• Korean Journal of Plant Resources
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• v.36 no.4
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• pp.275-281
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• 2023

Autophagy contributes to enhancing the immune system (innate and adaptive immune system) against foreign pathogens. Autophagy of macrophages is used as a major indicator for developing vaccine adjuvants to increase the adaptive immune response. In this study, PLR activated autophagy and increased p62/SQSTM1. The knockdown of p62/SQSTM1 attenuated PLR-mediated autophagy. Inhibition of TLR4 blocked PLR-mediated increase in p62/SQSTM1 level and autophagy induction. In addition, inhibition of PI3K blocked HSL-mediated increase of p62/SQSTM1. PLR increased Nrf2 level and the inhibition of TLR4 and PI3K reduced PLR-mediated increase of Nrf2. Taken together, it is believed that PLR may induce autophagy through upregulating p62/SQSTM1 via TLR4/PI3K/Nrf2 signaling pathway.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2023.04a
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• pp.44-44
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• 2023

Syneilesis palmata (SP) has been used as a traditional medicinal plant and vegetable. SP was reported to exert pharmacological activities such as anti-inflammation, anti-cancer, and anti-HIV. However, there are no studies on the immunostimulatory activity of SP. Thus, in this study, we report that S. palmata leaves (SPL) induce the activation of macrophages. An increase in both secretions of immunostimulatory mediators and phagocytotic activity was observed in SPL-treated RAW264.7 cells. However, this was reversed by inhibition of TLR2/4. In addition, the p38 inhibition reduced the SPL-mediated secretion of immunostimulatory mediators, and the SPL-mediated p38 activation was blocked by the TLR2/4 inhibition. SPL augmented both p62/SQSTM1 and LC3-II. TLR2/4 inhibition blocked the SPL-mediated increase of p62/SQSTM1 and LC3-II. These findings indicate that SPL may activate macrophages through TLR2/4-dependent p38 activation and activate autophagy through TLR2/4 stimulation.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2019.04a
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• pp.94-94
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• 2019

In this study, we elucidated the anti-inflammatory mechanisms of leaves extracts from Rodgersia podophylla (RPL) in RAW264.7 cells. RP-L significantly inhibited the production of the proinflammatory mediators such as NO, iNOS, IL-$1{\beta}$ and IL-6 in LPS-stimulated RAW264.7 cells. RPL increased HO-1 expression in RAW264.7 cells, and the inhibition of HO-1 by ZnPP reduced the inhibitory effect of RPL against LPS-induced NO production in RAW264.7 cells. Inhibition of p38, ROS and $GSK3{\beta}$ attenuated RPL-mediated HO-1 expression. Inhibition of ROS inhibited p38 phosphorylation and $GSK3{\beta}$ expression induced by RPL. In addition, inhibition of $GSK3{\beta}$ blocked RPL-mediated p38 phosphorylation. RPL induced nuclear accumulation of Nrf2, and Inhibition of p38, ROS and $GSK3{\beta}$ abolished RPL-mediated nuclear accumulation of Nrf2. Furthermore, RPL blocked LPS-induced degradation of $I{\kappa}B-{\alpha}$ and nuclear accumulation of p65. RP-L also attenuated LPS-induced phosphorylation of ERK1/2 and p38. Our results suggest that RPL exerts potential antiinflammatory activity by activating ROS/$GSK3{\beta}$/p38/Nrf2/HO-1 signaling and inhibiting NF-${\kappa}B$ and MAPK signaling in RAW264.7 cells. These findings suggest that RPL may have great potential for the development of anti-inflammatory drug.

