• Title, Summary, Keyword: mitogen

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The response of peripheral blood lymphocytes against in vivo stimulation with mitogen in carp, Cyprinus carpio (Mitogen 투여에 대한 잉어 순환혈액 림프구의 반응)

  • Cho, Mi-Young;Park, Soo-Il
    • Journal of fish pathology
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    • v.9 no.1
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    • pp.95-109
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    • 1996
  • This work was carried out to investigate the functional heterogeneity of peripheral blood lymphocytes(PBLs) in carp, Cyprinus carpio. PHA, Con A, LPS and BCG were injected intraperitoneally into carp to determine the blastogenic response and rosette formation activity. In each group of fish treated with stimulators, the cell numbers and DNA contents of lymphocytes were higher than those of untreated control group and reached the highest level between 1 week and 2 weeks after injection with mitogens. These results showed that BCG and Con A were strong stimulators of proliferation compared to PHA and LPS. However, PHA-treated fish twice showed the highest rosette formation response among the consecutive stimulations with the same mitogen. Alase, the results on consecutive mitogen stimulation revealed that carps reinjected by different mitogens led to an increased stimulation higher than the one reinjected after 1 week with same mitogen. It seems that different mitogens may stimulate different cell populations and implies functionally separated subpopulations of lymphocytes in carp.

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Effect of T-2 Toxin on the Mitogen-Induced Blastogenesis in Chick Splenic Cell (T-2 Toxin이 병아리 비장세포의 유전질 발생에 미치는 영향)

  • Chun, Hyang-Sook;Chung, Duck-Hwa;Lee, Su-Rae
    • Korean Journal of Food Science and Technology
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    • v.26 no.5
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    • pp.585-589
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    • 1994
  • The effects of T-2 toxin on mitogen-induced blastogenesis of chick splenic cells were investigated. The [$^3H$] thymidine incorporation in splenic cells stimulated by lipopolysaccharide and concanavalin A were equally inhibited as the concentration of T-2 toxin was increased. The effective dose of T-2 toxin causing a 50% reduction of [$^3H$] thymidine incorporation was inbetween 1.0 and 5.0 ng/ml for both mitogens. Mitogen-induced blastogenesis in chick splenic cells showed differences among experimental groups with different exposure time of T-2 toxin, exhibiting the most inhibition in the experimental group exposed to T-2 toxin at both embryonic and chick periods.

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Total ginsenosides suppress monocrotaline-induced pulmonary hypertension in rats: involvement of nitric oxide and mitogen-activated protein kinase pathways

  • Qin, Na;Yang, Wei;Feng, Dongxu;Wang, Xinwen;Qi, Muyao;Du, Tianxin;Sun, Hongzhi;Wu, Shufang
    • Journal of Ginseng Research
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    • v.40 no.3
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    • pp.285-291
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    • 2016
  • Background: Ginsenosides have been shown to exert beneficial pharmacological effects on the central nervous, cardiovascular, and endocrine systems. We sought to determine whether total ginsenosides (TG) inhibit monocrotaline (MCT)-induced pulmonary hypertension and to elucidate the underlying mechanism. Methods: MCT-intoxicated rats were treated with gradient doses of TG, with or without $N^G$-nitro-$\small{L}$-arginine methyl ester. The levels of molecules involving the regulation of nitric oxide and mitogen-activated protein kinase pathways were determined. Results: TG ameliorated MCT-induced pulmonary hypertension in a dose-dependent manner, as assessed by the right ventricular systolic pressure, the right ventricular hypertrophy index, and pulmonary arterial remodeling. Furthermore, TG increased the levels of pulmonary nitric oxide, endothelial nitric oxide synthase, and cyclic guanosine monophosphate. Lastly, TG increased mitogen-activated protein kinase phosphatase-1 expression and promoted the dephosphorylation of extracellular signal-regulated protein kinases 1/2, p38 mitogen-activated protein kinase, and c-Jun NH2-terminal kinase 1/2. Conclusion: TG attenuates MCT-induced pulmonary hypertension, which may involve in part the regulation of nitric oxide and mitogen-activated protein kinase pathways.

