Demonstration of the induction of apoptosis (programmed cell death) by tetrandrine, a novel anti-inflammatory agent

1991 ◽  
Vol 13 (8) ◽  
pp. 1117-1126 ◽  
Author(s):  
B.S. Teh ◽  
P. Chen ◽  
M.F. Lavin ◽  
W.K. Seow ◽  
Y.H. Thong
1997 ◽  
Vol 328 (1) ◽  
pp. 307-316 ◽  
Author(s):  
Rei-Huang HU ◽  
E. Anthony PEGG

Treatment of Chinese hamster ovary cells with α-difluoromethylornithine for 3 days, followed by exposure to cycloheximide, led to an unregulated, rapid and massive accumulation of polyamine analogues. This accumulation led to cell death by apoptosis within a few hours. Clear evidence of DNA fragmentation was seen in response to both N-terminally ethylated polyamines and to polyamines containing methyl groups on the terminal carbon atoms. Programmed cell death was induced within 2-4 h of exposure to 1 μM or higher concentrations of N1,N11-bis(ethyl)norspermine. The presence of cycloheximide increased the uptake of the polyamine analogues and therefore led to cell death at lower analogue concentrations, but it was not essential for the induction of apoptosis, since similar effects were seen when the protein synthesis inhibitor was omitted and the concentration of N1,N11-bis(ethyl)norspermine was increased to 5 μM or more The induction of apoptosis was blocked both by the addition of the caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, or by the addition of the polyamine oxidase inhibitor N1-methyl-N2-(2,3-butadienyl)butane-1,4-diamine (MDL 72,527). These experiments provide evidence to support the concepts that: (1) polyamines or their oxidation products may be initiators of programmed cell death; (2) regulation of polyamine biosynthesis and uptake prevents the accumulation of toxic levels of polyamines; and (3) the anti-neoplastic effects of bis(ethyl) polyamine analogues may be due to the induction of apoptosis in sensitive tumour cells.


1993 ◽  
Vol 61 (12) ◽  
pp. 5044-5048 ◽  
Author(s):  
Y H Zhang ◽  
K Takahashi ◽  
G Z Jiang ◽  
M Kawai ◽  
M Fukada ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yumei Zhong ◽  
Deli Lai ◽  
Linlin Zhang ◽  
Wenting Lu ◽  
Yanan Shang ◽  
...  

Objective. Rheumatoid arthritis (RA) is an autoimmune disease that starts with inflammation of the synovium. The pain and joint dysfunction caused by RA urgently need an effective treatment to alleviate the inflammatory reaction and delay the progression of the disease. The pathological damage of RA is proposed to associate with the dysfunction of the programmed cell death 1/programmed cell death ligand 1 (PD-1/PD-L1) pathway. Moxibustion, as a main complementary therapy of traditional Chinese medicine (TCM), has been proved effective to reduce chronic inflammatory reaction on RA, but whether the anti-inflammatory effects are mediated by PD-1/PD-L1 pathway is still unclear. Therefore, moxibustion was conducted in the rats with RA to investigate its effect on PD-1/PD-L1. Methods. The rats' right hind paws were injected with Freundʼs complete adjuvant (FCA) to establish the model of RA. Seven days after the injection of FCA, moxibustion therapy was performed on the acupoints of Shenshu (BL23) and Zusanli (ST36) once a day for three weeks. Then, ELISA and immunohistochemical methods were used to analyze the influence of moxibustion on the expression of PD-1/PD-L1. If the moxibustion had an effect on the expression of PD-1/PD-L1-related molecules, we would knock down PD-1 with adenovirus vector. After moxibustion therapy, ELISA and histological analysis were performed to observe the anti-inflammatory effect of moxibustion. Results. The results demonstrated that moxibustion had an effect on the expression of PD-1-related molecules. The results of ELISA manifested that moxibustion decreased the level of IFN-γ and increased the level of IL-4 and IL-10. HE staining revealed that moxibustion alleviated the proliferation of synovial tissue. However, the anti-inflammatory effect and pathological improvement were weakened when PD-1 was blocked. Conclusions. The results indicate that moxibustion affected the expression of PD-1/PD-L1-related molecules and can effectively treat RA damage. The anti-inflammatory effect of moxibustion was weakened when PD-1 was knocked down.


