• Title/Summary/Keyword: lung damage

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Effects of Several Medicine Herb Prescriptions on Lung Carcinoma Cells (수종의 한약처방이 폐암세포에 미치는 영향)

  • Kang, Pil-Gu;Park, Dong-Il;Choi, Won-Choul;Jeon, Jong-Choul
    • The Journal of Internal Korean Medicine
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    • v.21 no.4
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    • pp.621-631
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    • 2000
  • Objective : In this study, the medicine herbs above were directly treated to cultured normal lung cells and lung carcinoma cells, and the effects were investigated to develope new cancer treatments with increased anti-cancer efficiency as well as decreased side-effects and to suggest more useful clinical therapies. Materials and Methods : In the experiment, WI-26 VA lung normal cell line and A-427 lung carcinoma cell line were cultured. To observe the morphological change of the treated cells, were subjected to Giemsa staining and observed under Reflected Fluorescence microscope. To examine whether cell death occurred, cells observed under Reflected Fluorescence microscope, To investigate the degree of cell death in the nucleus, cells were screened by Laser cytometry ACAS 570. Results : Samgibopye-tang(Shenqibufei-tang) stimulated not only the growth of the normal cells but also that of the carcinoma cells, Wikyeung-tang(Weijing-tang) induced morphological change such as cytoplasmic constriction in the normal cells and the carcinoma cells, but it did not show any strong inhibitory effect on the cell growth. Samso-eum(Shensu-yin) caused severe cell damage in both cell lines, Eunkyo San(Yinqiao-san) significantly damaged the nuclei and caused weak cytoplasmic constriction in both cell lines, Normal cells treated with Gilgyeung-tang(Jingeng-tang) did not show any significant morphological change while some Gilgyeung-tang(Jingeng-tang) treated carcinoma cells were observed to have a normal cell-like shape, interestingly, conclusions : As the results above, Samgibopye-tang(Shenqibufei-tang), Wikyeung-tang(Weijing-tang), and Gilgyeung-tang(Jingeng-tang) helped the growth of both cell lines, and especially Samgibopye-tang(Shenqibufei-tang) showed the best effect, However, Samso-eum(Shensuyin) and Eunkyo-san(Yinqiao-san) caused lethal damage in the normal cells and also showed strong toxicity in the carcinoma cells.

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Chemopreventive Effect of Quercetin, Vitamin C and Trolox Against the Organic Extract of Airborne Particulate Matter Induced Genotoxicity in A549 Human Lung Carcinoma Cells (대기부유분진추출물로 야기된 DNA 손상에 대한 Quercetin, Vitamin C 및 Trolox 의 보호효과)

  • Kim, Nam-Yee;Heo, Moon-Young
    • YAKHAK HOEJI
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    • v.51 no.4
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    • pp.239-245
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    • 2007
  • In order to evaluate the genotoxicity of airborne particulate matter extracted with dichloromethane (APE), the rat microsome mediated (S-9) or DNA repair enzyme treated Comet assays were performed using the single cell gel electrophoresis in A549 human lung carcinoma cells. It was found that the cells interacting with APE showed more DNA single-strand breaks relative to untreated cells. The genotoxicity of APE was increased with the treatment of S-9 mixture. Microsome mediated DNA damage was inhibited by CYP1Al inhibitor, quercetin. The APE also showed oxidative DNA damage evaluated by endonuclease III treatment. Oxidative DNA damage of APE was inhibited by antioxidants such as vita- min C and Trolox. We also found that the vegetables or fruits extract may reduce APE-induced genotoxicity by their anti- oxidant activity and CYP1A1 inhibition.

Effects of Platycodi Radix on Passive Smoking in Rats (간접흡연에 노출시킨 흰쥐의 폐조직 손상에 대한 길경의 보호효과)

  • Kim, Bum-Hoi
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.26 no.1
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    • pp.40-46
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    • 2012
  • Cigarette smoking is known to be associated with various chronic pulmonary and cardiovascular diseases ranging from inflammation to cancer. Not only first-hand smoke but also second-hand smoke is suggested to be a factor of health risk. This study was to investigate whether Platycodi Radix extract administration would alter oxidative stress in lung leading to protection of cigarette smoke-induced lung damage. Sprague-Dawley rats were randomly divided into 3 groups; Intact, Smoke+PR and Smoke+Vehicle. In Smoke+PR and Smoke+Vehicle group, the exposure to cigarette smoke was performed for 15 min/day for 4 weeks in ventilated smoking chamber. The Platycodi Radix extract and saline were orally administrated to Smoke+PR and Smoke+Vehicle group each. The rats of Intact group were just kept in ventilated chamber without cigarette smoke. After the experiment for 4 weeks, the lung tissues were collected for histological observation and immunohistochemistry. In Results, airspace enlargement and goblet cell hyperplasia were observed after 4 weeks' exposure to cigarette smoke. Whereas, the oral administration of Platycodi Radix extract for 4 weeks reduced airspace enlargement and goblet cell hyperplasia. Moreover, the alterations of BAX/Bcl-2 proteins in lung tissues were observed. These results suggest that Platycodi Radix extract ameliorates lung damage in cigarette smoke-exposed rats and has protective effects on second-hand smoke injury.

