암환자의 혈청 중 Putrescine, Spermidine 및 Spermine의 분리 정량

신태용,이석봉,김대근,채병숙 우석대학교 의약품개발연구소 1997 藥學硏究誌 Vol.2 No.-

A high performance liquid chromatographic method developed for the determination of polyamines(putrescine, spermidine and spermine) in the serum of normal human and cancer patients. The benzoyi chloride derivatives of polyamines are separated on a uBondapak C_18 reverse-phase column with methanol/water(50v/50v) as the mobile phase. The results show that the mean level of polyamines in concer patients serum is much higher than that in normal human serum.

사인에 의한 즉시형 과민반응의 억제 효과

신태용,염정열,김원,김현미,박해정,장진이,조성룡,채병숙 우석대학교 생명과학연구소 1998 생명과학연구소 논문집 Vol.2 No.-

We investigated the effect of aqueous extract of Ammomum xanthioides(AXAE) on immediate hypersensitivity. AXAE inhibited systemic anaphylaxis induced by compound 48/80 in mice. AXAE inhibited serum histamine levels induced by compound 48/80 in mice. Moreover, AXAE dose-dependently inhibited histamine release in peritoneal mast cells activated by compound 48/80. These results indicate that the AXAE may be benificial in the regulation of immediate type allergic reaction.

승마 추출물의 항알레르기 효과

신태용(Tae Yong Shin),서형만(Hyung Man Seo),채병숙(Byeong Suk Chae) 대한약학회 1998 약학회지 Vol.42 No.4

Effects of the aqueous extract of Cimicifuga heracleifolia (CHAE) on the allergic reactions were investigated. CHAE inhibited systemic anaphylaxis induced by compound 48/80 in mice dose-dependently. Especially, CHAE inhibited compound 48/80-induced systemic anaphylaxis 100% with a dose of 0.5mg/g body weight. CHAE significantly inhibited serum histamine levels induced by compound 48/80. CHAE inhibited histamine release from the rat peritonea] mast cells activated by compound 48/80 or anti-DNP IgE. Our studies provide evidence that CHAE will be beneficial in the treatment of anaphylias.

Persistent development of LPS-induced acute lung injury in pristane-primed chronic inflammation mice : the role of IL-6

Byeong Suk Chae,Jeong Suk Park,Hye Young Shin,Dae Keun Kim,Tae Yong Shin 환경독성보건학회 2005 한국독성학회 심포지움 및 학술발표회 Vol.- No.-

Prostaglandin $E_2-Mediated$ Dysregulation of Proinflammatory Cytokine Production in Pristane-Induced Lupus Mice

Chae, Byeong-Suk,Shin, Tae-Yong,Kim, Dae-Keun,Eun, Jae-Soon,Leem, Jae-Yoon,Yang, Jae-Heon 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.4

Systemic lupus erythematosus (SLE) is characterized by inflammatory and dysregulatory immune responses including overactive B cells, overproduction of proinflammatory cytokines, and T cell hyperactivity. $PGE_2$ modulates a variety of immune processes at sites of inflammation, including production of inflammatory cytokines. However, the role of $PGE_2$ in dysregulatory inflammatory and immune responses in lupus remains unclear. We investigated whether $PGE_2$ mediates production of inflammatory cytokines in pristane-induced lupus BALB/c mice. Our results showed that levels of serum and BAL $PGE_2$ and LPS-stimulated production of $PGE_2$ by peritoneal macrophages were remarkably increased in pristane-induced lupus mice compared to healthy controls. Exogenous $PGE_2$ enhanced production of IL-6, IL-10, and NO but decreased $TNF-{\alpha}$ by macrophages and augmented $IFN-{\gamma}$, IL-6, and IL-10 by splenocytes from pristane-induced lupus mice compared to healthy controls. Exogenous $PGE_2$ also enhanced production of $IFN-{\gamma}$, IL-6, and IL-10 by thymocytes from pristane-induced lupus mice. Indomethacin (Indo), a $PGE_2$ synthesis inhibitor, greatly inhibited LPS-induced production of IL-6 and IL-10 by macrophages from pristane-induced lupus mice, while enhanced $TNF-{\alpha}$. Indo remarkably inhibited Con A-increased production of $IFN-{\gamma}$, IL-6, and IL-10 by splenocytes and thymocytes from pristane-induced lupus mice. Therefore, our findings suggest that endogenous $PGE_2$ may mediate dysregulation of production of proinflammatory cytokines, such as IL-6, IL-10, and $IFN-{\gamma}$, and NO in pristane-induced lupus mice.