2011 ◽  
Vol 213 (3) ◽  
pp. S54-S55
Author(s):  
Sean F. Monaghan ◽  
Rajan K. Thakkar ◽  
Chun S. Chung ◽  
Yaping Chen ◽  
Daithi S. Heffernan ◽  
...  

2005 ◽  
Vol 20 (3) ◽  
pp. 482-484 ◽  
Author(s):  
Tarek A. Taha ◽  
Kazuyuki Kitatani ◽  
Mazen El‐Alwani ◽  
Jacek Bielawski ◽  
Yusuf A. Hannun ◽  
...  

2021 ◽  
Author(s):  
Mehmet Evren Okur ◽  
Panoraia I. Siafaka ◽  
Merve Tutar ◽  
Yusuf Tutar

Apoptosis, known as programmed cell death, has been considered a potent target for the pharmacy industry. The scientific community has actively participated to research which evaluate active molecules for possible inhibition or induction of apoptosis. Nanocarriers especially for cancer targeting are widely found through literature; they mainly based on inorganic, lipid or polymer nanoparticles which incorporate anticancer drugs. Another important and innovative category of anticancer agents is that of microRNAs. In this chapter, a discussion about the most recent applications of apoptosis-based agents mainly focusing on cancer target is done.


2018 ◽  
Vol 19 (9) ◽  
pp. 2695 ◽  
Author(s):  
Eun-A Kim ◽  
Yuling Ding ◽  
Hye-Won Yang ◽  
Soo-Jin Heo ◽  
Seung-Hong Lee

Marine-derived extract and/or bioactive compounds have attracted increasing demand due to their unique and potential uses as cures for various inflammation-based diseases. Several studies revealed anti-inflammatory candidates found in soft corals. However, the effects of soft corals on inflammation in an in vivo model remain to be determined. Therefore, the extract of soft coral Dendronephthya puetteri (DPE) was investigated for an in vivo anti-inflammatory effect in a lipopolysaccharide (LPS)-stimulated zebrafish model to determine its potential use as a natural anti-inflammatory agent. We also investigated whether DPE has toxic effects in a zebrafish model. No significant changes were observed in terms of survival, heart beat rate, or developmental abnormalities in the zebrafish embryos exposed to a concentration below 100 µg/mL of DPE. Treating the zebrafish model with LPS-treatment significantly increased the ROS, NO generation, and cell death. However, DPE inhibited this LPS-stimulated ROS, NO generation, and cell death in a dose-dependent manner. In addition, DPE significantly reduced the mRNA expression of both iNOS and COX-2 and markedly suppressed the expression levels of the proinflammatory cytokines, TNF-α and IL-6, in an LPS-stimulated zebrafish model. These findings demonstrate that DPE has profound anti-inflammatory effect in vivo, suggesting that DPE might be a strong natural anti-inflammatory agent.


2011 ◽  
Vol 63 (3) ◽  
pp. 527-535
Author(s):  
G. Brajuskovic ◽  
Milica Strnad ◽  
Snezana Cerovic ◽  
Stanka Romac

Apoptosis or programmed cell death is a genetically regulated process of cellular suicide. Apoptosis has been implicated in a wide range of pathological conditions, and mutations in apoptotic genes play important roles in the process of malignant transformation. Chronic leukemia represents a neoplastic disorder caused primarily by defective programmed cell death, as opposed to increased cell proliferation. This paper presents the main results of our ten-year research on the apoptosis of leukemia cells. The research included the morphological aspects of the process, the effect of antineoplastic agents on the induction of apoptosis in leukemia cells and expression analysis of the proteins involved in programmed cell death. Special attention was paid to the expression and interaction of the Bcl-2 family of proteins in leukemia cells. The ultimate aim of the study of apoptosis of leukemic cells is the discovery of new biological agents that might be used in the treatment of chronic leukemia.


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