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소목(蘇木)이 사람 간암 세포주인 HepG2의 세포사멸에 미치는 영향과 그 경로
김판준,윤현정,이영태,서교수,박선동,Kim, Pan-Jun,Yun, Hyun-Joung,Lee, Young-Tae,Seo, Kyo-Soo,Park, Sun-Dong 대한한의학방제학회 2005 大韓韓醫學方劑學會誌 Vol.13 No.2
The purpose of this study was to investigate the anticancer effects of Caesalpiniae Lignum (Somok) on HepG2 cells, a human liver cancer cell line. To study the cytotoxic effect of Caesalpiniae Lignum methanol extract (CL-MeOH) on HepG2 cells, the cells were treated with various concentrations of CL-MeOH and then cell viability was determined by XTT reduction method and trypan blue exclusion assay. CL-MeOH reduced proliferation of HepG2 cells in a dose-dependent manner. To confirm the induction of apoptosis, HepG2 cells were treated with various concentrations of CL-MeOH. The activation of caspase 3 and the cleavage of poly ADP-ribose polymerase (PARP), a substrate for caspase-3 and a typical sign of apoptosis, was examined by western blot analysis. CL-MeOH decreased procaspase 3 level in a dose-dependent manner and induced the clevage of PARP at concentration> $200{\mu}/ml$. Mitogen-activated protein (MAP) kinase signaling cascades are multi-functional signaling networks that influence cell growth, differentiation, apoptosis, and cellular responses to stress. CL-MeOH-induced MAPK activation was examined by Western blot for phosphorylated ERK, p38 and JNK. CL-MeOH significantly increased p38 phosphorylation and JNK phosphorylation in a dose-dependent manner. Inhibition of p38 function using the selective inhibitor SB20358O results in inhibition of apoptosis by CL-MeOH. These results suggest that CL-MeOH-induced apoptosis is MAP kinase-dependent apoptoric pathway. These results suggest that CL-MeOH is potentially useful as a chemotherapeutic agent in human liver cancer.
최재우,배창욱,박소영,윤현정,박선동,Choi, Jae-Woo,Bae, Chang-Wook,Park, So-Young,Yun, Hyun-Joung,Park, Sun-Dong 대한한의학방제학회 2005 大韓韓醫學方劑學會誌 Vol.13 No.1
Acetaminophen, which causes acute liver min in humans and animals, has made useful inducer of hepatoxicity for studying hepatopreventive drugs. Injinhotang is known as one of the hepatopreventive drugs. However, its mechanism of recovery of hepatoxicity treated with acetaminophen is poorly understood. this study was performed to observe the antioxidative effect of injinhotang extract and its several combination groups. The results were obtained as follows:1. In the study on free radical scavenging effect in vitro(the suppressing effect on peroxidation of linoleic acid on concentration, the scavenging effect of DPPH radical, inhibitory effect of superoxide in xanthine-xanthine oxidase system and the inhibitory effect on lipid peroxidation reaction by hydroxy radical in H2O2-Fe2+system, injinhotang have more effect than its components groups relatively. 2. In the study on antioxidants system in vivo(the level of serum LPO, the level of hepatic LPO, catalase, GSH, GST), only injnhotang has a significant effect. 3. In the study on hepatotoxicity(GOT, GPT, $\gamma$-GTP, ALP, LDH, b ilirubin), only injinhotang has a significant effect. These results suggest that injinhotang has the protective effect on acetaminophen-induced hepatoxicity. The mechanisms of these are supposed to be involved in antioxidant and three drugs' cooperative synergy effect.