Effects of Swainsonine on the Humoral Immune Response of Lipopolysaccharide

Chae, Byeong-Suk,Ahn, Young-Keun,Kim, Joung-Hoon The Pharmaceutical Society of Korea 1997 Archives of Pharmacal Research Vol.20 No.6

Effects of swainsonine (SW;8${\alpha}$, ${\beta}$-indolizidine-${\alpha}$, $2{\alpha}$8-triol from Locoweed) on the humoral immune responses of lipopolysaccharide (LPS) wer studied in ICR mice. Mice were divided into 4 groups (10 mice/group), and LPS was given to each mouse 1 hr after i.p. injection with 3.7 mg/kg of swainsonine, by i.p. injection twice a week for 14 days at a dose of 2 mg/kg. Humoral immune responses were evaluated by hemagglutination (HA) titer and splenic plaque forming cells (PFC). The results of this study were summarized as follows: Mice administrated each of LPS and SW showed significant enhancement of the weight ratios of spleen to body, HA titer, 2-mercaptoethanol-resistant HA(MER-HA) titer and PFC compared with those in controls. However, the LPS plus SW treatment decreased HA titer, MER-HA titer and PFC corresponding to humoral immunity, as compared with those in the mice treated with LPS alone. These findings indicated that LPS significantly enhanced humoral immune responses, but their enhancement effects were lowered somewhat by SW.

Comparative Study of the Endotoxemia and Endotoxin Tolerance on the Production of Th Cytokines and Macrophage Interleukin-6: Differential Regulation of Indomethacin

Chae, Byeong-Suk The Pharmaceutical Society of Korea 2002 Archives of Pharmacal Research Vol.25 No.6

Endotoxin tolerance reduces the capacity of monocytes to produce proinflammatory cytokines, results in cellular immune paralysis, and down-regulates the production of helper T (Th)1 type cytokines with a shift toward a Th2 cytokine response. Prostaglandin (PG)E$_2$ in the immune system also results in macrophage inactivation and the suppression of Th1 activation and the enhancement of Th2 activation. However, the inhibitory effects of PGE$_2$ on the altered polarization of the Th cell and macrophage interleukin (IL)-6 production characterized in part by cellular immune paralysis in a state of endotoxin tolerance is unclear. This study was undertaken, using indomethacin, to investigate the role of endogenous PGE$_2$ on the Th cytokines and macrophage IL-6 production in a state of endotoxin tolerance compared to those with endotoxemia mice, wherein, in this latter case, the increased production of proinflammatory cytokines and PGE$_2$ is exhibited. Endotoxemia was induced by injection of lipopolysaccharide (LPS; 10 mg/kg in saline) i.p. once in BALB/c mice, and endotoxin tolerance was induced by pretreatment with LPS (1 mg/kg in saline) injected i.p. daily for two consecutive days and then with LPS 10 mg/kg on day 4. Splenocytes or macrophages were obtained from endotoxemia and endotoxin tolerance models pretreated with indomethacin, and then cytokine production was induced by Con A-stimulated splenocytes for the Th cytokine assays and LPS-stimulated macrophages for the IL-6 assay. Our results showed that endotoxemia led to significantly reduced IL-2 and IL-4 production, to significantly increased IL-6 production, whereas interferon $(IFN)-{\gamma}$ production was not affected. Indomethacin in the case of endotoxemia markedly attenuated $IFN-{\gamma}$ and IL-6 production and didnt reverse IL-2 and IL-4 production. Endotoxin tolerance resulted in the significantly reduced production of IL-2 and $IFN-{\gamma}$ and the significantly increased production of IL-4 and IL-6. Indomethacin in endotoxin tolerance greatly augmented IL-2 production, significantly decreased IL-4 production, and slightly attenuated IL-6 production. These findings indicate that endogenous PGE$_2$ may mediate the suppressed Th1 type immune response, with a shift toward a Th2 cytokine response in a state of endotoxin tolerance, whereas endotoxemia may be regulated differentially. Also, endogenous PGE$_2$ may mediate macrophage IL-6 production in the case of endotoxemia to a greater extent than in the case of endotoxin tolerance.

Endotoxin Induces Late Increase in the Production of Pulmonary Proinflammatory Cytokines in Murine Lupus-Like Pristane-Primed Modelp

Chae Byeong-Suk,Park Jeong-Suk,Shin Tae-Yong The Pharmaceutical Society of Korea 2006 Archives of Pharmacal Research Vol.29 No.4

Lupus-like syndrome is characterized by multiple organ injuries including lungs and kidneys. Endotoxin induces a transiently intent systemic inflammatory response and indirectly transient acute lung injury in normal condition. However, whether endotoxin may trigger the persistent development of lung injury in chronic, inflammatory lupus-like syndrome compared with normal condition remains unclear. We examined the pulmonary vascular permeability and production of proinflammatory cytokines, such as TNF-${\alpha}$, IL-6, IL-10 and IFN-${\gamma}$, which play prominent roles in the pathogenesis of lupus-like tissue injury, 6 hand 72 h after i.p. lipopolysaccharide (LPS; endotoxin) injection in pristane-primed chronic inflammation ICR mice characterized by a lupus-like syndrome. These results demonstrated that levels of serum IL-6, IL-10 and IFN-${\gamma}$ and bronchoalveolar lavage (BAL) IL-6 and IFN-${\gamma}$ were remarkably increased 6 h in LPS-exposed pristane-primed mice compared with pristane-primed controls, while pulmonary vascular permeability and levels of serum and BAL TNF-${\alpha}$ were not. And levels of BAL TNF-${\alpha}$, IL-6 and IL-10 were significantly enhanced 72 h in LPS-exposed pristane-primed mice compared with pristane-primed controls. Also, LPS significantly induced the increased in vitro production of TNF-${\alpha}$, IL-6 and IL-10 by lung cells obtained from LPS-exposed pristane-primed mice compared with LPS-exposed normal mice. Our findings indicate that LPS may trigger persistent progression of lung injury through late overproduction of BAL TNF-${\alpha}$, IL-6, and IL-10 in lupuslike chronic inflammation syndrome compared with normal condition.

