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T 세포 및 대식세포 기능에 대한 Silybin의 조절효과
조재열,Cho, Jae-Youl 대한약학회 2007 약학회지 Vol.51 No.4
Silybin is known to be a major active flavonoid component isolated from Silybum marianum, a hepatoprotective medicinal plant. In this study, we examined the immunomodulatory role of silybin on T cell and macrophage-mediated immune responses. To do this, the proliferation of splenic lymphocytes and CD8+ CTLL-2 cells under mitogenic stimulation with lipopolysaccharide (LPS), concanavalin (Con) A and interleukin (IL)-2 and the production of $TNF-{\alpha}$ and NO from LPS- and $IFN-{\gamma}$-activated macrophages was evaluated under silybin treatment. The mitogenic proliferation of splenic lymphocytes induced by LPS and Con A was strongly diminished by silybin in a dose-dependent manner. Moreover, the proliferation of CD8+ CTLL-2 cells was also negatively modulated by the compound. In contrast, silybin did not strongly suppress the proliferation of normal splenocytes and T cell line Sup-T1 cells, indicating that the inhibitory effect of silybin may be due to blocking only mitogenic responses of splenic lymphocytes. In addition, silybin inhibited $TNF-{\alpha}$ production in LPS-stimulated RAW264.7 cells. Effect of silybin however was distinct, according to NO-inducing stimuli. Thus, silybin only blocked NO production induced by $IFN-{\gamma}$ but not LPS and the inhibition was increased when PMA was co-treated with $IFN-{\gamma}$. Unlike NO inhibition, however, this compound protected the cytotoxic damage of RAW264.7 cells induced by both LPS and $IFN-{\gamma}$. Therefore, our data suggest that silybin may participate in host immune responses mediated by T cells and macrophages via regulating mitogenic proliferation, and the production of $TNF-{\alpha}$ and NO, depending on cellular stimuli.
S. abortus 유래 LPS와 E. coli 유래 LPS에 의한 패혈증성 쇽 유도 작용 비교
조재열,유은숙,Cho, Jae-Youl,Yoo, Eun-Sook 대한약학회 2007 약학회지 Vol.51 No.1
Acute septic shock is one of inflammatory diseases mediated by pro-inflammatory cytokines such as tumor necrosis factor (TNF)-${\alpha}$. In this study, we examined the pathological difference and mechanism of lipopolysaccharides isolated from E. coli (E-LPS) or S. abortus (S-LPS) on inducing acute septic shock in ICR mouse. All mice were died by intraperitoneal treatment of S-LPS with 0.75 mg/kg, whereas E-LPS treated with even 3 mg/kg only showed 30% of mice lethal, indicating that S-LPS may be more feasible in triggering a strong septic shock condition. The secretion pattern of TNF-${\alpha}$, a critical pro-inflammatory cytokine in septic shock condition, was also distinct between E-LPS- and S-LPS-treated groups. Thus, S-LPS strikingly increased serum level of TNF-${\alpha}$ (6 ng/ml) at 1 h, while E-LPS just displayed at 2 ng/ml level. However the interaction of S-LPS with LPS receptor toll like receptor (TLR)-4, was not stronger than that of E-LPS, according to experiments with macrophage cell line RAW264.7 cells. Thus, E-LPS rather than S-LPS strongly enhanced the production of TNF-${\alpha}$. Interestingly, S-LPS more strongly up-regulated splenocyte proliferation, compared to E-LPS group, whereas there was no difference between S- or E-LPS treated groups in proliferation of Balb/c- or C57BL/6-originated splenic lymphocytes. Therefore, our data suggest that S-LPS is a more active endotoxin and that the strong septic shock-inducing effect of S-LPS seems due to the enhancement of early TNF-${\alpha}$ production and S-LPS-sensitive lymphocyte proliferation.