• The Journal of Korean Society of Virology
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• v.28 no.1
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• pp.39-52
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• 1998

HIV-1 tat, a strong transactivator, is essential for the HIV-1 replication and AIDS progression. The Tat function is markedly inhibited by human anti-oncogene p53. This work was initiated to identify the p53-associated inhibitory mechanism on tat-mediated transactivation. Inhibitory function of p53 was confirmed by co-transfection of tat-expressing Jurkat cells with LTR-CAT plasmid, or H3T1 cells (LTR-CAT integrated HeLa cells) with different ratio of pSV-tat/pCDNA-p53 plasmids. Results from the direct protein-protein interaction between soluble p53 and tat, and yeast two-hybrid experiments showed that the co-suppression mechanism is unlikely to be due to the direct interaction. CAT activity was not affected by tat in Jurkat cells which were transfected with p53-promoter-CAT or p53-enhancer-CAT, suggesting that the tat-mediated p53 suppression is not directly associated with p53-promoter. Finally, we have tested protein kinase activity in p53-tranfected Jurkat cells, which might phosphorylate HIV-1 tat, resulting in inhibition of tat function. Some of our data lead us to assume that the p53-mediated tat inhibition is likely to be associated with p53-associated, signaling-mediated phosphorylation of tat, resulting in the dysfunction of tat. This study is now under investigation.

• Proceedings of the Ginseng society Conference
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• 1990.06a
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• pp.36-44
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• 1990

The analgesic effect of morphine was antagonized and the development of tolerance was suppressed by the modification of the neurologic function in the animals treated with ginseng saponins. The activation of the spinal descending inhibitory systems as well as the supraspinal structures by the administration of morphine was inhibited in the animals treated with ginseng saponins intracerebrally or intrathecally The development of morphine tolerance and dependence, and the abrupt expression of naloxone induced abstinence syndrome were also inhibited by ginsenoside Kbl , Rba, Rgl and Re. These results suggest that ginsenoside Kbl, Rba, Rgl and Re are the bioactive components of panax ginseng on the inhibition of the development of morphine tolerance and dependence, and the inhibition of abrupt abstinence syndrome. In addition, further research on the minor components of Panax ginseng should be investigated. A single or daily treatment with ginseng saponins did not induce any appreciable changes in the brain level of monoamines at the various time intervals and at the various day intervals, respectively The inhibitory or facilitated effects of ginseng saponins on electrically evoked contractions in guinea pig ileum (U-receptor) and mouse was definers (5·receptor) were not mediated through opioid receptors. The antagonism of a x receptor agonist, U-, iO.488H was also not mediated through opioid receptors in the animals treated with ginseng saponins, bolt mediated through serotonergic mechanisms. Ginseng saponins inhibited morphine S-dehydrogenase that catalyzed the production of morphine from morphine, and increased hepatic glutathione contents for the detoxification of morphine. This result suggests that the dual action of the above plays an important role in the inhibition of the development of morphine tolerance and dependence.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2020.08a
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• pp.86-86
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• 2020

The leaves of Staphylea bumalda (S. bumalda) as a deciduous tree distributed in Korea, China and Japan are used to treat respiratory diseases or inflammation. However, there is no scientific research on the immune-enhancing activity of S. bumalda leaves. Thus, in this study, we investigated the effect of water extracts from S. bumalda leaves (SBL) on the macrophage activity using mouse macrophage cells, RAW264.7. SBL increased production of immunomodulators such as NO, iNOS, IL-1β, IL-6, TNF-α and MCP-1 in RAW264.7 cells and activated phagocytic activity of RAW264.7 cells. Inhibition of TLR2 and TLR4 blocked SBL-mediated production of immunomodulators in RAW264.7 cells. In addition, SBL-mediated production of immunomodulators was attenuated by JNK inhibition in RAW264.7 cells. SBL increased JNK phosphorylation, while Inhibition of TLR2 and TLR4 blocked SBL-mediated JNK phosphorylation in RAW264.7 cells. These results are thought to be evidence that SBL activates JNK through stimulation of TLR2 and TLR4 in macrophage to induce the production of immunomodulators. In LPS-stimulated RAW264.7 cells, SBL inhibited over-production of immunomodulators. Summarizing the results, SBL showed immunostimulatory activity under normal conditions and immunosuppressive activity under LPS-induced excessive immune response conditions.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.6
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• pp.399-405
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• 2010

