Ro Jai Youl;Yoon Suk Jong;Lee Jong Wha;Kim Kyung Hwan
Proceedings of the Ginseng society Conference
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1993.09a
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pp.84-93
/
1993
It has been reported that ginseng is effective in the central nervous system, immune system, and the strong inflammatory responses. However, there has been no research report yet about the effect of ginseng on allergic hypersensitivity reactivity. To confirm the ginseng effects on the release of mediators(histamine. leukotrienes etc.) which cause the hypersensitivity reactivity and inflammatory response, we used actively sensitized guinea pig airway tissues by utilizing the superfusion technique. In this procedure. the contractile response and mediators released after antigen stimulation of sensitized tissues, and IgG and IgE antibody products were measured in sera of immunized animals. Then the results of the controll group were compared to those of ginseng pretreatment groups. In the total saponin(TS) and panaxatriol(PT) pretreatment, histamine release decreased by $20\%$ in the tracheal tissues after active sensitization by ovalbumin(OVA, 10mg/kg), but in the lung parenchyma, histamine release decreased by $40\%.$ Panaxadiol(PD) significantly decreased histamine release by $40\%$ in the both tissues after active sensitization. TS, PT and PD of ginseng poorly blocked leukotrienes (LTs) and prostagrandin $D_2(PGD_2)$ release(less than $10\%$). Ginseng TS and PT had no effect on the serum IgG antibody production by ovalbumin, whereas PD significantly increased serum IgG antibody contents(approximately by 2 times). However, $IgG_1$ antibody products in the serum of guinea pig actively sensitized with ovalbumin after PD pretreatment were decreased, compared to that with ovalbumin alone. IgE antibody production by passive cutaneous anaphylaxis(PCA) titer in the TS pretreatment increased 3 times more than in the absence of TS(PCA titer by PT was not detected). These studies show that some ginseng saponins can in part act to inhibit mediator release in antigen - induced airway smooth muscle by inducing the IgG antibody production which has been changed in the specificity.
The intent of this study is to investigate whether two oriental medical prescriptions named haengsotang(HST) and gami-palmihwan(GPMH) significantly effect mucin release from cultured hamster tracheal surface epithelial(HTSE) cells, Confluent HTSE cells were metabolically radiolabeled with $^3H-glucosamine$ for 24 hrs and chased for 30 min in the presence of HST or GPMH to assess the effect of each agent on $^3H-mucin$ release. Possible cytotoxicities of each agent were assessed by measuring lactate dehydrogenase(LDH) release. Also, the effects of HST and GPMH on contractility of isolated tracheal smooth muscle were investigated. The results are consistant with the following assertions: (1) HST significantly inhibited mucin release from cultured HTSE cells, without cytotoxicity; (2) GPMH did not effect mucin release without cytotoxicity; (3) HST and GPMH did not effect contractility of isolated tracheal smooth muscle. These results suggest a need for further investigation of HST and its components, for its potential in oriental medicine prescriptions and novel agents that effectively regulate (inhibit) mucin secretion from airway goblet cells.
Park Jin Young;Shim Jin Chan;Kim Ho Keun;Sun Sung Gyu;Jin Sang Sik;Kim Jong Chun;Han Jong Hyun
Journal of Physiology & Pathology in Korean Medicine
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v.16
no.2
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pp.322-326
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2002
Artemisia iwayomogi has been used in Korea for many centuries as a treatment for anemia. The effect of Artemisia iwayomogi on tracheal smooth muscle is not known. The purpose of the present study is to determine the effect of Artemisia iwayomogi on histamine induced tracheal smooth muscle contraction in guinea pigs. Guinea pigs(500g, male) were killed by CO₂ exposure and a segment (8-10mm) of the thoracic trachea from each rat and guinea pig was cut into equal segments and mounted ‘in pairs’ in a tissue bath. Contractile force was measured with force displacement transducers under 0.5g loading tension. The dose of histamine (His) which evoked 50% of maximal response (ED/sub 50/) was obtained from cumulative dose response curves for histamine (10/sup -7/~10/sup -4/M). Contractions evoked by His (ED/sub 50/) were inhibited significantly by Artemisia iwayomogi. In guinea pig tracheal smooth muscle, the mean percent inhibition of histamine induced contraction was 31.9% (p<0.05) after 100㎕/㎖ Artemisia iwayomogi. L-NNA slightly but significantly attenuated the inhibitory effects of Artemisia iwayomogi. Following treatment with L-NNA, the mean percent inhibition caused by 100㎕/㎖ Artemisia iwayomogi fell to 44.6% in guinea pig induced by histamine contraction. Propranolol, indomethacin and methylene blue did not significantly alter the inhibitory effect of Artemisia iwayomogi. These results indicate that Artemisia iwayomogi can relax histamine induced contraction of guinea pig, and that this inhibition related to nitric oxide formation.
