Artemisia argyi is used as a health supplement, tea, and food source in Korea. This study aimed to evaluate the effect of Artemisia argyi (AA) and its active compound, dehydromatricarin A (DA), on the attenuation of airway inflammation in a murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). The C57BL/6 mice were administered AA (50 mg/kg or 100 mg/kg) and DA (10 mg/kg or 20 mg/kg) by oral gavage from day 0 to 7 days and LPS treated by intranasal instillation 48 hours before the sacrifice. The treatment of AA and DA markedly decreased inflammatory cells in the bronchoalveolar lavage fluid (BALF) compared with that in ALI-induced mice, which was accompanied by a significant reduction in the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in BALF. Furthermore, the administration of AA and DA clearly decreased inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in comparison with that in the ALI-induced mice. The histological examination of the lung tissue revealed that the administration of AA and DA suppressed the inflammatory cell infiltration into the peribronchial and alveolar lesions induced by LPS instillation. Collectively, our results indicated that AA and DA effectively decreased the airway inflammatory response induced by LPS instillation. Therefore, AA and DA may offer a potential therapy for airway inflammatory disease.
Acute Lung Injury* ; Animals ; Artemisia* ; Bronchoalveolar Lavage Fluid ; Inflammation* ; Interleukins ; Korea ; Lung ; Mice ; NF-kappa B ; Nitric Oxide Synthase Type II ; Phosphorylation ; Tea ; Tumor Necrosis Factor-alpha

Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of Pycnogenol® (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth factor-β1 (TGF-β1) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in TGF-β1/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.
Animals ; Bronchoalveolar Lavage Fluid ; Collagen ; Humans ; Inflammation ; Lung ; Lung Diseases, Obstructive ; Mice ; Phosphorylation ; Pulmonary Disease, Chronic Obstructive ; Pulmonary Fibrosis ; Smoke ; Tobacco Products*

HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-α, interleukin (IL)-6 and IL-1β in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.
Animals ; Cell Count ; Immune System ; Inflammation* ; Interleukins ; Lung ; MAP Kinase Signaling System ; Matrix Metalloproteinase 9 ; Mice ; Phosphorylation ; Plant Preparations* ; Pneumonia ; Pulmonary Disease, Chronic Obstructive ; Receptors, Tumor Necrosis Factor ; Smoke* ; Therapeutic Irrigation ; Tobacco Products*

In this study, the potential hepatotoxicity of 1,3-dichloro-2-propanol and its hepatotoxic mechanisms in rats was investigated. The test chemical was administered orally to male rats at 0, 27.5, 55, and 110 mg/kg body weight. 1,3-Dichloro-2-propanol administration caused acute hepatotoxicity, as evidenced by an increase in serum aminotransferases, total cholesterol, and total bilirubin levels and a decrease in serum glucose concentration in a dose-dependent manner with corresponding histopathological changes in the hepatic tissues. The significant increase in malondialdehyde content and the significant decrease in glutathione content and antioxidant enzyme activities indicated that 1,3-dichloro-2-propanol-induced hepatic damage was mediated through oxidative stress, which caused a dose-dependent increase of hepatocellular apoptotic changes in the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay and immunohistochemical analysis for caspase-3. The phosphorylation of mitogen-activated protein kinases caused by 1,3-dichloro-2-propanol possibly involved in hepatocellular apoptotic changes in rat liver. Furthermore, 1,3-dichloro-2-propanol induced an inflammatory response through activation of nuclear factor-kappa B signaling that coincided with the induction of pro-inflammatory mediators or cytokines in a dose-dependent manner. Taken together, these results demonstrate that hepatotoxicity may be related to oxidative stress-mediated activation of mitogen-activated protein kinases and nuclear factor-kappa B-mediated inflammatory response.
Animals ; Bilirubin ; Blood Glucose ; Body Weight ; Caspase 3 ; Cholesterol ; Cytokines ; Glutathione ; Humans ; Liver ; Male ; Malondialdehyde ; Mitogen-Activated Protein Kinases* ; Oxidative Stress ; Phosphorylation ; Rats ; Transaminases

