• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.492-501
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• 1995

Background: Transforming growth factor- alpha(TGF-$\alpha$) may play important roles in carcinogenesis, tumor growth, and angiogenesis. Transforming growth factor-beta(TGF-$\beta$) are known to be involved in cell-cycle control and regeneration. TGF-$\alpha$ positively acts on growth control of many epithelial cells in contrast to the negative role of TGF-$\beta$. Method: To evaluate the possible role of TGF-$\alpha$ and TGF-$\beta$ in human primary lung cancers, the expression of TGF-$\alpha$ and TGF-$\beta$ were immmunohistochemically investigated in tissue sections from forty seven cases with lung cancers and ten cases with non-cancerous lung tissues. Recombinant cloned monoclonal antibody of TGF-$\alpha$ and neutralizing antibody of TGF-$\beta$ were employed as primary antibodies after dewaxing the formalin-fixed, paraffinized tissue sections. Results: TGF-$\alpha$ was expressed in the cytoplasms of tumor cells in thirty five cases of forty seven(74.5%) primary lung cancers, whereas the control expressed in two of ten brochial epithelial cells. The expression of TGF-$\alpha$ was disclosed in four cases of eleven(36.4 %) small cell carcinomas and thirty one cases of thirty six(86.1%) non-small cell carcinomas of the lung. Expressions of TGF-$\beta$ was discernible in bronchial epithelium in eight of ten non-cancerous lung tissues. The expression of TGF-$\beta$ was noted in the cytoplasms of tumor cells in eight cases of forty seven(17.0%) primary lung cancers. The expression of TGF-$\beta$ disclosed in two cases of eleven(18.2%) small cell carcinomas and six cases of thirty six(16.7%) non- small cell carcinomas of the lung. Conclusion: These findings suggest that up-regulation of TGF-$\alpha$ and down-regulation of TGF-$\beta$ are involved during development and growth of primary lung cancers.

• Journal of Life Science
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• v.33 no.9
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• pp.713-723
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• 2023

Lung cancer is a type of cancer that has the highest mortality rate. It is mainly classified into small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC). Chemotherapy is used to treat lung cancer, but long-term treatment causes side effects and drug resistances. Curcumin is a bright yellow polyphenol extracted from the root of turmeric. It has biological activities, such as anti-oxidant, anti-cancer, and anti-inflammatory effects. In this study, we observed differential cell death in human lung cancer cells. Based on the results, curcumin at 10, 30, and 50 μM exhibited a dose-dependent inhibition on the cell survival of several lung cancer cells, with minor differential phenotypes. In addition, apoptosis, autophagy, and reactive oxygen species (ROS) regeneration were observed through flow cytometry. Curcumin dose-dependently increased these phenotypes in A549 (NSCLC) and DMS53 (SCLC), which were restored by corresponding inhibitors. Western blotting was performed to measure the level of expression of apoptosis- and autophagy-related proteins. The results indicate that Bax, PARP, pro-caspase-3, and Bcl-2 were dose-dependently regulated by curcumin, with seemingly higher Bax/Bcl-2 ratios in DMS53. In addition, autophagic proteins, p-AKT, p62, and LC3B, were dose-dependently regulated by curcumin. ROS inhibition by diphenyleneiodonium reduced the induction of apoptosis and autophagy generated by curcumin. Taken together, it is suggested that curcumin induces apoptosis and autophagy via ROS generation, leading to cell death, with minor differences between human lung cancer cells.

• Journal of Chest Surgery
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• v.30 no.6
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• pp.559-565
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• 1997

