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鄭敏燮,吳旼錫,宋泰元 대전대학교 한의학연구소 2001 혜화의학회지 Vol.10 No.1
Through study of movement of Tae-Geuk-Guan(太極拳), we understand Tae-Geuk-Guan(太極拳) & essential movement. Theory about creator of Tae-Geuk-Guan(太極拳) is indistinct. there are Jangsampung-theory(張三豊設), Wangjongak-theory(王宗岳設), Jinwangjung-theory(陳王廷設), Jinbok-theory(陳卜設). Tae-Geuk-Guan(太極拳) is military arts developed before Song empire(宋). Tae-Geuk-Guan(太極拳) has many branch.(Jin-sik陳式, Yang-sik楊式, Mu-sik武式 O-sik吳式, Son-sik孫式) Tae-Geuk-Guan(太極拳) manual movement use fist(拳), palm(掌), hook shape(鉤), its using form has many type like Bung, Yi, Jae, An, Chae, Yul, Ju, Go. Its gait has many type like Sang-bo(上步), Tae-bo(退步), Jin-bo(進步), Deng-gak(댕脚), Bun-gak(分脚), Bak-gak(拍脚). Essential theory of Tae-Geuk-Guan(太極拳) is Yi-Sim-Hang-Gi(以心行氣) & Yi-Gi-Un-Sin(以氣運身). It means mind(心) moves and qi(氣) moves body(身).
Inhibitory Effects of Bee Venom on Growth of A549 Lung Cancer Cells via Induction of Death Receptors
Jang, Dong Min,Song, Ho Sueb Korean AcupunctureMoxibustion Medicine Society 2013 대한침구의학회지 Vol.31 No.4
This study was to investigated the effects of the bee venom on inhibition of cell growth via upregulation of death receptor expression in the A549 human lung cancer cells. Bee venom(1-5 ${\mu}g$/ml) inhibited the growth of A549 lung cancer cells by the induction of apoptotic cell death in a dose dependent manner. Consistent with apoptotic cell death, expression of TNFR1, Fas, death receptors(DR) 3, 4 and 6 was increased in the cells. Expression of DR downstream pro-apoptotic proteins including caspase-3, -9 and Bax was concomitantly increased, but the expression of Bcl-2, NF-${\kappa}B$ were inhibited by treatment with bee venom in A549 cells. Moreover, deletion of DR3, DR4 by small interfering RNA significantly reversed bee venom-induced cell growth inhibitory effect, whereas Apo3L strengthened anti-proliferative effect of bee venom through enhancement of DR3 expression. These results suggest that bee venom should exert anti-tumor effect through induction of apoptotic cell death in lung cancer cells via enhancement of death receptor expression, and that bee venom could be a promising agent for preventing and treating lung cancer.
민웅기 ( Woong Ki Min ),여수정 ( Su Jung Yeo ),김이화 ( Ee Hwa Kim ),송호섭 ( Ho Sueb Song ),구성태 ( Sung Tae Koo ),이재동 ( Jae Dong Lee ),임사비나 ( Sa Bi Na Lim ) 경락경혈학회 2013 Korean Journal of Acupuncture Vol.30 No.1
Objectives: The aim of this study was to investigate whether warm-needling is more effective than acupuncture in relieving the pain and improving the symptoms of knee osteoarthritis(OA). Methods: 76 volunteers with knee OA participated in the study. The subjects were randomly assigned to one of two groups. One group received warm-needling(n=38), while the other group received acupuncture(n=38). Sixteen sessions of warm-needling or acupuncture were conducted on the pain region of each problematic knee over a period of 8 weeks. The Western Ontario and McMaster Universities Osteoarthritis Index(WOMAC) scores, physical health score based on the 36-Item Short-Form Health Survey(SF-36) and the Global Assessment(PGA) was measured. Results: Compared to the acupuncture group, the warm-needling group showed a significant decrease in pain, function, and total WOMAC scores according to the Mann-Whitney U-test. The PGA scores of the warm-needling group also showed a significant improvement compared to the acupuncture group. Conclusions: Warm-needling showed a greater pain relief effect on knee OA compared to the acupuncture group. These findings suggest that warm-needling may be a promising alternative therapy for treating knee OA.
Kollipara, Pushpa Saranya,Kim, Jung Hyun,Won, Dohee,Lee, Sang Min,Sung, Ha Chang,Chang, Hyun Sok,Lee, Kang Tae,Lee, Kang Sik,Park, Mi Hee,Song, Min Jong,Song, Ho Sueb,Hong, Jin Tae 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.3
In the present study we experimented on a multimodal therapeutic approach, such as combining chemotherapy agent (Bee venom) with cellular (NK-92MI) immunotherapy. Previously bee venom has been found to show anti-cancer effect in various cancer cell lines. In lung cancer cells bee venom showed an $IC^{50}$ value of $3{\mu}g/ml$ in both cell lines. The co-culture of NK-92MI cell lines with lung cancer cells also show a decrease in viability upto 50 % at 48 h time point. Hence we used bee venom treated NK-92MI cells to co-culture with NSCLC cells and found that there is a further decrease in cell viability upto 70 and 75 % in A549 and NCI-H460 cell lines respectively. We further investigated the expression of various apoptotic and anti-apoptotic proteins and found that Bax, cleaved caspase-3 and -8 were increasing where as Bcl-2 and cIAP-2 was decreasing. The expression of various death receptor proteins like DR3, DR6 and Fas was also increasing. Concomitantly the expression of various death receptor ligands (TNFalpha, Apo3L and FasL) was also increasing of NK-92MI cells after co-culture. Further the DNA binding activity and luciferase activity of NF-${\kappa}B$ was also inhibited after co-culture with bee venom treated NK-92MI cell lines. The knock down of death receptors with si-RNA has reversed the decrease in cell viability and NF-${\kappa}B$ activity after co-culture with bee venom treated NK-92MI cells. Thus this new approach can enhance the anti-cancer effect of bee venom at a much lower concentration.
