scholarly journals Induction of human leukemia U937 cell apoptosis by an ethanol extract of Dendropanax morbifera Lev. through the caspase-dependent pathway

2013 ◽  
Vol 30 (3) ◽  
pp. 1231-1238 ◽  
Author(s):  
JOON WOO LEE ◽  
CHEOL PARK ◽  
MIN HO HAN ◽  
SU HYUN HONG ◽  
TAE KYUNG LEE ◽  
...  
1999 ◽  
Vol 5 (3) ◽  
pp. 37
Author(s):  
Koichiro Kuwahara ◽  
Yoshihiko Saito ◽  
Ichiro Kishimoto ◽  
Masaki Harada ◽  
Ichiro Hamanaka ◽  
...  

2016 ◽  
Vol 7 (10) ◽  
pp. 1360-1373 ◽  
Author(s):  
Tsung Chi Lu ◽  
Guan- Hao Zhao ◽  
Yao Yun Chen ◽  
Chia-Ying Chien ◽  
Chi-Hung Huang ◽  
...  

Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3313 ◽  
Author(s):  
Seung-Sik Cho ◽  
Seung-Hui Song ◽  
Chul-Yung Choi ◽  
Kyung Park ◽  
Jung-Hyun Shim ◽  
...  

Dendropanax morbifera H. Levis a medicinal plant native to South Korea, East Asia, and South America. Among some 75 species, one species grows in Korea. In previous studies, D. morbifera extracts with anti-oxidant, anti-inflammatory, anti-complementary and anti-cancer activities were reported. The present study aims to investigate optimization of extraction and evaluation of anti-hyperuricemic effects of D. morbifera leaf and the phytochemicals contained therein. Ethanol and hexane extract were found to display the best xanthine oxidase inhibition among six types of solvent and water extract. The antioxidant effect of the ethanol extract was superior to that of the hexane extract. The DPPH radical scavenging effect of the ethanol and hexane extracts were 81.52 ± 1.57% and 2.69 ± 0.16. The reducing power of the ethanol and hexane extracts were 9.71 ± 0.15 and 0.89 ± 0.01 mg/g equivalent of gallic acid. Total phenols of the ethanol and hexane extracts were 6.53 ± 0.16 and 0.63 ± 0.001 mg/g equivalent of gallic acid. In addition, we compared the two marker compounds from D. morbifera, chlorogenic acid and rutin, which were determined in the ethanol extract at 0.80 ± 0.03% and 0.52 ± 0.01%, respectively. We found that the ethanol extracts showed better xanthine oxidase inhibition than hexane extracts. Especially, ethanol extracts showed higher antioxidant activity than hexane extracts. Based on these results, we selected the ethanol extract as an effective xanthine oxidase inhibitor and confirmed whether ethanol extracts showed xanthine oxidase inhibition in animal experiments. The in vivo mouse study demonstrated that ethanol extract of D. morbifera leaf at the dose of 300 mg/kg could inhibit blood/hepatic xanthine oxidase activity and this result shows that the xanthine oxidase inhibitory activity in vitro is reproduced in vivo. The present study showed that ethanol extract was optimal xanthine oxidase inhibitor which can be applied to prevent diseases related to hyperuricemia.


FEBS Journal ◽  
2009 ◽  
Vol 276 (7) ◽  
pp. 2022-2036 ◽  
Author(s):  
Xin Lin ◽  
Yu-Jun Wang ◽  
Qing Li ◽  
Yuan-Yuan Hou ◽  
Min-Hua Hong ◽  
...  

1998 ◽  
Vol 16 ◽  
pp. S221
Author(s):  
Stephen Brenneman ◽  
Robert Burns ◽  
Ard Vink ◽  
Erika Gaines ◽  
Anne Haake ◽  
...  

2004 ◽  
Vol 311 (1) ◽  
pp. 115-122 ◽  
Author(s):  
Masuo Kondoh ◽  
Ikue Suzuki ◽  
Masao Sato ◽  
Fumihiro Nagashima ◽  
Siro Simizu ◽  
...  

2019 ◽  
Vol 47 (04) ◽  
pp. 895-912 ◽  
Author(s):  
Ming-Chung Lin ◽  
Yuan-Wen Lee ◽  
Yuan-Yun Tseng ◽  
Yung-Wei Lin ◽  
Jui-Tai Chen ◽  
...  

In children, neuroblastomas are the most common and deadly solid tumor. Our previous studies showed that honokiol can cross the blood–brain barrier and kill neuroblastoma cells. In this study, we further evaluated if exposure to honokiol for short periods could induce autophagy and subsequent apoptosis of neuroblastoma cells and possible mechanisms. Exposure of neuroblastoma neuro-2a cells to honokiol for 24[Formula: see text]h induced morphological shrinkage and cell death. As to the mechanisms, honokiol consecutively induced cytochrome c release from mitochondria, caspase-3 activation, DNA fragmentation and cell apoptosis. Separately, honokiol time-dependently augmented the proportion of autophagic cells and the ratio of light chain 3 (LC3)-II/LC3-I. Pretreatment of neuro-2a cells with 3-methyladenine, an inhibitor of autophagy, attenuated honokiol-induced cell autophagy, caspase-3 activation, DNA damage and cell apoptosis. In contrast, stimulation of autophagy by rapamycin, an inducer of autophagy, significantly enhanced honokiol-induced cell apoptosis. Furthermore, honokiol-induced autophagic apoptosis was confirmed in neuroblastoma NB41A3 cells. Knocking down translation of p53 using RNA interference attenuated honokiol-induced autophagy and apoptosis in neuro-2a and NB41A3 cells. Taken together, this study showed that at early periods, honokiol can induce autophagic apoptosis of neuroblastoma cells through activating a p53-dependent mechanism. Consequently, honokiol has the potential to be a therapeutic option for neuroblastomas.


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