Donor airway ischemia is a significant problem after tracheal replacement with homograft or lung transplantation, Several factors such as omentopexy, heparin, PGl2 and fibroblast growth factor, have been shown to induce angiogenesis in vitro and in vivo. This study was designed to investigate whether omentopexy and basic flbroblast growth factor can enhance rabbit tracheal revascularization and epithelial regeneration, Three different experiments were performed with New Zealand white rabbit. In group I(n= 15 control group), only coNical tracheal autotransplantation was done. In group II(n= 15), cervical tracheal autotransplantation with omentopexy was done through subcutaneous route. In group III(n= 15), cervical tracheal autotransplantation was done and lug basic flbroblast growth factor was applied. After 3, 7 and 14 days, the animals were sacrificed. The extent of revascularization was investigated by means of uptake of the human serum albumin labelled with 99m technetium, and epithelial regeneration were assessed by means of light microscope. In the group investigated at day 3, there was statistically significant high tracheal revascularization in group III(p<0.05), but no difference at 7 and 14 days. And epithelial regenerations at day 3 were better in group III(p<0.05), and at day 7 in group II and III. But there was no difference at day 14. We concluded that b-FGF can enhance the revascularization and epithelial regeneration of the tracheal autograft especially in early phase.

• KSBB Journal
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• v.27 no.6
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• pp.367-374
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• 2012

Cigarette smoking (SM) is considered to be well known environmental toxin which contributes to the onset of various diseases. SM cause direct lungs damage, activate lungs inflammatory responses, and in some cases leads to the development of lung cancer. Cytokines in injured starfish (Asterina pectinifera) is the potential changes in its expression during the regeneration process. Especially, expression of TGF-${\beta}1$ has increased in arm cut starfish extract after eight days. Also, starfish including saponin like the ginseng. Saponin is widely used in the world because of some effective pharmacological activities. Therefore, the current study was designed to elucidate the pharmacological activities of starfish extract against cigarette smoking induced damage in cell line and pulmonary tissue. We investigate that the effect of eight days starfish extract after arm cut (8d) and intact starfish extract on cell line and mouse lung injury by SM. In cell proliferation analysis, although cigarette smoking extract (CSE) was co-treated, the higher proliferation ability is shown in 8d treatment than intact starfish extract. 8d and intact starfish extract was directly transported to pulmonary cells through respiratory organ by nebulizer inhalation. In this case of cigarette smoking, the pulmonary structure was damaged and functions become abnormal. However, 8d treated groups showed similar with the control group compared with SM group. Among them, 8d was proved to be more effective than intact starfish extract. These results demonstrate that 8d could more protect pulmonary structure and function than intact starfish extract against cigarette smoking by ginseng like saponin and regulation of inflammatory cytokines.

• BMB Reports
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• v.53 no.2
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• pp.65-73
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• 2020

Life expectancy has dramatically increased around the world over the last few decades, and staying healthier longer, without chronic disease, has become an important issue. Although understanding aging is a grand challenge, our understanding of the mechanisms underlying the degeneration of cell and tissue functions with age and its contribution to chronic disease has greatly advanced during the past decade. As our immune system alters with aging, abnormal activation of immune cells leads to imbalance of innate and adaptive immunity and develops a persistent and mild systemic inflammation, inflammaging. With their unique therapeutic properties, such as immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs) have been considered to be a promising source for treating autoimmune disease or as anti-aging therapy. Although direct evidence of the role of MSCs in inflammaging has not been thoroughly studied, features reported in senescent MSCs or the aging process of MSCs are associated with inflammaging; MSC niche-driven skewing of hematopoiesis toward the myeloid lineage or oncogenesis, production of pro-inflammatory cytokines, and weakening their modulative property on macrophage polarization, which plays a central role on inflammaging development. This review explores the role of senescent MSCs as an important regulator for onset and progression of inflammaging and as an effective target for anti-aging strategies.

• The Journal of Internal Korean Medicine
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• v.33 no.2
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• pp.126-144
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• 2012