Edaravone alleviates lung damage in mice with hypoxic pulmonary hypertension by increasing nitric oxide synthase 3 expression

  • Wan Zheng;Tianfa Li;Junping Wei;Yani Yan;Shanshan Yang
    • The Korean Journal of Physiology and Pharmacology
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    • v.27 no.3
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    • pp.209-220
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    • 2023
  • This study is to determine the regulation of nitric oxide synthase 3 (NOS3) by edaravone in mice with hypoxic pulmonary hypertension (HPH). C57BL/6J mice were reared in a hypoxic chamber. HPH mice were treated with edaravone or edaravone + L-NMMA (a NOS inhibitor). Lung tissue was collected for histological assessment, apoptosis analysis, and detection of malondialdehyde, superoxide dismutase, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and NOS3. The levels of serum TNF-α and IL-6 were also measured. Immunohistochemistry was used to visualize the expression of α-smooth muscle actin (SMA) in pulmonary arterioles. Edaravone treatment improved hemodynamics, inhibited right ventricular hypertrophy, increased NOS3 expression, and reduced pathological changes, pulmonary artery wall thickness, apoptotic pulmonary cells, oxidative stress, and the expression of TNF-α, IL-6, and α-SMA in HPH mice. L-NMMA treatment counteracted the lung protective effects of edaravone. In conclusion, edaravone might reduce lung damage in HPH mice by increasing the expression of NOS3.

Ethanolic extract of Condurango (Marsdenia condurango) used in traditional systems of medicine including homeopathy against cancer can induce DNA damage and apoptosis in non small lung cancer cells, A549 and H522, in vitro

  • Sikdar, Sourav;Mukherjee, Avinaba;Boujedaini, Naoual;Khuda-Bukhsh, Anisur Rahman
    • CELLMED
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    • v.3 no.1
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    • pp.9.1-9.10
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    • 2013
  • In traditional systems of medicine including homeopathy, the Condurango extract (Con) is often used to cure stomach cancer mainly, without having any scientific validation of its anti-cancer ability. Con has therefore been tested against non-small-cell lung cancer cells (NSCLC) A549 and NCI-H522 (H522) known to contain the KRAS mutation, making them resistant to most chemotherapeutic agents. As cancer cells generally defy cytotoxicity developed by chemopreventive agents and escape cell death, any drug showing the capability of preferentially killing cancer cells through apoptosis is worth consideration for judicious application. A549 and H522 cells were exposed to $0.35{\mu}g/{\mu}l$ and $0.25{\mu}g/{\mu}l$ of Con, respectively, for 48 h and analysed based on various protocols associated with apoptosis and DNA damage, such as MTT assay to determine cell viability, LDH assay, DNA fragmentation assay, comet assay, and microscopical examinations of DNA binding fluorescence stains like DAPI, Hoechst 33258 and acridine orange/ethidium bromide to determine the extent of DNA damage made in drug-treated and untreated cells and the results compared. Changes in mitochondrial membrane potential and the generation of reactive oxygen species were also documented through standard techniques. Con killed almost 50% of the cancer cells but spared normal cells significantly. Fluorescence studies revealed increased DNA nick formation and depolarized membrane potentials after drug treatment in both cell types. Caspase-3 expression levels confirmed the apoptosis-inducing potential of Con in both the NSCLC lines. Thus, overall results suggest considerable anticancer potential of Con against NSCLC in vitro, validating its use against lung cancer by practitioners of traditional medicine including homeopathy.

