• 한방안이비인후피부과학회지
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• 제20권1호통권32호
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• pp.177-194
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• 2007

Fructus of Rubus coreanus $M_{IQ.}$. (FRCM) has been used for stuttering urination, prostate gland disease, and impotence in Korean traditional medicine. Water extract of FRCM (WFRCM) treatment significantly attenuated airway hyperreactivity (AHR). Airway recruitment of leukocytes and eosinophils was also markedly reduced by WFRCM administration, suggesting that WFRCM can alleviate the airway inflammation. However, the level of cytokine (IL-4, IL-5, and IL-13) in bronchoalveolar lavage fluid (BALF) and lung was not different compared with positive control. WFRCM reduced the number of draining lymph node cells during OVA-induced allergic asthma. I further examined transcription level of cytokine in lung. WFRCM treatment reduced IL-4 and IL-13 mRNA in lung and inhibited IgE and IgG1 but not IgG2a. My data suggest that WFRCM attenuates OVA-induced allergic asthma through inhibition of Th2 cell response.

• 대한예방한의학회지
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• 제27권3호
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• pp.35-46
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• 2023

Objectives : Gumiganghwal-tang and its main components have been used for treatment of cough, headache, joint pain and fever. Using a respiratory inflammatory model, we intend to demonstrate the its anti-inflammatory effect and immune mechanism of Gumiganghwal-tang. Methods : We induced the respiratory inflammation mouse model by papain treatment. Female BALB/C mice (8 weeks old) were divided into three groups as follows: saline control group, papain treatment group (vehicle), papain and Gumiganghwal-tang (200 mg/kg) treatment group (n=4). To verify the anti-inflammatory effect of Gumiganghwal-tang extracts, we measured the infiltration of inflammatory cells in bronchoalveolar lavage fluid (BALF) and nasal lavage fluid (NALF). Additionally, the efficacy of Gumiganghwal-tang extracts on Th2 cell population and alveolar macrophage in lung were analyzed by using flow cytometry. Results : Gumiganghwal-tang extracts administration decreased inflammatory cell infiltration in BALF and NALF, especially of eosinophils. Furthermore, interleukin-5 level was reduced in lung by drug administration. Interestingly, Gumiganghwal-tang extracts treatment also decreased the Th2 cell (CD4⁺GATA3⁺) population and increased the alveolar macrophage (CD11b⁺CD11c⁺) population in lung. Conclusions : Our findings indicate that Gumiganghwal-tang extracts have anti-inflammatory effects by mediating Th2 cell and alveolar macrophage cell activation.

• Journal of Ginseng Research
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• 제42권4호
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• pp.476-484
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• 2018

Background: Korean Red Ginseng (steamed and dried white ginseng, Panax ginseng Meyer) is well known for enhancing vital energy and immune capacity and for inhibiting cancer cell growth. Some clinical studies also demonstrated a therapeutic potential of ginseng extract for treating lung inflammatory disorders. This study was conducted to establish the therapeutic potential of ginseng saponins on the lung inflammatory response. Methods: From Korean Red Ginseng, 11 ginsenosides (Rb1, Rb2, Rb3, Rc, Rd, Re, Rf, Rg1, Rg2, Rg3, and Rh2) were isolated. Their inhibitory potential and action mechanism were evaluated using a mouse model of lung inflammation, acute lung injury induced by intranasal lipopolysaccharide administration. Their anti-inflammatory activities were also examined in lung epithelial cell line (A549) and alveolar macrophage (MH-S). Results: All ginsenosides orally administered at 20 mg/kg showed 11.5-51.6% reduction of total cell numbers in bronchoalveolar lavage fluid (BALF). Among the ginsenosides, Rc, Re, Rg1, and Rh2 exhibited significant inhibitory action by reducing total cell numbers in the BALF by 34.1-51.6% (n = 5). Particularly, Re showed strong and comparable inhibitory potency with that of dexamethasone, as judged by the number of infiltrated cells and histological observations. Re treatment clearly inhibited the activation of mitogen-activated protein kinases, nuclear factor-${\kappa}B$, and the c-Fos component in the lung tissue (n = 3). Conclusion: Certain ginsenosides inhibit lung inflammatory responses by interrupting these signaling molecules and they are potential therapeutics for inflammatory lung diseases.

• Archives of Pharmacal Research
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• 제29권4호
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• pp.302-309
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• 2006

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.

• Tuberculosis and Respiratory Diseases
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• 제67권5호
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• pp.436-444
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• 2009

Background: Micro computed tomography (CT) is rapidly developing as an imaging tool, especially for mice, which have become the experimental animal of choice for many pulmonary disease studies. We evaluated the usefulness of micro CT for evaluating lung fibrosis in the murine model of bleomycin-induced lung inflammation and fibrosis. Methods: The control mice (n=10) were treated with saline. The murine model of lung fibrosis (n=60) was established by administering bleomycin intra-tracheally. Among the 70 mice, only 20 mice had successful imaging analyses. We analyzed the micro CT and pathological findings and examined the correlation between imaging scoring in micro CT and histological scoring of pulmonary inflammation or fibrosis. Results: The control group showed normal findings on micro CT. The abnormal findings on micro CT performed at 3 weeks after the administration of bleomycin were ground-glass opacity (GGO) and consolidation. At 6 weeks after bleomycin administration, micro CT showed various patterns such as GGO, consolidation, bronchiectasis, small nodules, and reticular opacity. GGO (r=0.84) and consolidation (r=0.69) on micro CT were significantly correlated with histological scoring that reflected pulmonary inflammation (p<0.05). In addition, bronchiectasis (r=0.63) and reticular opacity (r=0.83) on micro CT shown at 6 weeks after bleomycin administration correlated with histological scoring that reflected lung fibrosis (p<0.05). Conclusion: These results suggest that micro CT findings from a murine model of bleomycin-induced lung fibrosis reflect pathologic findings, and micro CT may be useful for predicting bleomycin-induced lung inflammation and fibrosis in mice.