Background : Peripheral nerves more rapidly recover than central nerves. However, it has been known that the degree of reaction of axons of peripheral nerves is affected by distinctive characteristics of axons and environmental factors near the axons. Taxol is a widely used medicine as for ovarian, breast, lung and gastric cancer. However it causes patients difficulties under treatment due to its toxic and side effects, which include persistent pain. Objectives : This study reviewed how SJT extract in vitro and in vivo affects nerve tissues of a sciatic nerve damaged by Taxol. It also studied how SJT extract in vivo affects axons of the sciatic nerve after the sciatic nerve was damaged by pressing. Methods : After vehicle, Taxol, and Taxol plus SJT were treated respectively for tissue of the sciatic nerve in vitro and then tissues were observed using Neurofilament 200, Hoechst, ${\beta}$-tubulin, $S100{\beta}$, caspase-3 and anti-cdc2. SJT was also oral medicated by injecting Taxol into the sciatic nerve of in vivo rats. Tissues of the sciatic nerve and axons of DRG sensory nerves were then observed using Neurofilament 200, Hoechst, ${\beta}$-tubulin, $S100{\beta}$, caspase-3 and p-Erk1/2. After inflicting pressing damage to the sciatic nerve of in vivo rats, tissues of the sciatic nerve and DRG sensory nerve were observed using Neurofilament 200, Hoechst, $S100{\beta}$, caspase-3, anti-cdc2, phospho-vimentin, ${\beta}1$-integrin, Dil reverse tracking and p-Erk1/2. Results : The group of in vitro Taxol plus SJT treatment had meaningful effects after sciatic nerve tissue was damaged by Taxol. The group of in vivo SJT treatment had effects of regenerating Schwann cells and axons which were damaged by Taxol treatment. The group of in vivo SJT had effects of regenerating axons in damaged areas after the sciatic nerve was damaged by pressing, and also had variations of distribution in Schwann cells at DRG sensory nerves and axons. Conclusions : This study confirmed that SJT treatment is effective for growth of axons in the sciatic nerve tissues and improvement of Schwann cells after axons of the sciatic nerve tissues was damaged. After tissues of sciatic nerve was damaged by pressing in vivo, SJT treatment had effects on promoting regeneration of axon in the damaged area and reactional capabilities in axons of DRG sensory nerves.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.397-405
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• 2005

Background : Laminin-1 is known to have regular functions in the development and course of differentiation of the lungs. The morphogenesis and distribution of laminin-1 still remains as a mystery and its distribution and changes in the molecular structure of laminin-1 in the pathogenesis of the lung still is a subject of great controversy. In this study, experiments were done to delineate the distribution and changes in the amount of laminin-1 after inducing inflammation of the lungs by exposing experimental animals to CS gas and especially, to find compositions of laminin-1 within type II pneumocytes. Materials and Methods : The experimental subjects of study were newborn rats and the extracted tissue from the experimental rats were viewed under light microscope and electron microscope after the sections were treated with immunohistochemical methods and immunogold reaction methods using bounded gold particles. Results : 1) Lymphocytes and mononuclear phagocytes invaded the alveolar septa in the 2 day group rats after CS gas exposure and intense interstitial inflammation was seen in the 3 day group. 2) Laminin immunoreactions decreased to a moderate degree in the 2 and 3 day group rats after CS gas exposure and strong laminin immunoreactions were seen again in the 5 and 7 day group rats. 3) Gold particles in basal lamina of the lung blood-air barrier decreased and in the type I pneumocytes decreased in the 2 and 3 day group rats after CS gas exposure. 4) Gold particles were seen only on the surface of the cell membranes of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure. 5) Few gold particles around the lamellar bodies and cytoplasm of type II pneumocytes in the control rat group and at 12 hours after CS gas exposure. Gold particles are seen only on the surface of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure and are evenly distributed in small amounts in the cells of the 3 day group after CS gas exposure. Conclusion : CS gas exposure in the rats caused inflammation of lung alveolar septa and also induced a decrease in laminin-1 in basal lamina and loss of laminin-1 in the cytoplasm of type II pneumonocytes. As the inflammatory cells disappeared, an increase in the distribution of laminin-1 occurred. This reflects tissue regeneration functions of laminin-1 in the pneumocytes of rats and the distribution of laminin-1 in type II pneumocytes can be seen through the electron microscope using immunogold methods.