Objectives In the present study, the author intended to investigate whether bojung-ikgitang-gamibang(BJGB) and seonbang-paedoktang(SBPT) significantly affect in vivo and in vitro mucin secretion from airway epithelial cells. Methods In vivo experiment, mice's mucin which is on a hypersecretion of airway mucin, mice's tracheal goblet cells in hyperplasia and mice's intraepithelial mucosubstances were exposed with SO2for3weeks. Effects of orally-administered BJGB and SBPT during 1 week on vivo mucin secretion and hyperplasia of tracheal goblet cells were assessed by using both enzyme-linked immunosorbent assay(ELISA) and staining goblet cells with alcian blue. In vitro experiment, confluent hamster tracheal surface epithelial(HTSE) cells were metabolically radiolabeled with 3H-glucosamine for 24hrs and chased for 30 min in the presence of each agent to figure out the effectiveness of 3H-mucin secretion. Total elution profiles of control spent media and treatment sample through Sepharose CL-4B column were analyzed. The effects of each agent on contractility of isolated tracheal smooth muscle and effects of each agent on MUC5AC gene expression in cultured HTSE cells were investigated. Also, possible cytotoxicities of each agent were assessed by measuring lactate dehydrogenase(LDH) release. Additionally, effects of BJGB and SBPT on both MUC5AC gene expression in cultured HTSE cells and TNF- or EGF-induced MUC5AC gene expression in human airway epithelial cells (NCI-H292) were investigated. Results (1) BJGB and SBPT inhibited hypersecretion of in vivo mucin. SBPT also inhibited the increase the number of goblet cells. However, BJGB did not affect the increase of number of goblet cells; (2) BJGB significantly increased mucin secretion from cultured HTSE cells, without significant cytotoxicity, and chiefly affected the 'mucin' secretion; (3) SBPT did not affect mucin secretion from cultured HTSE cells without significant cytotoxicity, and also did not affect the secretion of the other releseable glycoproteins; (4) BJGB and SBPT did not affect Ach-induced contraction of isolated tracheal smooth muscle; (5) SBPT significantly inhibit the expression levels of MUC5AC gene and BJGB significantly increased the expression levels of MUC5AC gene in both HTSE cells and NCI-H292 cells. Conclusions BJGB and SBPT can not only affect the secretion of mucin but also affect the expression of mucin gene. The author suggests that the effects BJGB and SBPT with their components should be further investigated and it is highly desirable to find from oriental medical prescriptions, novel agents which might regulate hypersecretion of mucin from airway epithelial cells.
