋亡基因Caspase-3,Caspase-9和Bax的表达上调,抗凋亡基因Bcl-2的表达下调.由此表明VEAE能抑制癌细胞的增殖,诱导细胞发生凋亡,其机制可能是通过调控与细胞凋亡相关基因的表达来实现. 相似文献
23.
C. Akgul 《Cellular and molecular life sciences : CMLS》2009,66(8):1326-1336
Resistance to apoptosis is a common challenge in human malignancies contributing to both progress of cancer and resistance
to conventional therapeutics. Abnormalities in a variety of cell intrinsic and extrinsic molecular mechanisms cooperatively
promote tumor formation. Therapeutic approaches that specifically target components of these molecular mechanisms are getting
widespread attention. Mcl-1 is a highly expressed pro-survival protein in human malignancies and its cellular expression is
tightly regulated via multiple mechanisms. Mcl-1 differs from other members of the Bcl-2 family in having a very short half-life. So inhibition
of its expression and/or neutralization of its anti-apoptotic function will rapidly make Mcl-1-dependent cells more susceptible
to apoptosis and provide an opportunity to combat several types of cancers. This review summarizes the current knowledge on
the regulation of Mcl-1 expression and discusses the alternative approaches targeting Mcl-1 in human cancer cells whose survivals
mainly depend on Mcl-1.
Received 6 October 2008; received after revision 21 October 2008; accepted 10 November 2008 相似文献
24.
Yun Zhang Zhong-yan Liang Shao-yang Zhang Fang-fang Huang Wei Wu Yuan Gao Zuo-bing Chen 《浙江大学学报(自然科学英文版)》2008,9(11):871-878
Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer's lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuated injury of the lung and decreased the concentration of lactic acid and the number of in situ TdT-mediated dUTP nick-end labelling (TUNEL)-positive cells. Moreover, immunohistochemistry performed 24 h after reperfusion revealed increases in the level of nuclear factor κB (NF-κB), and phosphorylated p38 mitogen-activated protein kinase (MAPK) in the albumin-untreated group was down-regulated by albumin treatment when compared with the sham rats. Conclusion: Resuscitation with albumin attenuates tissue injury and inhibits T/HS-induced apoptosis in the lung via the p38 MAPK signal transduction pathway that functions to stimulate the activation of NF-κB. 相似文献
25.
Zaitseva II Størling J Mandrup-Poulsen T Berggren PO Zaitsev SV 《Cellular and molecular life sciences : CMLS》2008,65(7-8):1248-1255
An insufficient number of insulin-producing β-cells is a major cause of defective control of blood glucose in both type 1
and type 2 diabetes. The aim of this study was to clarify whether the insulinotropic imidazolines can affect the survival
of highly proliferating insulin-secreting cells, here exemplified by the MIN6 cell line. Our data demonstrate that RX871024,
but not efaroxan, triggered MIN6 cell death and potentiated death induced by a combination of the pro-inflammatory cytokines
interleukin-1β, interferon- γ and tumor necrosis factor-α. These effects did not involve changes in nitric oxide production
but correlated with stimulation of c-jun N-terminal kinase (JNK) activity and activation of caspases-1, -3, -8 and -9. Our
results suggest that the imidazoline RX871024 causes death of highly proliferating insulin-secreting cells, putatively via augmentation of JNK activity, a finding that may impact on the possibility of using compounds of similar activity in the
treatment of diabetes.
Received 13 December 2007; received after revision 5 February 2008; accepted 6 February 2008 相似文献
26.
Gavin C. Higgins Philip M. Beart Phillip Nagley 《Cellular and molecular life sciences : CMLS》2009,66(16):2773-2787
To characterize neuronal death, primary cortical neurons (C57/Black 6 J mice) were exposed to hydrogen peroxide (H2O2) and staurosporine. Both caused cell shrinkage, nuclear condensation, DNA fragmentation and loss of plasma membrane integrity.
Neither treatment induced caspase-7 activity, but caspase-3 was activated by staurosporine but not H2O2. Each treatment caused redistribution from mitochondria of both endonuclease G (Endo G) and cytochrome c. Neurons knocked down for Endo G expression using siRNA showed reduction in both nuclear condensation and DNA fragmentation
after treatment with H2O2, but not staurosporine. Endo G suppression protected cells against H2O2-induced cell death, while staurosporine-induced death was merely delayed. We conclude that staurosporine induces apoptosis
in these neurons, but severe oxidative stress leads to Endo G-dependent death, in the absence of caspase activation (programmed
cell death-type III). Therefore, oxidative stress triggers in neurons a form of necrosis that is a systematic cellular response
subject to molecular regulation.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
27.
