• 대한한방내과학회지
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• 제28권2호
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• pp.377-384
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• 2007

Objective : Immune potentiation including activation of T cells, B cells, macrophages, and dendritic cells is known to play a key role in prevention and treatment of patients with cancer. In this study, we investigated the effects of Acanthopanax sessiliflorus (AR) on the immune system, especially on thymocytes, splenocytes, and macrophages. Methods : We investigated the effects of AR on proliferation of splenocytes in normal mice, and the effects on proliferation of splenocytes and thymocytes in tumor-bearing mice. In addition, the effect of AR on NO production using macrophages was investigated. Results : Treatment with AR accelerated proliferation of splenocytes in vitro. AR also accelerated thymocyte proliferation, but did not affect splenocytes proliferation in normal mice. In contrast, AR accelerated proliferation of splenocytes and thymocytes significantly in tumor bearing mice. In addition, NO production level from macrophages was elevated by treatment with AR. Conclusion : These results demonstrate that AR has anti-cancer activities and related mechanisms are involved in immune potentiation such as acceleration of immune cell proliferation and elevation of NO production level in macrophages. In addition, we also demonstrate the possibilities of AR as complementary and alternative medicine to standard anti-cancer drugs.

• 대한수의학회지
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• 제44권3호
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• pp.329-334
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• 2004

Ischemia/reperfusion(I/R) injury of the rat testis causes germ cell death and infiltration of inflammatory cells. To investigate the mechanism of germ cell death in torsion of the rat testis, apoptosis and macrophage activation were studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling(TUNEL) method and immunohistochemistry in the testes of Sprague-Dawley rats subjected to 1.5 h of ischemia, followed by 0, 1, 3, 6, 12, 24, 48 and 96 h of reperfusion. Apoptotic, TUNEL-positive cells were found at the base of the seminiferous epithelia after I/R. TUNEL-positive cells were significantly increased 6 h after repair of the torsion, and there was a significant peak in apoptosis 24 h after reperfusion, as compared with normal or sham-operated controls. In contrast, histological evidence of germ cell necrosis in the seminiferous tubules was first visible 24 h after reperfusion. In the testis of sham-operated rats, ED2-positive resident macrophages were found diffusely in the interstitial space, while ED1-positive monocyte-like macrophages were rarely found. After I/R, ED1-positive cells were significantly increased beginning 12 h after reperfusion, while ED2-positive immunoreactivity did not change during the experimental period. Together, the results of this study confirmed that increased numbers of ED1-positive macrophages, but not resident ED2-positive macrophages, infiltrated the interstitial space surrounding damaged tubules and induced germcell death.

• 동의생리병리학회지
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• 제17권4호
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• pp.991-995
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• 2003

The purpose of this research was to investigate the effects of unripened fruits and ripened fruits of Rubus coreanus Miquel on murine peritoneal macrophages. The 70% ethyl alcohol extracts (20 or 100 mg/kg) of unripened fruits (RCE-I) and of ripened fruits (RCE-II) were administered p.o. once a day for 7 days to mice. RCE-I and RCE-II decreased the phagocytic activity of murine peritoneal macrophages and the production of nitric oxide. Also, RCE-I and RCE-II increased the production of tumor necrosis factor- a from peritoneal macrophages. In general, the immuno-suppressive action of RCE-I on macrophages was more potent than those of RCE-II. These results suggest that the fruits of Rubus coreanus Miquel regulates the non-specific immune response via decrease of phagocytic activity and increase of production of tumor necrosis factor- a from murine peritoneal macrophages.

• 동의생리병리학회지
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• 제20권5호
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• pp.1217-1222
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• 2006

The purpose of this research was to investigate the effects of the administration of Juglandis Semen without inner cortex (JE) or with inner cortex (JEIC) on activity of splenocytes and peritoneal macrophages in BALB/C mice. JE (300 mg/kg, p.o.) did not affect the cell viability of T- and B-lymphocytes in murine splenocytes, but JEIC (300mg/kg, p.o.) increased the cell viability of T- and B-lymphocytes. Furthermore, JE decreased the population of B220$^+$ cells in splenocytes, but JEIC enhanced the population of Thyl$^+$ cells. Also, JEIC enhanced the population of splenic CD4$^+$ cells. JE decreased the production of nitric oxide and the phagocytic activity of peritoneal macrophages, but JEIC increased the production of nitric oxide and the phagocytic activity of peritoneal macrophages. These results suggest that JEIC is more potent than JE against the immune response induced by splenocytes and macrophages.