Comparison of the efficacy of the herbs for upper medication on glucose tolerance induced by high fat/high sucrose feeding-induced mice (본초 귀경에 따른 상소한약의 당내성 유발 마우스에서의 개선 효능 비교 연구)

  • Kang, Seok Yong;Park, Yong-Ki
    • The Korea Journal of Herbology
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    • v.29 no.5
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    • pp.1-8
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    • 2014
  • Objectives : To prove the channel-tropism theory of herbal medicines on diabetes mellitus as emaciation-thirst disease in Korean Medicine Theory, we investigated the selective therapeutic effects of Mori Cortex Radidus (MCR), Schisandrae Fructus (SF), Anemarrhenae Rhizoma (AR) for the upper emaciation on different organs in high fat and high sucrose (HF/HS) feeding-induced prediabetic mice. Methods : Diabetes in C57BL/6 mice was induced by the administration of high fat (45 kal%) and high sucrose (32 kal%) for 8 weeks, and them treated with each extract at 250 or 500 mg/kg body weight for 4 weeks (once a day). Oral glucose tolerance test and body weight was measured once a week. Insulin, total cholesterol, triglyceride, ${\gamma}GTP$, GOT and GPT were measured in the sera of all mice. Histopathological changes of different organs, lung, heart, pancreas, stomach, liver, and kidney were observed by H&E staining. Results : The results revealed that MCR extract inhibited the impaired glucose tolerance and lung damage, and increased serum insulin levels in HF/HS-induced prediabetic mice. SF extract inhibited the impaired glucose tolerance and lung damage, increased serum insulin levels, and decreased serum triglycerige levels. Meanwhile, AR extract inhibited the impaired glucose tolerance and lung damage, and decreased serum levels of insulin, total cholesterol and triglycerige levels. Conclusions : These results demonstrated that MCR, SF, and AR extract as the upper emaciation herbal medicines were followed their channel-tropism theory like a lung, and may have a selective therapeutic potential for control of diabetic stage.

A study on the effects of Insambaekhabtang and Insambaekhabtanggamibang on the Experimental lung damage and the hemostasis (인삼백합탕(人蔘百合湯) 및 인삼백합탕가미방(人蔘百合湯加味方)의 효능(效能)에 관(關)한 부험적(實驗的) 연구(硏究))

  • Kim, Nak-Ki;Jeong, Hee-Jae;Jung, Sung-Ki;Rhee, Hyung-Koo
    • The Journal of Korean Medicine
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    • v.16 no.2 s.30
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    • pp.271-280
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    • 1995
  • The experimental studies were done to research the clinical effects of lnsambaekhabtang and Insambaekhabtanggamibang on the xylene-poisoned-lung damage and hypoprothrombinemia induced by warfarin injection in rats and mice. The results are as follows: 1. As to the hemostatic time in mice, lnsambaekhabtang was recongnized no significance but Insambaekhabtanggamibang was recognized significance( P<0.02 ). 2. As to the prothrombine time in rats. lnsambaekhabtang and lnsambaekhabtanggamibang Were recognized significance ( P<0.05, P<0.05 ). 3. As to the recalcification in rats, Insambaekhabtang and lnsambaekhabtanggamibang Were recognized significance ( P<0.05, P<0.02). 4. As to the lung TBA values in Xylene intoxicated rats, Insambaekhabtang was recognized significance but Insambaekhabtanggamibang was no recognized significance ( P<0.05). 5. As to the oxygen consumption in Xylene intoxicated rats, Insambaekhabtang and lnsambaekhabtanggamibang were no recognized significance. According to the above findings, it is suggested that the solid extract of Insambaekhabtang and Insambaekhabtanggamibang revealed effects on the xylene-poisoned-Iung damage and hypoprothrombinemia induced by warfarin injection in rats and mice.

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Effects of Oxidative DNA Damage Induced by Polycyclic Aromatic Hydrocarbons and Genetic Polymorphism of the Paraoxonase-1 (PON1) Gene on Lung Cancer (다환성 방향족 탄화수소 노출에 의한 DNA 산화적 손상과 Paraoxonase-1(PON1) 유전자 다형성이 폐암 발생에 미치는 영향)

  • Lee, Chul-Ho;Lee, Kye-Young;Choe, Kang-Hyeon;Hong, Yun-Chul;Kim, Yong-Dae;Kang, Jong-Won;Kim, Heon
    • Journal of Preventive Medicine and Public Health
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    • v.38 no.3
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    • pp.345-350
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    • 2005
  • Objectives : Polycyclic aromatic hydrocarbons (PAHs), which are risk factors for lung cancer, have been reported to induce oxidative DNA damage. The paraoxonase (PON) plays a significant role in the detoxification of a variety of organophosphorous compounds, with paraoxonase-1 (PON1) being one of the endogenous free-radical scavenging systems in the human body. The aim of this case-control study was to investigate the effects of PAH exposure, oxidative stress and the Q192R polymorphism of PON1 genes, and their interactions in the carcinogenesis of lung cancer. Methods : One hundred and seventy seven lung cancer patients and 177 age- and sex-matched controls were enrolled in this study. Each subject was asked to complete a questionnaire concerning their smoking habits and environmental exposure to PAHs. The Q192R genotypes of the PON1 gene was examined, and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8-hydroxydeoxyguanosine (8-OH-dG) measured. Results : Cigarette smoking was found to be a significant risk factor for lung cancer. The urinary 8-OH-dG level was higher in the patients, whereas the urinary 1-OHP and 2-naphthol levels were higher in the controls. There was a significant correlation between the urinary levels of 8-OHdG and 1-OHP in both the cases and controls. The PON1 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Q/Q genotype of the PON1 gene were found to be at higher risk of developing lung cancer. There was a significant correlation between the urinary levels of 8-OH-dG and 1-OHP in those with the PON1 Q/Q genotype. Conclusions : These results lead to the conclusion that PAHs would induce oxidative DNA damage, especially in individuals with the PON1 Q/Q genotype. Therefore, people with the PON1 Q/Q genotype would be more susceptible to lung cancer than those with the R/R or Q/R genotypes of the PON1 gene.