Maldonado-Celisa ME Roussia S Foltzer-Jourdainne C Gossé F Lobstein A Habold C Roessner A Schneider-Stock R Raul F 《Cellular and molecular life sciences : CMLS》2008,65(9):1425-1434
We showed previously that inhibition of polyamine catabolism with the polyamine oxidase inhibitor MDL 72527 (MDL) potentiates
the apoptotic effects of apple procyanidins (Pcy) in SW620 cells. Here we report that Pcy caused an activation of the intrinsic
apoptotic pathway through enhanced polyamine catabolism and mitochondrial membrane depolarization. MDL in the presence of
Pcy caused a profound intracellular depletion of polyamines and exerted a protective effect on mitochondrial functions. MDL
potentiation of Pcy-triggered apoptosis was reversed by addition of exogenous polyamines. In addition, MDL in combination
with Pcy activated the extrinsic apoptotic pathway through enhanced TRAIL-death receptor (DR4/DR5) expression. Potentiation
of Pcy-triggered apoptosis by MDL was inhibited when cells were exposed to specific inhibitors of DR4/DR5. These data indicate
that the depletion of intracellular polyamines by MDL in the presence of Pcy caused a switch from intrinsic to extrinsic apoptotic
pathways in human colon cancer-derived metastatic cells.
Received 15 January 2008; received after revision 19 February 2008; accepted 7 March 2008 相似文献
28.
Clinical implications of p53 mutations 总被引:5,自引:0,他引:5
The ultimate goal of basic cancer research is to provide a theoretical foundation for rational approaches to improve cancer
therapy. Our extensive insight into the biology of the p53 tumour suppressor and the clinical behaviour of tumours harbouring
p53 mutations indicates that information concerning p53 will be useful in diagnosis and prognosis, and may ultimately produce
new therapeutic strategies. At the same time, efforts to understand the clinical implications of p53 mutations have revealed conceptual and technical limitations in translating basic biology to the clinic. The lessons learned
from p53 may lay the groundwork for future efforts to synthesize cancer gene function, cancer genetics and cancer therapy. 相似文献
29.
从有机胂的角度出发,结合丹皮酚的抗炎、活血和抗肿瘤等特性,合成了一系列的有关丹皮酚和有机胂的衍生物,均为创新化合物;采用正交实验和方差分析对合成化合物的条件进行了探讨,同时对丹皮酚的提取条件进行了优化研究;以创新化合物对人肝癌细胞株HepG2细胞的抗肿瘤活性进行了筛选,获得效果较佳的化合物和最佳的试验浓度,通过对HepG2细胞生长抑制实验、诱导HepG2细胞凋亡分析及机制等的探讨,探索了一类结构简单、较低浓度下可以诱导体外及体内肿瘤细胞凋亡,而对正常细胞影响较小的新型有机胂药物. 相似文献
30.
Liu ZM Chen GG Vlantis AC Tse GM Shum CK van Hasselt CA 《Cellular and molecular life sciences : CMLS》2007,64(11):1428-1436
The molecular mechanism responsible for cadmium-induced cell death in thyroid cancer cells (FRO) is unknown. We demonstrated
that apoptosis of FRO cells induced by cadmium was concentration and time dependent. Cadmium caused the rapid elevation of
intracellular calcium and induced phosphorylation of Akt, p53, JNK, ERK and p38. Inhibition of PI3K/Akt attenuated the cadmium-induced
apoptosis, but the inhibition of JNK inhibitor, ERK or p38 aggravated it, indicating that activation of PI3K/Akt was a pro-apoptosis
signal in response to cadmium treatment, whereas the activation of stress-activated protein kinase JNK, ERK and p38 functioned
as survival signals to counteract the cadmium-induced apoptosis. Buffering of the calcium response attenuated mitochondrial
impairment, recovered the cadmium-activated Akt, p53, JNK, ERK and p38, and subsequently blocked the apoptosis. These results
suggested that apoptosis induced by cadmium in FRO cells was initiated by the rapid elevation of intracellular calcium, followed
by calcium-mediated activation of PI3K/Akt and mitochondrial impairment.
Received 28 February 2007; received after revision 2 April 2007; accepted 23 April 2007 相似文献