Journal of The Korean Dental Society of Anesthesiology
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v.6
no.2
s.11
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pp.121-126
/
2006
Generalized anaphylaxis is a most dramatic and acutely life-threatening allergic reaction. Most fatalities from anaphylaxis occur within the first 30 minutes postantigenic exposure. The mechanism of generalized anaphylaxis is the reaction of IgE antibodies to an allergen that causes the release of histamine, bradykinin, and others. These chemical mediators cause the contraction of smooth muscles of the respiratory and intestinal tracts, as well as increased vascular permeability. Four major clinical symptoms are recognized: skin reactions, smooth muscle spasm (gastrointestinal and genitourinary tracts and respiratory smooth muscle), respiratory distress, and cardiovascular collapse. Epinephrine is the drug of choice for the management. Its syrnpathomimetic effects directly counteract most aspects of the attack. Respiration must be immediately supported by the establishment of a patent airway along with artificial ventilation. The circulation should be supported and the existing hypotension overcome by placing the victim in a position to allow gravity to aid venous return and by administering intravenous fluids, vasopressors, and corticosteroids. When an imperceptible pulse is evident, external cardiac compression must also be instituted. This is a case report of anaphylactic shock care during general anesthesia, possibly due to penicillin, pancuronium and others.
Objectives : In the present study, the author intended to investigate Gagam-jeonggitang(GJT), Gami-hwajeongjeon(GHJ) and Gami-tonggyutang(GTT) significantly affect in vivo and in vitro mucin secretion from airway epithelial cells. Methods : In vivo experiment, the author induced hypersecretion of airway mucin, hyperplasia of tracheal goblet cells and the increase in intraepithelial mucosubstances by exposing rats to SO2 during 3 weeks. Effects of orally-administered GJT, GHJ and GTT during 1 week on in vivo mucin secretion and hyperplasia of tracheal goblet cells were assesed using ELISA and staining goblet cells with alcian blue. For in vitro experiment, confluent HTSE cells were metabolically radiolabeled with 3H-glucosamine for 24 hrs and chased for 30 min in the presence of each agent to assess the effects of each agent on 3H-mucin secretion. Possible cytotoxicities of each agent were assessed by measuring lactate dehydrogenase release. Also, the effects of each agent on contractility of isolated tracheal smooth muscle and effects of each agent on MUC5AC gene expression in cultured HTSE cells were investigated. Results : GJT, GHJ and GTI inhibited hypersecretion of in vivo mucin: GJT and GHJ inhibited the increase of number of goblet cells. However, GTT did not affect the increase of number of goblet cells; GJT and GTT significantly increased mucin secretion from cultured HTSE cells, without significant cytotoxicity. GHJ increased mucin secretion and showed mild cytotoxicity at the highest concentration: GJT, GHJ and GTT chiefly affected the 'mucin' secretion; GJT, GHJ and GTT did not affect Ach-induced contraction of isolated tracheal smooth muscle; GTT did not significantly affect the expression levels of MUC5AC gene. However, GJT significantly. inhibit the expression levels of MUC5AC gene and GHJ significantly increased the expression levels of MUC5AC gene. These results suggest that GJT, GHJ and GTI can increase mucin secretion during short-term treatment(in vitro), whereas it can inihibit hypersecretion of mucin during long-term treatment(in vivo) and GJT and GHJ can not only affect the secretion of mucin but also affect the expression of mucin gene. Conclusions : The author suggests that the effects GJT, GHJ and GTT with their components should be further investigated and it is valuable to find, from oriental medical prescriptions, novel agents which might regulate hypersecretion of mucin from airway epithelial cells.
Choi, In Ho;Song, Dae Hyun;Kim, Jhingook;Han, Joungho
Tuberculosis and Respiratory Diseases
/
v.76
no.1
/
pp.34-37
/
2014
Glomus tumors of the lung are rare benign neoplasm, originating from modified smooth muscle cells. The patients are usually presented with no or non-specific symptoms such as cough, dyspnea or hemoptysis. Although surgical treatment is considered as the treatment of choice, the endobronchial therapy can be applied to the patients who are unfit for surgical excision. Herein, we describe two rare cases of glomus tumor originated at large airway (trachea and main bronchus) without respiratory symptoms and review their characteristic radiologic, macroscopic and pathological features.