Lipid A of Salmonella typhimurium Suppressed T-cell Mitogen-Induced Proliferation of Murine spleen Cells in the Presence of Macrophage (Salmonella typhimurium lipid A를 처리한 식세포 존재 조건에서 mitogen에 유도되는 이자 세포의 증식억제)

  • Kang, Gyong-Suk;Chung, Kyung-Tae
    • Journal of Life Science
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    • v.17 no.1
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    • pp.31-38
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    • 2007
  • Infection with virulent or attenuated Salmonella typhimuriumhas known to induce reduction in proliferative responses of spleen cells. We investigated a role of lipid A from S. typhimurium, a B cell mitogen, on proliferation of spleen cells by T cell mitogens such as concanavaline A and phytohemagglutinin under in vitro and ex vivo conditions. Lipid A alone induced proliferation of spleen cells in vitroin a dose-dependent manner. However, subsequent treatment of concanavaline A or phytohemagglutin in after lipid A treatment induced proliferation suppression of murine spleen cells in vitro and ex vivo. Removal of macrophages from spleen cells, which were obtained from a lipid A-injected mouse, restored proliferation by concanavaline A and phytohemagglutinin, indicating that macrophages appeared to play a role in lipid A-induced suppression. Secreted molecules from macrophages did not accounted for the suppression because suppressive effect was not achieved when the supernatant from macrophage-containing spleen cell culture was conditoned to macrophage-depleted spleen cell culture. Co-culture of spleen cells from lipid A-treated and - untreated mice showed proliferation suppression as increasing cell numbers of lipid A-treated mouse. These data suggested that the cell-to-cell contact of macrophage with splenic lymphocyte cells is responsible for immune responses against lipid A, which is applicable to the case of human S. typhi infection.

p38 mitogen-activated protein kinase-dependent activation of contractility in rat thoracic aorta

  • Yeol, An-Hui
    • Proceedings of the Korean Biophysical Society Conference
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    • pp.24-24
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    • 2001
  • The present study was undertaken to determine whether p38 mitogen-activated protein kinase participates in the regulation of vascular smooth muscle contraction by endothelin-I (ET-1) in rat thoracic aorta. ET-1 induced a sustained contraction. In contrast, both the intracellular Ca$\^$2+/ and myosin light chain (MLC) phosphorylations were not sustained.(omitted)

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Comparative Study of 3 kinds of Black Soybean on Murine Immune Cells (생쥐의 면역세포에 대한 검은콩 3종의 비교 연구)

  • Seo, Seung-Yong;Pang, Jinye;Eun, Jae-Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.24 no.4
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    • pp.668-673
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    • 2010
  • The purpose of this research was the comparative study of 3 kinds of black soybean on murine immune cells. The 3 kinds of black soybean are Glycine max Merr. with inner color-yellow (GY), Glycine max Merr. with inner color-greenish (GG) and Rhynchosia volubilis Lour. (RV). All of the black soybean increased the viability of murine thymocytes in vitro. The combined treatment of GY or GG and mitogen did not affect the viability of splenic T- and B-lymphocytes compared with mitogen-treated group, but the combined treatment of RV and mitogen increased their action compared with mitogen-treated group. Also, the 3 kinds of black soybean were given p.o. once a day for 7 days, respectively. RV increased the population of thymic-$CD8^+$, splenic-$CD8^+$ and $B220^+$ cells in vivo. Furthermore, GY and GG did not affect the phagocytic activity and the production of nitric oxide in peritoneal macrophages in vitro, but RV enhanced their action. These results suggest that immunopotentiative action of Rhynchosia volubilis Lour. is more potent than their of Glycine max Merr.

Effects of Curcumin, the Active Ingredient of Turmeric(Curcuma longa), on Regulation of Glutamate-induced Toxicity and Activation of the Mitogen-activated Protein Kinase Phosphatase-1 (MKP-1) in HT22 Neuronal Cell

  • Lee, Sang-Hyun;Yun, Young-Gab
    • Natural Product Sciences
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    • v.15 no.1
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    • pp.32-36
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    • 2009
  • Glutamate causes neurotoxicity through formation of reactive oxygen species and activation of mitogen-activated protein kinase (MAPK) pathways. MAPK phosphatase-1 (MKP-1) is one of the phosphatases responsible for dephosphorylation/deactivation of three MAPK families: the extracellular signal-regulated kinase-1/2 (ERK-1/2), the c-Jun N-terminal kinase-1/2 (JNK-1/2), and the p38 MAPK. In this report, the potential involvement of MKP-1 in neuroprotective effects of curcumin, the active ingredient of turmeric (Curcuma longa), was examined using HT22 cells. Glutamate caused cell death and activation of ERK-1/2 but not p38 MAPK or JNK-1/2. Blockage of ERK-1/2 by its inhibitor protected HT22 cells against glutamate-induced toxicity. Curcumin attenuated glutamate-induced cell death and ERK-1/2 activation. Interestingly, curcumin induced MKP-1 activation. In HT22 cells transiently transfected with small interfering RNA against MKP-1, curcumin failed to inhibit glutamate-induced ERK-1/2 activation and to protect HT22 cells from glutamate-induced toxicity. These results suggest that curcumin can attenuate glutamate-induced neurotoxicity by activating MKP-1 which acts as the negative regulator of ERK-1/2. This novel pathway may contribute to and explain at least one of the neuroprotective actions of curcumin.