Effect of low-dose corticosterone pretreatment on the production of inflammatory mediators in super-low-dose LPS-primed immune cells

Chae Byeong Suk 한국독성학회 2021 Toxicological Research Vol.37 No.1

Pretreatment of super-low-dose lipopolysaccharide (SL-LPS) induces a more hyperresponsive state on the production of proinflammatory mediators to a subsequent secondary challenge with high-dose LPS in innate immune cells. Low-dose glucocorticoids (GCs) are also known to induce inflammation and immunosuppression in the immune cells. However, there is limited knowledge on whether preconditioning of low-dose GCs enhances inflammatory responses and dysregulates T lymphocyte responses to secondary LPS in SL-LPS-primed immune cells. In the present study, RAW 264.7 and EL4 cells were pretreated with SL-LPS (50 pg/ml) or low-dose corticosterone (CORT50: 50 ng/ml and CORT100: 100 ng/ml) in fresh complete medium once a day for 2–3 days, consecutively, and then cultured in fresh complete medium for 6 or 24 h in the presence or absence of LPS (1–10 μg/ml) or concanavalin A (Con A). The results demonstrated that the repeated pretreatment of CORT50 strongly enhanced production of IL-6, IL-10, TNF-α, and nitric oxide (NO) by RAW 264.7 cells in EP (SL-LPS-primed cells: endotoxin priming) in the absence of LPS compared to those in control (vehicle-pretreated cells), whereas CORT100 reduced production of TNF-α and IL-10. Further, the repeated pretreatment of CORT50 markedly enhanced LPS-induced production of IL-6, IL-10, TNF-α, PGE2, and NO by RAW 264.7 cells in EP compared to those in control, whereas CORT100 attenuated LPS-induced production of IL-6, IL-10, and NO. Moreover, the repeated pretreatments of CORT50 and CORT100 greatly attenuated the Con A-stimulated production of IFN-γ and IFN-γ/IL-10 and LPSstimulated production of IL-10, IFN-γ, and IFN-γ/IL-10 by SL-LPS-primed EL4 cells (EP). These findings suggest that double preconditionings of low grade hypercortisolemia and metabolic endotoxemia may act as important risk factors for metabolic disorder and severe morbidity and mortality in septic shock via upregulated production of inflammatory mediators and immunosuppression of IFN-γ-mediated responses.

Pretreatment of Low-Dose and Super-Low-Dose LPS on the Production of In Vitro LPS-Induced Inflammatory Mediators

Byeong Suk Chae 한국독성학회 2018 Toxicological Research Vol.34 No.1

Pretreatment of low-dose lipopolysaccharide (LPS) induces a hyporesponsive state to subsequent secondary challenge with high-dose LPS in innate immune cells, whereas super-low-dose LPS results in augmented expression of pro-inflammatory cytokines. However, little is known about the difference between super-low-dose and lowdose LPS pretreatments on immune cell-mediated inflammatory and hepatic acute-phase responses to secondary LPS. In the present study, RAW 264.7 cells, EL4 cells, and Hepa-1c1c7 cells were pretreated with super-low-dose LPS (SL-LPS: 50 pg/mL) or low-dose LPS (L-LPS: 50 ng/mL) in fresh complete medium once a day for 2~3 days and then cultured in fresh complete medium for 24 hr or 48 hr in the presence or absence of LPS (1~10 μg/mL) or concanavalin A (Con A). SL-LPS pretreatment strongly enhanced the LPS-induced production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, TNF-α/IL-10, prostaglandin E2 (PGE2), and nitric oxide (NO) by RAW 264.7 cells compared to the control, whereas L-LPS increased IL-6 and NO production only. SL-LPS strongly augmented the Con A-induced ratios of interferon (IFN)-γ/IL-10 in EL4 cells but decreased the LPS-induced ratios of IFN-γ/IL-10 compared to the control, while L-LPS decreased the Con A- and LPS-induced ratios of IFN-γ/IL-10. SL-LPS enhanced the LPS-induced production of IL-6 by Hepa1c1c-7 cells compared to the control, while L-LPS increased IL-6 but decreased IL-1β and C reactive protein (CRP) levels. SL-LPS pretreatment strongly enhanced the LPS-induced production of TNF-α, IL-6, IL-10, PGE2, and NO in RAW 264.7 cells, and the IL-6, IL-1β, and CRP levels in Hepa1c1c-7 cells, as well as the ratios of IFN-γ/IL-10 in LPS- and Con A-stimulated EL4 cells compared to L-LPS. These findings suggest that pre-conditioning of SL-LPS may contribute to the mortality to secondary infection in sepsis rather than pre-conditioning of L-LPS.