• 대한한의학회지
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• 제26권1호
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• pp.59-70
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• 2005

Objective: Tumor necrosis factor-a $(TNF-{\alpha})$, a potent immuno-modulator and pro-inflammatory cytokine, has been implicated in many pathological processes. In this study, the author examined whether promoter region polymorphism in the $TNF-{\alpha}$a gene at position-308 affect the odds of cerebral infarction (CI) and whether genetic risk is enhanced by sasang constitutional classification. Methods: 212 CI patients and 610 healthy controls were genotyped and determined according to sasang constitutional classification. The amplified genotypes were analyzed on $8\%$ polyacrylamide gel. The alleles were visualized by ethidium bromide staining. Primers for $TNF-{\alpha}$ were designed to incorporate a polymorphic site at a position -308 bp of the $TNF-{\alpha}$ gene into an NcoI restriction site. Restriction digests generated products of 87 and 20 bp for G allele and 107 bp for A allele. Results : A significant decrease was found for the $TNF-{\alpha}$ A allele in CI patients compared with controls (P=0.033, odds ratio, O.R.: 0.622). However, there was no significant association between $TNF-{\alpha}$ polymorphism and sasang constitution in CI patients. Conclusion: My finding suggests that $TNF-{\alpha}$promoter region polymorphism is responsible for susceptibility to CI in Koreans.

• The Korean journal of internal medicine
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• 제33권6호
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• pp.1103-1110
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• 2018

Background/Aims: Several epidemiological studies have validated the association of interleukin gene polymorphisms with acute pancreatitis (AP) in different populations. However, there have been few studies in Asian ethnic groups. We aimed to investigate the relationships between inflammatory cytokine polymorphisms and AP as pilot research in a Korean ethnic group. Methods: Patients who had been diagnosed with AP were prospectively enrolled. DNA was extracted from whole blood, and DNA sequencing was subsequently performed. Single-nucleotide polymorphisms (SNPs) of the interleukin $1{\beta}$ (IL1B), interleukin 1 receptor antagonist (IL1RN), and tumor necrosis factor ${\alpha}$ (TNFA) genes of patients with AP were compared to those of normal controls. Results: Between January 2011 and January 2013, a total of 65 subjects were enrolled (40 patients with AP vs. 25 healthy controls). One intronic SNP (IL1RN -1129T>C, rs4251961) was significantly associated with the risk of AP (odds ratio, 0.304; 95% confidence interval, 0.095 to 0.967; p = 0.043). However, in our study, AP was not found to be associated with polymorphisms in the promoter regions of inflammatory cytokine genes, including IL1B (-118C>T, c47+242C>T, +3954C/T, and -598T>C) and TNFA (-1211T>C, -1043C>A, -1037C>T, -488G>A, and -418G>A). Conclusions: IL1RN -1129T>C (rs4251961) genotypes might be associated with a significant increase of AP risk in a Korean ethnic group.

• 동의신경정신과학회지
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• 제12권2호
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• pp.157-171
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• 2001

Astrocytes are glial cells that play a major role in the inflammation observed in Alzheimer's disease (AD). Upon stimulation from various agents, these cells adopt a reactive phenotype, a morphological hallmark in AD pathology, during which they themselves may produce still more inflammatory cytokines. Substance P (SP) can stimulate secretion of tumor necrosis $factor-\;{\alpha}$ $(TNF-\;{\alpha})$ from astrocytes stimulated with lipopolysaccharide (LPS). Here I report that Sunghyangjungkisan- ga- pogokyoung(Sgp) can modulate cytokines secretion from primary cultures of rat astrocytes. Sgp $(10\;to\;1000\;{\mu}g/ml)$ significantly inhibited the $TNF-\;{\alpha}$ secretion by astrocytes stimulated with LPS and SP. Interleukin-1 (IL-1) has been shown to elevate $TNF-\;{\alpha}$ secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. Treatment of Sgp $(10\;to\;1000\;{\mu}g/ml)$ to astrocytes stimulated with both LPS and SP decreased IL-1 secretion significantly. The secretion of $TNF-\;{\alpha}$ by LPS and SP in astrocytes was progressively inhibited with increasing amount of IL-1 neutralizing antibody. Neurodegenerative processes in AD are thought to be driven in part by the deposition of ${\beta}\;-amyloid\;(A\;{\beta})$, a 39- to 43-amino acid peptide product resulting from an alternative cleavage of amyloid precursor protein. Sgp $(10\;to\;1000\;{\mu}g/ml)$ significantly inhibited the $TNF-\;{\alpha}$ secretion by astrocytes stimulated with $A-{\beta}-$and IL-1. These results suggest that Sgp may inhibit $TNF-\;{\alpha}$ secretion by inhibiting IL-1 secretion and that Sgp has an antiinflammatory activity in AD brain