• Journal of Ginseng Research
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• v.34 no.2
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• pp.77-88
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• 2010

Ginseng has been reported to reduce the risk of cancer in diverse organs, including the lip, oral cavity, pharynx, larynx, esophagus, lung, liver, pancreas, ovary, colon, rectum, and stomach, as demonstrated in clinical and epidemiological studies. studies, base on which findings, Panax ginseng has been classified as a "non-organ-specific cancer preventive." However, the recent keen interest in traditional medicinal herbs has been frequently questioned, about exact mode of action and the use of panaceic compounds has been a prime issue discussed in terms of complementary and alternative medicine. Several in vitro and in vivo studies have shown the mitigating effects of Korean red ginseng on Helicobacter pylori (H. pylori)-associated atrophic changes and carcinogenesis; However, evidence-based medicine, consisting of large-scale or well designed clinical studies, is still warranted whether Korean red ginseng is to be recognized as an essential therapeutic strategy regarding a "H. pylori-associated gastric cancer preventive." Specifically, comprehensive clinical trials of Korean red ginseng are needed to demonstrate that mucosal regeneration in patients with atrophic gastritis is feasible using Korean red ginseng supplements after the eradication of H. pylori infection. Ginseng is a good example of a natural herb and its ubiquitous properties may include the reduction or delay of inflammation carcinogenesis. Korean red ginseng contains ample amounts of active ginsenosides and we have demonstrated their effects in in vitro and in vivo studies with positive outcomes. In this review, the quantitative and qualitative benefits of Korean red ginseng in the treatment of H. pylori infection are described.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.17 no.3
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• pp.181-191
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• 2007

With the 2-Butanethiol, which is an unidentified inhalation toxic material, acute inhalation toxicity was tested with SD rats. The $LC_{50}$ was evaluated to be 2,500 ppm (9.22 mg/L) or higher which falls under the criteria of acute toxicity Category 3 (500<$LC_{50}$<2,500 ppm) in the Industrial Safety and Health Act. In the subchronical inhalation toxicity test by 0, 25, 100, and 400 ppm, 6 hours a day, 5 days a week, for 13 weeks repeated exposure, though no death or particular clinical presentation was observed, in the female 25 and 400 ppm group, including weight change, and in each concentration group including 400 ppm, change of feed rate, eye stimulation, motility change in male group, and lesions in blood and blood biochemical were observed. In the internal organs weight, 25, 100, and 400 ppm groups in male and 400 ppm group in female showed significant (p<0.05) changes in kidney, liver, thymus, and lung. In the pathological tissue test, severe cortical tubular hyaline droplets were observed in the male 400 ppm group, and all male rats of 400 ppm group and 2 female individuals showed tubular degeneration/regeneration accompanied with pigmentation, showing that the target organs of inhalation exposure of 2-Butanethiol are spleen, kidney, nasal cavity, and adrenal. Through the tests, the NOEL of 2-Butanethiol was evaluated to be 25 ppm (0.092 mg/L) or less for both male and female.

• Experimental and Molecular Medicine
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• v.50 no.11
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• pp.9.1-9.10
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• 2018

Although the positive effects of recombinant fibroblast growth factor-2 (rFGF-2) in chronic obstructive pulmonary disease (COPD) have been implicated in previous studies, knowledge of its role in COPD remains limited. The mechanism of FGF2 in a COPD mouse model and the therapeutic potential of rFGF-2 were investigated in COPD. The mechanism and protective effects of rFGF-2 were evaluated in cigarette smoke-exposed or elastase-induced COPD animal models. Inflammation was assessed in alveolar cells and lung tissues from mice. FGF-2 was decreased in the lungs of cigarette smoke-exposed mice. Intranasal use of rFGF-2 significantly reduced macrophage-dominant inflammation and alveolar destruction in the lungs. In the elastase-induced emphysema model, rFGF-2 improved regeneration of the lungs. In humans, plasma FGF-2 was decreased significantly in COPD compared with normal subjects (10 subjects, P = 0.037). The safety and efficacy of inhaled rFGF-2 use was examined in COPD patients, along with changes in respiratory symptoms and pulmonary function. A 2-week treatment with inhaled rFGF-2 in COPD (n = 6) resulted in significantly improved respiratory symptoms compared with baseline levels (P < 0.05); however, the results were not significant compared with the placebo. The pulmonary function test results of COPD improved numerically compared with those in the placebo, but the difference was not statistically significant. No serious adverse events occurred during treatment with inhaled rFGF-2. The loss of FGF-2 production is an important mechanism in the development of COPD. Inhaling rFGF-2 may be a new therapeutic option for patients with COPD because rFGF-2 decreases inflammation in lungs exposed to cigarette smoke.