Combination of Vitamin C and Rutin on Neuropathy and Lung Damage of Diabetes Mellitus Rats

  • Sohn, Uy-Dong;Je, Hyun-Dong;Shin, Chang-Yell;Park, Sun-Young;Yim, Sung-Hyuk;Kum, Chan;Huh, In-Hoi;Kim, Jin -Hak
    • Archives of Pharmacal Research
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    • v.25 no.2
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    • pp.184-191
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    • 2002
  • We investigated the role of vitamin C or rutin on neuropathy and lung damage of diabetic mellitus(DM) rats. Norepinephrine content was significantly decreased in sciatic nerves of DM rats compared with non-DM controls but vitamin C had no effect on decreases of norepinephrine. 2,4-dinitrophenylhydrazine (DNPH) incorporation, which is biomarker of protein oxidation, was increased in sciatic nerve of DM rats as compared with normal control. However, vitamin C had no effects on increases of DNPH incorporation . We measured the content of conjugated dienes (CD) as a biomarker of lipid oxidation in sciatic nerve. CD was increased in DM as compared with normal control, Vitamin C or rutin had no effects on increases of CD. However, Rutin plus vitamin C significantly decreased the content of CD as compared with CIM rats. In lung of DM rats, DNPH incorporation or CD was increased as compared with normal control. Vitamin C or Rutin had no effects on increases of CD However, Rutin plus vitamin C significantly decreased the content of DNPH incorporation or CD in lung tissue. Vitamin C caused marked pathological changes such as the increases of parenchyma and the thickening of alveolar septa in the lung of DM. Rutin had protective effects on the pathological changes in the lung of DM rats. In conclusion, Vitamin C had no effects on oxidative parameter, such as DNPH incorporation or CD, and on the decreases of norepinephrine content in DM rats. Vitamin C caused the marked pathological changes in the lung of DM rats but rutin had protective efforts against the pathological changes.

Therapeutic Effects of (+)-Afzelechin on Particulate Matter-Induced Pulmonary Injury

  • Sanghee Cho;Yun Jin Park;Jong-Sup Bae
    • Biomolecules & Therapeutics
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    • v.32 no.1
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    • pp.162-169
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    • 2024
  • Particulate matter (PM) constitutes a hazardous blend of organic and inorganic particles that poses health risks. Inhalation of fine airborne PM with a diameter of ≤ 2.5 ㎛ (PM2.5) can lead to significant lung impairments. (+)-afzelechin (AZC), a natural compound sourced from Bergenia ligulata, boasts a range of attributes, including antioxidant, antimicrobial, anticancer, and cardiovascular effects. However, knowledge about the therapeutic potential of AZC for patients with PM2.5-induced lung injuries remains limited. Thus, in this study, we investigated the protective attributes of AZC against lung damage caused by PM2.5 exposure. AZC was administered to the mice 30 min after intratracheal instillation of PM2.5. Various parameters, such as changes in lung tissue wet/dry (W/D) weight ratio, total protein/total cell ratio, lymphocyte counts, levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF), vascular permeability, and histology, were evaluated in mice exposed to PM2.5. Data demonstrated that AZC mitigated lung damage, reduced W/D weight ratio, and curbed hyperpermeability induced by PM2.5 exposure. Furthermore, AZC effectively lowered plasma levels of inflammatory cytokines produced by PM2.5 exposure. It reduced the total protein concentration in BALF and successfully alleviated PM2.5-induced lymphocytosis. Additionally, AZC substantially diminished the expression levels of Toll-like receptors 4 (TLR4), MyD88, and autophagy-related proteins LC3 II and Beclin 1. In contrast, it elevated the protein phosphorylation of the mammalian target of rapamycin (mTOR). Consequently, the anti-inflammatory attribute of AZC positions it as a promising therapeutic agent for mitigating PM2.5-induced lung injuries by modulating the TLR4-MyD88 and mTOR-autophagy pathways.