인삼 사포닌류가 종양괴사인자의 생성 및 T 세포 증식에 미치는 효과
조재열(Jae Youl Cho),박지수(Ji Soo Park),유은숙(Eun Sook Yoo),백경업(Kyong Up Baik),박명환(Myung Hwan Park),한병훈(Byung Hoon Han) 대한약학회 1998 약학회지 Vol.42 No.3
To investigate the effects of ginsenosides from Panax ginseng on mitogenic responses in macrophages and splenocytes from murine, we examined the effects of representative protopanaxadiol and protopanaxatriol ginsenosides (Rb1, Rb2, Re and Rg1) on tumor necrosis factor-alpha (TNF-(alpha) production in and smurine macrophage cell line (RAW264.7 cells) stimulated by lipopolysaccharide (LPS) and T cell proliferation in splenocytes stimulated by concanavalin A (Con A). Among the ginsenosides tested, protopanaxadiol ginsenosides (Rb1 and Rb2) significantly inhibited TNF-alpha production in a dose-dependent manner. However, protoppanaxatriol ginsenosides (Re and Rg1) showed little inhibitory activity. The molar concentrations of Rb1 and Rb2 producing 50% inhibition (IC50) of TNF-alpha production were 55.8mcg/ml (48.0mcM) and 31.8mcg/ml (27.9mcM), respectively. As a positive control, prednisolone also exhibited inhibitory activity with an IC50 value of 21.7mcM. In T cell proliferation, Rg1, was not effective but Rb1 and Re or Rb2 significantly increased or inhibited at high concentration, 75 and 100mcg/ml. In contrast, prednisolone showed potent inhibitory activity with an IC50 value of 6.1nM. These results suggest that ginsenosides may take part in the mitogen-induced signaling pathway for TNF-alpha production and T cell proliferation from macrophages splenocytes.
조재열(Jae Youl Cho),김성수(Hyang Woo Lee),이향우(Hyang Woo Lee),홍성렬(Sungyoul Hong) 대한약학회 2001 약학회지 Vol.45 No.1
Protein carboxy O-methylation is a kind of enzymatic reaction producing carboxy methylester catalyzed protein carboxyl O-methyltransferases at the carboxyl group of amino acid residues in polypeptide. Since the finding of carboxyl methylester, many studies have been focused on the understanding of biological functions in eukaryotes but still not clear except for roles in Ras attachment to membrane and protein repair. In this study, we investigated the protein carboxyl methylation in porcine liver and testis in repect of identification and characterization of carboxyl methylesters and natural proteinous substrates using pH stability of the esters and electrophoresis under acidic and bacis conditions. We detected several kinds of methyl esters, 3 kimds each in cytosolic fractions from liver and testis. Under the treatment of strong acid and base, the ratio between base- stable substrates and unstable ones in liver (4:6) was different from the ratio obtainde in testis (6:4). The methyl accepting capacities were affected by enzymatic proteolysis between the range of 55 to 65% in liver and of 35 to 45% in testis. Separation of the methylated proteins by acidic elelctrophoresis in the presesnce of urea and SDS revealed distinctively natural substrates of 26, 33 and 80kD in the cytosol from liver, and of 14, 25, 32 and 86kD from testis. Most of the labelling, however, were lost following electrophoreses under moderare alkaline condition, except fot molecules of newly detected 7 and 17kD in liver, and 15, 29, 40 and 80kD in testis. From these results, it was proposed that protein carboxyl O-methylation in each organs may be catalyzed by different classes of protein carboxyl O- methyltransferases. In addition, it is suggested that the protein carboxyl methylation in liver and testis may have different patterns in respect of natural substrates.
Ginsenoside Rg3 및 그 유도체 Ginsenoside Rg3-2H의 NO 생성 및 lymphocyte 분열 억제 효과
조재열(Jae Youl Cho) 고려인삼학회 2008 Journal of Ginseng Research Vol.32 No.3
Ginsenosides are major components in Panax ginseng and known to have numerous pharmacological activities such as anti-cancer, anti-diabetes, anti-viral and anti-atherosclerosis effects. In this study, the regulatory activities of G-Rg3 and its derivative 25-hydroxy Rg3 (G-Rg3-2H) on the production of nitric oxide (NO) in macrophages and the proliferation of lymphocytes prepared from spleen and bone marrow under treatment of lipopolysaccharide (LPS) or concanavalin (Con) A were examined. G-Rg3 and G-Rg3-2H dose-dependently inhibited NO production from LPS-activated RAW264.7 cells and in agreement, these compounds protected RAW264.7 cells from LPS-mediated cytotoxicity. In contrast, G-Rg3-2H dose-dependently inhibited lymphocyte proliferation induced by both LPS and Con A, while there was no inhibition by G-Rg3. Therefore, our data suggest that these compounds may be applied for NO-mediated or lymphocyte- mediated immunological diseases.