• Laboraroty Animal Research
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• 제34권4호
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• pp.133-139
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• 2018

Nonalcoholic steatohepatitis (NASH) is becoming common chronic liver disease because of the increasing global prevalence of obesity and consequently Nonalcoholic fatty liver disease (NAFLD). However, the mechanism for progression of NAFLD to NASH and then cirrhosis is not completely understood, yet. The triggering of these hepatic diseases is thought from hepatocyte injury caused by over-accumulated lipid toxicity. Injured hepatocytes release damage-associated molecular patterns (DAMPs), which can stimulate the Kupffer cells (KCs), liver-resident macrophages, to release pro-inflammatory cytokines and chemokines, and recruit monocyte-derived macrophages (MDMs). The increased activation of KCs and recruitment of MDMs accelerate the progression of NAFLD to NASH and cirrhosis. Therefore, characterization for activation of hepatic macrophages, both KCs and MDMs, is a baseline to figure out the progression of hepatic diseases. The purpose of this review is to discuss the current understanding of mechanisms of NAFLD and NASH, mainly focusing on characterization and function of hepatic macrophages and suggests the regulators of hepatic macrophages as the therapeutic target in hepatic diseases.

• 대한본초학회지
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• 제29권1호
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• pp.1-6
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• 2014

Objectives : Many of currently used anti-cancer drugs were developed to target cell death mechanisms and had serious side effects by causing damage to normal cells. Hangambujeongsan or Kangai Fuzheng Powder was a mixture based on the traditional Chinese medicine. It had been used in the local Chinese hospitals to treat cancer patients for decades and had shown a certain level of beneficial effects without major toxic effects. But its mechanism of action had not been elucidated yet. Thus this study aimed to investigate the effects of Kangai Fuzheng Powder in an in vitro experiment. Methods : Cancer lines or RAW264.7 mouse macrophage cells were treated with Kangai Fuzheng Powder. Cell viability was measured by MTT assay, and morphological observation was also performed. Gene expression of cytokines in macrophages was determined by real-time polymerase chain reaction. Phagocytic function assay was also performed in macrophage cells. Results : Kangai Fuzheng Powder had no direct detrimental effect on cancer cells. When macrophages were co-cultured with cancer cells, Kangai Fuzheng Powder had toxic effect on cancer cells. After exposing macrophages to Kangai Fuzheng Powder, macrophages transformed into activated form and the mRNA level of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, interleukin-10 and monocyte chemotactic protein-1 was significantly enhanced. Phagocytic activity of macrophages was dramatically potentiated. Conclusions : We demonstrated that anti-cancer effect of Kangai Fuzheng Powder was related to activation of macrophages including enhanced cytokine production and phagocytic function.

• 방사선산업학회지
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• 제18권1호
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• pp.63-70
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• 2024

Phlorocyclin (PC) and isophorocyclin (IPC) are rare benzofuran derivaitves obtained from the representive dihydrochalcone glucoside, phloridzin (PZ) and are a type of neolignan backbone with a potential anti-glycative agents. However, research related to the enhancement of biological functionallites to inflammation of the newly converted products is very limited. This research was directed with the purpose of discovery more effective anti-inflammatory agents in macrophages of newly radiolysis products PC and IPC. The anti-inflammatory capacities of the characterized products in RAW 264.7 and DH82 macrophages treated with lipopolysaccharide (LPS) to stimulate an inflammation response were examined. The pro-inflammatory factors such as prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), nitric oxide (NO), interleukin-6 (IL-6), and IL-10, without cytotoxicity in LPS-stimulated macrophages, were significantly inhibited after treatment with PC and IPC, when compared to PZ. Moreover, PC and IPC decreased the appearance of cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) proteins in macrophages. The cyclization products modified by radiolysis showed the greatest anti-inflammatory effects in macrophage cells, indicating PC and IPC are a potential candidate for use in anti-inflammatory agents.