This study investigated the protective effects of diallyl disulfide (DADS) against acetaminophen (AAP)-induced acute renal injury in male rats. We also investigated the effects of DADS on kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL), which are novel biomarkers of nephrotoxicity in renal tissues, in response to AAP treatment. The following four experimental groups were evaluated: (1) vehicle control, (2) AAP (1,000 mg/kg), (3) AAP&DADS, and (4) DADS (50 mg/kg/day). AAP treatment caused acute kidney injury evidenced by increased serum blood urea nitrogen (BUN) levels and histopathological alterations. Additionally, Western blot and immunohistochemistry analysis showed increased expression of KIM-1 and NGAL proteins in renal tissues of AAP-treated rats. In contrast, DADS pretreatment significantly attenuated the AAP-induced nephrotoxic effects, including serum BUN level and expression of KIM-1 and NGAL proteins. Histopathological studies confirmed the renoprotective effect of DADS. The results suggest that DADS prevents AAP-induced acute nephrotoxicity, and that KIM-1 and NGAL may be useful biomarkers for the detection and monitoring of acute kidney injury associated with AAP exposure.
Acetaminophen ; Acute Kidney Injury ; Animals ; Biomarkers ; Blood Urea Nitrogen ; Blotting, Western ; Humans ; Immunohistochemistry ; Kidney ; Lipocalins ; Male ; Neutrophils ; Rats*

The aim of this study was to verify subacute oral dose toxicity of positively charged 100 nm zinc oxide (ZnO(AE100[+])) nanoparticles (NPs) in Sprague-Dawley rats. ZnO(AE100[+]) NPs were administered to rats of each sex by gavage at 0, 500, 1,000, and 2,000 mg/kg/day for 14 days. During the study period, clinical signs, mortality, body weight, food consumption, hematology, serum biochemistry, gross pathology, organ weight, and histopathology were examined. Increased mortality and clinical signs, decreased body weight, feed consumption, hemoglobin (HB), hematocrit (HCT), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet (PT), and lymphocyte (LYM) and increased white blood cells (WBCs), neutrophils (NEUs), alkaline phosphatase (ALP), and histopathological alterations in the spleen, stomach, and pancreas were observed at 2,000 mg/kg/day. Increased clinical signs, decreased body weight, feed consumption, HB, HCT, MCV, MCH, MCHC, and LYM and increased WBCs, NEUs, ALP, and histopathological alterations in the spleen, stomach, and pancreas were seen at 1,000 mg/kg/day. Increased clinical signs, decreased MCV and MCH and increased histopathological alterations in the stomach and pancreas were found at 500 mg/kg/day. These results suggest that the target organs were the spleen, stomach, and pancreas in rats. The no-observed-adverse-effect level was <500 mg/kg for both sexes.
Alkaline Phosphatase ; Animals ; Biochemistry ; Blood Platelets ; Body Weight ; Erythrocyte Indices ; Hematocrit ; Hematology ; Leukocytes ; Lymphocytes ; Mortality ; Nanoparticles* ; Neutrophils ; No-Observed-Adverse-Effect Level ; Organ Size ; Pancreas ; Pathology ; Rats* ; Rats, Sprague-Dawley ; Spleen ; Stomach ; Zinc Oxide* ; Zinc*

A pancreatic fistula (PF) is an abnormal connection between the pancreas and adjacent or distant organs, structures, or spaces resulting from leakage of pancreatic secretions from disrupted pancreatic ducts. A PF is a rare complication that occurs during a acute and chronic pancreatitis or after traumatic or surgical disruption of the pancreatic duct. PFs are frequently classified as internal or external depending upon whether they communicate with an internal organ or the skin. Pancreatico- colonic fistulas are the most common, whereas pancreatico-gastric fistulas are the rarest. We report a rare case of a pancreatico-gastric fistula complicated by acute pancreatitis.
Colon ; Fistula ; Pancreas ; Pancreatic Ducts ; Pancreatic Fistula ; Pancreatitis ; Pancreatitis, Chronic ; Skin