Potassium $(K^+)$ channels are present in airway smooth muscle cells, and their activation results in hyperpolarization and relaxation. Because these effects may have therapeutic relevance to hypersensitivity and asthma, we examined the effect of a potassium channel activator, cromakalim (BRL 34915, CK) on the release of mediators from superfused tracheal and parenchymal strips after passive sensitization with $IgG_1$ antibody. Both tissues were superfused with CK $(2{\times}10^{-6}\;M)$ for 30 min and challenged with CK and antigen (Ox-HSA). Using monodispersed, partially purified, highly purified guinea pig lung mast cells, we also examined the effect of CK on mediator release from these cells after passive sensitization with $IgG_{1}$ antibody $({\alpha}-OA)$. Guinea pig lung mast cells were purified using enzyme digestion method, count current elutriation, and discontinuous Percoll density gradient. After CK pretreatment, passively sensitized mast cells were challenged with varying concentration of antigen (OA, immunological stimuli) or with varying concentration of calcium ionophore (CaI, non-immunological stimuli). Histamine (Hist) release was determined by spectrophotofluorometry, and leukotrienes (LT) by radioimmunoassy. CK pretreatment decreased Hist by 35% and LT release by 40% in the antigen-induced tracheal tissue after $IgG_1$ sensitization but did not decrease the contractile response. In the antigen-induced parenchymal tissue CK decreased Hist release by 25% but poorly decreased LT. Both immunologic and non-immunologic stimuli caused a dose-dependent release of Hist and LT from monodispersed, partially purified and highly purified lung mast cells. Verification of LT release was obtained by the use of 5-lipoxygenase inhibitor, A64077 (Zileuton). CK decreased Hist and LT release by 20% respectively in the OA-induced guinea pig lung mast cells after $IgG_1$ sensitization. The inhibitory effects of CK on the Hist and LT release in the Ox-HSA-induced airway smooth muscle tissues or in the OA-induced and CaI-induced mast cells after $IgG_1$ sensitization were completely blocked by TEA and GBC. These studies show that guinea pig lung mast cells seem to be an important contributor to LT release, and that CK (which has been known as an airway smooth muscle relaxant) can in part act to inhibit mediator release in the antigen-induced airway smooth muscle, and that CK may also act to inhibit mediator release in the OA-induced and CaI-induced highly purified mast cells. These results suggest that Hist and LT release evoked by mast cell activation might in part be associated with $K{^+}4 channel activity.
Kang, Ji Young;Kim, In Kyoung;Hur, Jung;Kim, Seok Chan;Lee, Sook Young;Kwon, Soon Seog;Kim, Young Kyoon
Tuberculosis and Respiratory Diseases
/
v.82
no.1
/
pp.71-80
/
2019
Background: Efficacy and safety of tiotropium bromide, a muscarinic receptor antagonist, in treatment of asthma have been reported. However, its effect on airway remodeling in chronic asthma of the elderly has not been clearly verified. The objective of this study was to investigate the effect of tiotropium and expression of muscarinic receptors as its related mechanism in an aged mouse model of chronic asthma with airway remodeling. Methods: BALB/c female mice age 6 weeks, 9 and 15 months were sensitized and challenged with ovalbumin (OVA) for three months. Tiotropium bromide was administered during the challenge period. Airway hyperresponsiveness (AHR) and pulmonary inflammation were measured. Parameters of airway remodeling, and expression levels of $M_2$ and $M_3$ receptors were examined. Results: Total cell with eosinophils, increased in the OVA groups by age, was decreased significantly after treatment with tiotropium bromide, particularly in the age group of 15 months. AHR and levels of interleukin (IL)-4, IL-5, and IL-13 were decreased, after tiotropium administration. In old aged group of 9- and 15-months-treated groups, hydroxyproline contents and levels of ${\alpha}$-smooth muscle actin were attenuated. Tiotropium enhanced the expression of $M_2$ but decreased expression of $M_3$ in all aged groups of OVA. Conclusion: Tiotropium bromide had anti-inflammatory and anti-remodeling effects in an aged mouse model of chronic asthma. Its effects seemed to be partly mediated by modulating expression $M_3$ and $M_2$ muscarinic receptors. Tiotropium may be a beneficial treatment option for the elderly with airway remodeling of chronic asthma.
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