• Journal of Chest Surgery
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• 제54권6호
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• pp.528-531
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• 2021

Pulmonary sclerosing pneumocytoma (PSP) is a tumor of pneumocytic origin that is classified as a benign neoplasm. To date, aggressive behavior of this tumor has rarely been reported. Here, we describe a case of a 56-year-old woman with a huge, 19-cm PSP that resulted in mediastinal shift and showed microscopic endobronchial invasion and necrosis. The differential diagnosis included malignant mesenchymal tumors, such as solitary fibrous tumor; however, PSP was confirmed based on the characteristic thyroid transcription factor 1 positivity and membranous expression of Ki-67 on immunohistochemical staining of tumor cells.

• BMB Reports
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• 제45권9호
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• pp.526-531
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• 2012

Many malignant tumors become resistant to tumor necrosis factor-alpha (TNF-${\alpha}$)-induced cell death during carcinogenesis. In the present study, we examined whether parkin acts as a tumor suppressor in HeLa cells, a human cervical cancer cell line resistant to TNF-${\alpha}$-induced cell death. TNF-${\alpha}$-treatment alone did not affect HeLa cell viability. However, expression of parkin restored TNF-${\alpha}$-induced apoptosis in HeLa cells. Increased cell death was due to the activation of the apoptotic pathway. Expression of parkin in TNF-${\alpha}$-treated HeLa cells stimulated cleavage of the pro-apoptotic proteins caspase-8, -9, -3, -7 and poly ADP ribose polymerase (PARP). In addition, parkin expression resulted in decreased expression of the caspase inhibitory protein, survivin. These results suggest that parkin acts as a tumor suppressor in human cervical cancer cells by modulating survivin expression and caspase activity. We propose that this pathway is a novel molecular mechanism by which parkin functions as a tumor suppressor.

• IMMUNE NETWORK
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• 제4권3호
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• pp.143-154
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• 2004

Background: CD27 is recently known as a memory B cell marker and is mainly expressed in activated T cells, some B cell population and NK cells. CD27 is a member of tumor necrosis factor receptor family. Like CD40 molecule, CD27 has (P/S/T/A) X(Q/E)E motif for interacting with TNF receptor-associated factors (TRAFs), and TRAF2 and TRAF5 bindings to CD27 in 293T cells were reported. Methods: To investigate the CD27 signaling effect in B cells, human CD40 extracellular domain containing mouse CD27 cytoplamic domain construct (hCD40-mCD27) was transfected into mouse B cell line CH12.LX and M12.4.1. Results: Through the stimulation of hCD40-mCD27 molecule via anti-human CD40 antibody or CD154 ligation, expression of CD11a, CD23, CD54, CD70 and CD80 were increased and secretion of IgM was induced, which were comparable to the effect of CD40 stimulation. TRAF2 and TRAF3 were recruited into lipid-enriched membrane raft and were bound to CD27 in M12.4.1 cells. CD27 stimulation, however, did not increase TRAF2 or TRAF3 degradation. Conclusion: In contrast to CD40 signaling pathway, TRAF2 and TRAF3 degradation was not observed after CD27 stimulation and it might contribute to prolonged B cell activation through CD27 signaling.

• 동의생리병리학회지
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• 제18권6호
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• pp.1805-1809
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• 2004

In order to validate the use of Radix Curcumae Aromaticae as an anti-inflammatory drug in the traditional Korean medicine, I have investigated the effect of water-soluble extract of Radix Curcumae Aromaticae (ECA) on the expression of inducible heme oxygenase-1 (HO-1), which ha.s anti-inflammatory and cytoprotective effects stimulates, in human umbilical vein endothelial cells (HUVECs) stimulated with a high dose of pro-inflammatory tumor necrosis factor-alpha (TNF-α). The extract protected dose-dependently HUVECs against TNF-α-induced apoptosis, as measured qualitatively by a nuclear staining method using the fluoresoence DAPI and quantitatively by a flow cytometry using fluoresce-enhanced Annexin V antibody, and significantly Increased HO-1 expression, as determined by Western blotting analysis using anti-HO-1 antibody. Biockage of HO-1 activity by a pharmacological inhibitor reversed cytoprotection afforded by the extract, and treatment with carbon monoxide, one of HO-1 metabolites, resulted in cytoprotection comparable to the extract. These results suggest that ECA may have therapeutic potential in the control of endothelial disorders caused by inflammatory cytokines.