The EST Knowledge Integrated System, EKIS (http://ekis.kribb.re.kr), was established as a part of Korea's Ministry of Education, Science and Technology initiative for genome sequencing and application research of the biological model organisms (GEAR) project. The goals of the EKIS are to collect EST information from GEAR projects and make an integrated database to provide transcriptomic and metabolomic information for biological scientists. The EKIS constitutes five independent categories and several retrieval systems in each category for incorporating massive EST data from high-throughput sequencing of 65 different species. Through the EKIS database, scientists can freely access information including BLAST functional annotation as well as Genechip and pathway information for KEGG. By integrating complex data into a framework of existing EST knowledge information, the EKIS provides new insights into specialized metabolic pathway information for an applied industrial material.
Data Mining ; Expressed Sequence Tags ; Genome ; Metabolic Networks and Pathways ; Metabolomics ; Models, Biological

BACKGROUND/AIMS: The therapeutic strategies of applying adefovir for treating lamivudine resistant HBV mutants are controversial. Thus, we observed the clinical outcomes after discontinuation of lamivudine to establish the timing to initiate adefovir therapy. METHODS: Fifty chronic hepatitis B (CHB) patients with lamivudine resistant HBV mutants who had received lamivudine for more than 12 months were included in the study. We investigated the clinical outcomes at 6 months after the end of treatment (EOT). We compared the serial clinical outcomes among respective groups based on serum ALT at the EOT and the clinical characteristics of patients with or without acute exacerbation (AE) and the HBeAg loss. We also investigated the predictive parameters of AE and HBeAg loss. RESULTS: Fifteen patients (30%) had experienced AE at 6 months after the EOT. Four patients received antiviral agents because of their hepatic decompensation. Patients with AE had higher serum ALT values and lower HBV DNA titers at EOT compared with those patients without AE. Serum ALT at the EOT was the predictive parameter of AE. Eight patients (21.6%) had newly developed HBeAg loss at 6 months after EOT. The total bilirubin at EOT was the predictive parameter of HBeAg loss. CONCLUSIONS: CHB patients with lamivudine resistant HBV mutants had favorable clinical outcomes at 6 months after EOT. Therefore, we can consider observing the clinical courses after discontinuation of lamivudine and it is not always required to overlap the adefovir for treating lamivudine resistant HBV mutants except for the treatment of patients with a high risk of developing decompensation.
Adenine/administration & dosage/analogs & derivatives ; Adult ; Antiviral Agents/*administration & dosage ; *Drug Resistance, Viral ; English Abstract ; Female ; Hepatitis B e Antigens/blood ; Hepatitis B virus/drug effects ; Hepatitis B, Chronic/*drug therapy/virology ; Humans ; Lamivudine/*administration & dosage ; Male ; Middle Aged ; Phosphonic Acids/administration & dosage ; Reverse Transcriptase Inhibitors/*therapeutic use ; Treatment Outcome

Hemobilia is a disease caused by injury or conditions that cause the abnormal communication between intrahepatic blood vessels and biliary tract, resulting in leakage of blood into the biliary tract. In the past, trauma had been the most common cause of hemobilia. However, with the increasing invasive procedures in the hepatobiliary tract, iatrogenic origin has become the major cause of hemobilia. Also, non-traumatic etiologies of hemobilia include vascular malformation such as aneurysm, gallstone, inflammation, biliary tumor, hepatocellular carcinoma and coagulopathy. Among these non-traumatic etiologies, choledocholithiasis is a rare cause of hemobilia. The authors have experienced two cases of hemobilia caused by choledocholithiasis, which was diagnosed by abdominal ultrasonography, abdominal CT and duodenoscopy. Both patients were treated by the endoscopic sphincterotomy and stone removal with basket.
Aneurysm ; Biliary Tract ; Blood Vessels ; Carcinoma, Hepatocellular ; Choledocholithiasis ; Common Bile Duct* ; Duodenoscopy ; Gallstones ; Hemobilia* ; Humans ; Inflammation ; Sphincterotomy, Endoscopic ; Tomography, X-Ray Computed ; Ultrasonography ; Vascular Malformations