• Clinical and Experimental Otorhinolaryngology
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• 제15권2호
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• pp.153-159
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• 2022

Objectives Noise exposure leads to an increase in the macrophage population. This increment is thought to be caused by the transformation of infiltrated monocytes into macrophages rather than by proliferation of the cochlear resident macrophages. However, studies on infiltrated monocytes in the cochlea are scarce. Thus, we aimed to investigate the infiltration of monocytes and their transformation into macrophages after noise exposure. Methods In wild-type and CX3CR1⁺/^GFPC57/B6 mice, inflammatory monocytes were identified by immunofluorescence of mouse cochlear cells. The findings were confirmed and quantitated by flow cytometry. Results One day after noise exposure, monocytes were identified in the spiral ligament. Flow cytometric analysis confirmed that the monocyte population peaked on post-noise exposure day 1 and decreased thereafter. On day 3 after noise exposure, amoeboid-type macrophages increased in the crista basilaris, and on day 5, they spread to the basilar membrane. Conclusion Infiltrated monocytes were successfully observed 1 day after noise exposure, preceding the increase in the macrophage population. This finding supports the proposal that infiltrated monocytes transform into macrophages.

• IMMUNE NETWORK
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• 제3권1호
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• pp.53-60
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• 2003

Background: The role of macrophages in tumor angiogenesis is known to be the production of angiogenic cytokines and growth factors including TNF-${\alpha}$. Recently, macrophage also can produce the INF-${\gamma}$ that is being studied to be involved in angiogenic inhibition. Thus, the importance of macrophages in tumor angiogenesis is might being an angiogenic switch. Thus, the hypothesis tested here is that TNF-${\alpha}$ can modulate the INF-${\gamma}$ production in the macrophages from tumor environment as a part of tumor angiogenic switch. Methods: Macrophages in tumor environment were obtained from the peritoneal cavity of C57BL/6 mice injected with B16F10 melanoma cell line for 6 or 11 days. $Mac1^+$-macrophages were purified using magnetic bead ($MACs^{TM}$; Milteny Biotech, Germany) and cultured with various concentrations of TNF-${\alpha}$ for various time points at $37^{\circ}C$. The supernatants were analyzed for IFN-${\gamma}$ or VEGF by ELISA kit (Endogen, Woburn, MA). Results: Residential macrophages from the peritoneal cavity did not respond to LPS or TNF-${\alpha}$ to produce INF-${\gamma}$. However, the cells from tumor environment produced IFN-${\gamma}$ as well as VEGF and upregulated by the addition of LPS or TNF-${\alpha}$. RT-PCR analysis revealed the external TNF-${\alpha}$-induced IFN-${\gamma}$ gene expression in the macrophages from tumor environment. Conclusion: The overall data suggest that the macrophages in tumor environment might have an important role not only in angiogenic signal but also in anti-angiogenic signal by producing related cytokines. And TNF-${\alpha}$ might be a key cytokine in tumor angiogenic switch.

• 대한미생물학회지
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• 제35권3호
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• pp.251-261
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• 2000

V. vulnificus is an estuarine bacterium which causes septicemia and shock in susceptible patients. The organism produces a hemolytic cytolysin (VvH), which has a membrane damaging effect on erythrocytes. To clarify the mechanisms by which VvH might contribute to virulence, we examined its effect on macrophages. When mouse peritoneal macrophages were harvested and co-cultured with hemolysin-positive V. vulnificus strains (100 bacteria/cell), about 60% of the macrophages were killed; macrophages were not killed when co-cultured V. vulnificus strain CVD 707, a VvH-negative deletion mutant. Exposure of macrophages to filtered culture supernatants (2.5 HU/ml) and purified VvH (3 HU/ml) resulted in an increase in dead cells (80 and 90%, respectively), as determined by the trypan blue dye exclusion method and LDH release from macrophages was also increased (70 and 65.5%, respectively). The cytotoxic effect of VvH on macrophages was both the dose- and time-dependent. The VvH caused damage to the macrophage membrane and was blocked significantly by preincubation with cholesterol (p<0.01). Fetal bovine serum showed remarkable inhibition of VvH synthesis by V. vulnificus and inhibited VvH activity in culture supernatant. Cell viability was increased by 35% (p<0.01) and LDH release decreased by 28% (p<0.01) when macrophages were incubated with V. vulnificus (100 bacterial cell) in DMEM-10% FBS for 2 hr. Bacterial clearance activity of mice against V. vulnificus CVD 707 was decreased by pretreatment with 10 HU of VvH. This result suggests that the VvH can impair the membrane of macrophages and may playa role in the pathogenesis of V. vulnificus septicemia.