Gamma-aminobutyric acid (GABA)-ergic inhibition is important in the function of the visual cortex. In a previous study, we reported a developmental increase in $GABA_A$ receptor-mediated inhibition in the rat visual cortex from 3 to 5 weeks of age. Because this developmental increase is crucial to the regulation of the induction of long-term synaptic plasticity, in the present study we investigated in detail the postnatal development of phasic and tonic inhibition. The amplitude of phasic inhibition evoked by electrical stimulation increased during development from 3 to 8 weeks of age, and the peak time and decay kinetics of inhibitory postsynaptic potential (IPSP) and current (IPSC) slowed progressively. Since the membrane time constant decreased during this period, passive membrane properties might not be involved in the kinetic changes of IPSP and IPSC. Tonic inhibition, another mode of $GABA_A$ receptor-mediated inhibition, also increased developmentally and reached a plateau at 5 weeks of age. These results indicate that the time course of the postnatal development of GABAergic inhibition matched well that of the functional maturation of the visual cortex. Thus, the present study provides significant insight into the roles of inhibitory development in the functional maturation of the visual cortical circuits.

• YAKHAK HOEJI
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• v.52 no.5
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• pp.370-375
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• 2008

In this study, the anti-allergic activity and mechanim of Salviae radix (SR) were investigated. The ethanol extract of SR showed significant inhibitory effect on degranulation from antigen-stimulated mast cells and it also inhibited the expression and secretion of TNF-${\alpha}$ and IL-4 in antigen-stimulated RBL-2H3 cells. In the mast cell-mediated local animal allergy model, it suppressed the passive cutaneous anaphylaxis in a dose-dependent manner. As its mechanism of action, SR inhibited the activating phosphorylation of Syk, a downstream signaling molecule of Src-family kinase, for the activation of mast cells. The results of the study indicate that the anti-allergic activity of SR is mediated by the inhibition of Src-family kinase in mast cells.

• Microbiology and Biotechnology Letters
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• v.47 no.3
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• pp.350-353
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• 2019

The transcription factor, GATA-1, plays an important role in the $Fc{\varepsilon}RI$ ${\alpha}$ chain expression in mast cells and basophils. This study was conducted to investigate the downregulation of the transcription factor GATA-1 by kaempferol isolated from Nelumbo nucifera stamens in $Fc{\varepsilon}RI$-mediated allergic reactions. Kaempferol inhibited $Fc{\varepsilon}RI$-mediated histamine release. Western blotting analysis and RT-PCR showed that the protein and mRNA expression of GATA-1 was suppressed by kaempferol in a dose-dependent manner. These results suggest that kaempferol may inactivate basophils by downregulating the $Fc{\varepsilon}RI$ ${\alpha}$ chain expression via the inhibition of the GATA-1 expression.

• Microbiology and Biotechnology Letters
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• v.50 no.2
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• pp.293-300
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• 2022

Lipoteichoic acid (LTA) regulates the immune system, including inflammatory responses, through TLR2-mediated signaling pathways. LTA isolated from Staphylococcus aureus (aLTA) has been shown to induce apoptosis, but the detailed mechanism has not been identified. We found that aLTA induced apoptosis through an autocrine mechanism in the human monocyte-like cell line, THP-1. We observed that the expression level of the anti-apoptosis protein, Bcl2, was suppressed in LTA-treated THP-1 cells. In addition, the cytokines, TNF-α and IFN-γ, which have been shown to induce apoptosis in some cell lines, were involved in THP-1 cell death via the modulation of Bcl2. The suppression of Bcl2 by aLTA was recovered when the negative regulator, SOCS-1, was knocked down. Taken together, these results showed that aLTA induced apoptosis in THP-1 cells through an autocrine mechanism of cytokines and SOCS-1-mediated Bcl2 inhibition.