Park, Mi Hee,Jo, Miran,Won, Dohee,Song, Ho Sueb,Song, Min Jong,Hong, Jin Tae Rapid Science Publishers ; Kluwer Academic Publish 2012 Apoptosis Vol.17 No.12
<P>We investigated whether snake venom toxin (SVT) from Vipera lebetina turanica enhances the apoptosis ability of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in cancer cells. TRAIL inhibited HCT116 cell growth in a dose-dependent manner; however, this reduction did not occur in TRAIL resistant HT-29, A549 and HepG2 cells with an even higher dose of TRAIL. SVT, but not TRAIL enhanced expression of cell death receptor (DR) in TRAIL resistant cancer cells in a dose-dependent manner. A combination of SVT with TRAIL significantly inhibited cell growth of TRAIL resistant HT-29, A549 and HepG2 cells. Consistent with cell growth inhibition, the expression of TRAIL receptors; DR4 and DR5 was significantly increased as well as apoptosis related proteins such as cleaved caspase-3, -8, -9 and Bax. However, the expression of survival proteins (e.g., cFLIP, survivin, XIAP and Bcl2) was suppressed by the combination treatment of SVT and TRAIL. Depletion of DR4 or DR5 by small interfering RNA significantly reversed the cell growth inhibitory and apoptosis blocking effects of SVT in HCT116 and HT-29 cells. Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects. The collective results suggest that SVT facilitates TRAIL-induced apoptosis in cancer cells through up-regulation of the TRAIL receptors; DR4 and DR5 via ROS/JNK pathway signals.</P>
Ju Kyoung Song,Jin Tae Hong,Mi Ran Jo,Mi Hee Park,Ho Sueb Song,Byeong Jun An,Min Jong Song,Sang Bae Han 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.5
Snake venom toxin from Vipera lebetina turanica induces apoptosis in many cancer cell lines, but there is no study about the apoptotic effect of snake venom toxin on human ovarian cancer cells. In this study, we investigated the apoptotic effect of snake venom toxin in human ovarian cancer PA-1 and SK-OV3 cells. Snake venom toxin dose dependently (0~10 μg/mL) inhibited ovarian cancer cell growth with IC50 values 4.5 μg/mL in PA-1 cells, and 6.5 μg/mL in SKOV3 cells. Our results also showed that apoptotic cell death increased by snake venom toxin in a dose dependent manner (0~10 μg/mL). Consistent with increased cell death, snake venom toxin increased the expression of pro-apoptotic protein Bax and caspase-3, but down-regulated anti-apoptotic protein Bcl-2. Untreated ovarian cancer cells showed a high DNA binding activity of nuclear factor B (NF-κB), but it was inhibited by snake venom toxin accompanied by inhibition of p50 and p65 translocation into the nucleus as well as phosphorylation of inhibitory κB. Snake venom toxin also inhibited DNA binding activity of the signal transducer and activator of transcription 3 (STAT3). Moreover, the combination treatment of NF-κB (salicylic acid, 1 or 5 μM) and STAT3 (stattic, 1 μM) with snake venom toxin (1 μg/mL) further enhanced cell growth inhibitory effects of snake venom toxin. These results showed that snake venom toxin from Vipera lebetina turanica caused apoptotic cell death of ovarian cancer cells through the inhibition of NF-κB and STAT3 signal, and suggested that snake venom toxin may be applicable as an anticancer agent for ovarian cancer.
( Jin Tae Hong ),( Pushpa Saranya Kollipara ),( Do Hee Won ),( Chul Ju Hwang ),( Yu Yeon Jung ),( Heui Seoung Yoon ),( Mi Hee Park ),( Min Jong Song ),( Ho Sueb Song ) 한국응용약물학회 2014 Biomolecules & Therapeutics(구 응용약물학회지) Vol.22 No.2
In the present study, we investigated anti-cancer effect of snake venom activated NK cells (NK-92MI) in lung cancer cell lines. Weused snake venom (4 mg/ml) treated NK-92MI cells to co-culture with lung cancer cells. There was a further decrease in cancer cellgrowth up to 65% and 70% in A549 and NCI-H460 cell lines respectively, whereas 30-40% was decreased in cancer cell growthby snake venom or NK-92MI alone treatment. We further found that the expression of various apoptotic proteins such as that Bax,and cleaved caspase-3 as well as the expression of various death receptor proteins like DR3, DR4 and Fas was also further increased. Moreover, consistent with cancer cell growth inhibition, the DNA binding activity of NF-kB was also further inhibited aftertreatment of snake venom activated NK-92MI cells. Thus, the present data showed that activated NK cells could further inhibitlung cancer cell growth.