• 한국방사선학회논문지
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• 제10권3호
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• pp.195-200
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• 2016

급성전골수구성 백혈병(Acute promyelocytic leukemia, APL)은 혈액암의 일종으로 치료의 성적이 좋지 않을 뿐 아니라 항암요법과 병행 하였을 경우 큰 효과를 보이는 것으로 알려져 있는 방사선 치료를 병행함에도 불구하고 정상세포에도 작용하여 부작용을 초래한다. 본 연구에서는 이러한 부작용을 감소시키기 위하여 감마선을 $TNF-{\alpha}$와 같이 처리하였을 경우 정상세포와 암세포의 세포 죽음에 어떠한 영향을 미치는지 확인하였다. HL-60 세포는 APL 세포주로서 사용하였고 DMSO를 처리하여 분화시킨 HL-60 세포는 정상과립구의 성질을 나타내어 정상대조군으로 이용하였다. 그 결과 $TNF-{\alpha}$와 함께 감마선을 처리한 HL-60 세포에서만 세포독성효과를 나타내었고 세포자멸사를 유도하여 세포가 죽음에 이르게 하였다. 결론적으로 $TNF-{\alpha}$는 항암치료의 부작용을 없애기 위해 저농도 감마선 치료 시 함께 사용하여 암 세포의 제거를 증가시켜 암의 치료효율을 높일 수 있는 유효물질로 사료된다.

• 생약학회지
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• 제50권3호
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• pp.191-197
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• 2019

Sepsis, an infectious disease, is a life-threatening condition that arises when the response to infection causes injury to tissues and organs. The purpose of this study was to demonstrate whether ABHC-1 and ABHC-2, two functional extracts from herbal complex, have an anti-bacterial effect against Escherchia coli in vivo, in vitro experimental model. ABHC-1 and ABHC-2 showed the antibacterial activity against the bacteria by paper disc method. The minimum inhibitory concentration (MIC) was measured using alamar blue reagent. The MIC was shown at $60{\mu}g/ml$ from ABHC-1 and $500{\mu}g/ml$ from ABHC-2 against E. coli. We next examined the effect of ABHCs on the production of inflammatory cytokine, such as tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), which is related to the induction of inflammation, in RAW 264.7 cell. ABHC-1 and ABHC-2 increased $TNF-{\alpha}$ production of RAW 264.7 cell in a dose-dependent manner while two extract decreased $TNF-{\alpha}$ production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cell in a dose-dependent manner. At a dose of $1{\times}10^8$ E. coli. i.p., non-treated mice were succumbed, while most of mice treated with ABHC-1 were survived. Therefore, our results suggest that ABHC-1 has anti-bacterial activity and can be a novel therapeutic agent against infectious diseases.

• Journal of Ginseng Research
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• 제20권1호
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• pp.15-22
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• 1996

In order to investigate the Immunomodulatory effects of ginseng, we have studied the effects of ginseng saponin on the proliferation and cytosine gene expression of human pheripheral blood mononuclear cell (PBMC). In the PBMC proliferation assay, total saponin exhibited proliferation inhibition on the PBMC or phytohemagglutinin(PHA)-stimulated PBMC in a dose-dependent fashion. Immunomodulatory effects of ginseng were further investigated using the cytokine gene expression as the indicators. In the reverse transcription-polymerase chain reaction (RT-PCR) test, interleukin (IL)-1, IL-2, IL-3, IL-4, IL-6, IL-13, granulocyte macrophage-colony stimulating factor, tumor necrosis factor (TNF), migration inhibitory factor and transforming growth factor genes were expressed in the PHA-stimulated PBMC 48 hrs after cell culture. Among expressed cytokines, total saponin could increase the expression of IL-1 and TNF of PBMC without stimulation of PHA. All of ginsenosides, $Rb_1$, $Rb_2$, $Rg_1$, Rc, Re, incresed TNF gene expression. Especially, Rb2 (20 g/ml) showed most prominent effect on TNF gene expression and it also slightly increased IL-1 gene expression of PBMC.