Immunosuppressive Effects of Safrole in BALB/c Mice

  • Kim, Byung-Sam;Jeong, Tae-Cheon;Choe, Suck-Young;Yang, Kyu-Hwan
    • Toxicological Research
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    • v.8 no.2
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    • pp.191-203
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    • 1992
  • The immunosuppressive effects of safrole were studied in female BALB/c mouse. Mice were given 100,200and 400mg safrole/kg daily for 14days and evaluated on day 15. The day 4 immunogloblin-M antibody response to T-dependent antigen, sheep red blood cells (SRBC) was inhibited dose-dependently in all doses studied. In vitro antibody response to polyclonal antigen, lipopolysaccharide (LPS) by spleen cell suspensions from safrole-treated mice were also significantly inhibited. When safrole was treated for 14days to mice, and mitogen-induced proliferation of splenocytes were assayed on day 15, there were significant suppression of responses to B-cell mitogen, LPS and T-cell mitogen concanavalin A(Con A) at a dose of 400mg safrole/kg. Direct addition of safrole on the splenocyte culture also produced a dose dependent suppression on in vitro antibody response to LPS, and mitogen-induced lymphoproliferatin at doses of 100,200,400 and 800${\mu}M$ safrole. The role of metabolic activation in safrole-induced suppression of in vitro antibody response was studied using splenocyte-hepatocyte coculture system. The suppression of in vitro antibody respose to LPS by safrole was not altered when safrole were incubated in the splenocyte-hepatocyte system for 4hr as compared with direct addition of safrole in splenocytes culture. Neither the addition of salicylamide, sulfotransferase inhibitor, nor the addation of inorganic sulfate, sulfation cofactor to the splenocyte-hepatocyte coculture, altered the suppression of antibody response by safrole. These results suggest that the immunosuppression by safrole may not by produced by the reactive metabolites which are mediated in carcinogenesis of safrole.

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Repair of Chromate induced DNA-Protein Crosslinks in Rat Lymphocyte (크롬에 의해 유발된 백서 임파구 DNA-Protein Crosslinks의 복구)

  • Lee, Hun-Jae;Lee, Kwan-Hee;Hong, Yun-Chul
    • Journal of Preventive Medicine and Public Health
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    • v.29 no.3
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    • pp.597-607
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    • 1996
  • Genotoxic agents can induce various DNA lesions. DNA-Protein Crosslinks(DPCs) were known as the important DNA lesions which could impair gene expression because DPCs had a high probability of resisting repair and persisting through cell cycle. This repair resistance of DPCs could have biological significance but had not been evaluated clearly yet. Most of the studies that have evaluated the repair of DPCs only compared the extent of DPCs repair with other DNA lesions. We injected $K_2CrO_4$, a genotoxic agent, into Sprague-Dawley rats intraperitoneally(5mg/kg) and isolated blood lymphocytes 12 hours later. These lymphocytes were cultured in the mitogen added growth media and mitogen free media separately. The degree of the repair of DPCs was monitored for 4 days by the K-SDS assay. 4 days later, the amount of DPCs decreased by 4.6% in the mitogen added media high increased by 10.9% in the mitogen free media. These results showed that DPCs induced by $K_2CrO_4$ were not repaired easily and the DPCs were biologically significant DNA lesions. We thought the decrease of DPCs in the mitogen added media was not due to the repair of DPCs, but from the increase of normal cell proliferation. Therefore, it is very important to consider the proliferation of normal cells when estimating the repair of DPCs.

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Regulation of Mitogen-activated Protein Kinases by Translatoinally Controlled Tumor Protein in PC12 Cells (PC12 세포주에서 Translationally Controlled Tumor Protein에 의한 Mitogen-activated Protein Kinases 활성 조절)

  • Kim, Mi-Yeon;Kim, Mi-Young
    • YAKHAK HOEJI
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    • v.54 no.5
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    • pp.323-327
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    • 2010
  • Translationally controlled tumor protein (TCTP) activates basophils to release histamine and causes chronic inflammation. It was also reported that TCTP significantly reduced in brain of Alzheimer's Disease and Down Syndrome as compared to normal person, suggesting that TCTP might be involved in cognitive function. We wondered whether TCTP could act as a general inducer in neurotransmitters release in brain. We, therefore, investigated the role of TCTP in PC12 cell line which expressed neuronal properties. We found that TCTP could activate JNK, and the activity was inhibited by pretreatment of dicoumarol, a JNK inhibitor. However, TCTP could not activate ERK that has known to be involved in neurotransmitter release. These suggest TCTP did not participate in neurotransmitter release from PC12 cells, and TCTP might not be a general inducer in neurotransmitter release.