• Clinical and Experimental Pediatrics
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• 제62권10호
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• pp.367-373
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• 2019

Bronchopulmonary dysplasia (BPD) is a chronic lung disease of preterm infants with multiple factors affected from prenatal to postnatal periods. Despite significant advances in neonatal care over almost 50 years, BPD rates have not decreased; in fact, they may have even increased. Since more preterm infants, even at periviable gestational age, survive today, different stages of lung development affect the pathogenesis of BPD. Hence, the definition of BPD has changed from "old" to "new." In this review, we discuss the various definitions of BPD, risk factors from the prenatal to postnatal periods, management strategies by phase, and future directions for research.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
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• pp.27-27
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• 2001

Significant evidence exists which demonstrates that inflammation predisposes and promotes the cancer process in humans. Chronic inflammation can induce cancer in a variety of organ sites, including bowel and lung. There is also firm evidence that induced cyclooxygenases and nitric oxide synthetases, prostaglandins, and inflammatory cytokines can promote and accelerate the carcinogenic process.(omitted)

• Natural Product Sciences
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• 제22권1호
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• pp.70-75
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• 2016

A phytoformula containing the root barks of Morus alba, the fructus of Schizandra sinensis and the roots of Asparagus cochinchinensis (MSA) was prepared as a potential new herbal remedy, and its therapeutic potential for alleviating inflammatory lung conditions was examined. For in vivo evaluation, an animal model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice was used. With oral administration of 6 - 60 mg/kg, MSA potently and dose-dependently inhibited bronchitis-like symptoms in acute lung injury induced by intranasal treatment of LPS as judged by the number of cells in the bronchoalveolar lavage fluid (BALF) and histological observation. The inhibitory potency was comparable with that of dexamethasone. For in vitro assay, the effects on the production of proinflammatory molecules in lung epithelial cells and alveolar macrophages were examined. Although MSA inhibited IL-6 production in IL-$1{\beta}$-treated lung epithelial cells (A549) only at a high concentration ($300{\mu}g/ml$), the formula strongly and concentration-dependently inhibited NO production in LPS-treated alveolar macrophages (MH-S) at $20-300{\mu}g/ml$. Based on all of these findings, the new phytoformula MSA is suggested to have the potential to control inflammatory lung diseases including bronchitis, at least in part, by inhibiting inducible nitric oxide synthase-catalyzed NO production.

• Clinical and Experimental Pediatrics
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• 제57권5호
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• pp.211-216
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• 2014

Asthma comprises a heterogeneous group of disorders characterized by airway inflammation, airway obstruction, and airway hyperresponsiveness (AHR). Airway inflammation, which induces AHR and recurrence of asthma, is the main pathophysiology of asthma. The fractional exhaled nitric oxide (FeNO) level is a noninvasive, reproducible measurement of eosinophilic airway inflammation that is easy to perform in young children. As airway inflammation precedes asthma attacks and airway obstruction, elevated FeNO levels may be useful as predictive markers for risk of recurrence of asthma. This review discusses FeNO measurements among early-childhood wheezing phenotypes that have been identified in large-scale longitudinal studies. These wheezing phenotypes are classified into three to six categories based on the onset and persistence of wheezing from birth to later childhood. Each phenotype has characteristic findings for atopic sensitization, lung function, AHR, or FeNO. For example, in one birth cohort study, children with asthma and persistent wheezing at 7 years had higher FeNO levels at 4 years compared to children without wheezing, which suggested that FeNO could be a predictive marker for later development of asthma. Preschool-aged children with recurrent wheezing and stringent asthma predictive indices also had higher FeNO levels in the first 4 years of life compared to children with wheezing and loose indices or children with no wheeze, suggesting that FeNO measurements may provide an additional parameter for predicting persistent wheezing in preschool children. Additional large-scale longitudinal studies are required to establish cutoff levels for FeNO as a risk factor for persistent asthma.

• Biomolecules & Therapeutics
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• 제26권6호
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• pp.539-545
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• 2018

4-Hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione (PD1) is a synthetic phthalimide derivative of a marine compound. PD1 has peroxisome proliferator-activated receptor (PPAR) ${\gamma}$ agonistic and anti-inflammatory effects. This study aimed to investigate the effect of PD1 on allergic asthma using rat basophilic leukemia (RBL)-2H3 mast cells and an ovalbumin (OVA)-induced asthma mouse model. In vitro, PD1 suppressed ${\beta}$-hexosaminidase activity in RBL-2H3 cells. In the OVA-induced allergic asthma mouse model, increased inflammatory cells and elevated Th2 and Th1 cytokine levels were observed in bronchoalveolar lavage fluid (BALF) and lung tissue. PD1 administration decreased the numbers of inflammatory cells, especially eosinophils, and reduced the mRNA and protein levels of the Th2 cytokines including interleukin (IL)-4 and IL-13, in BALF and lung tissue. The severity of inflammation and mucin secretion in the lungs of PD1-treated mice was also less. These findings indicate that PD1 could be a potential compound for anti-allergic therapy.