Nicotine is a component of tobacco products and is one of the most commonly abused substances that leads to addiction. Therefore, the present study was performed to investigate the behavioral pattern and toxicity by nicotine exposure in planarians. Basically, planarians were exposed to different concentration of nicotine for 5 min. To investigate detoxification effect, planarians were exposed to nicotine for 5 min, and treated glycyrrhizin for 5 min, then motility and seizure-like behavior were observed for 5 min. As a result, the motility of nicotine-exposed planarians decreased approximately more than 50% compared to freshwater control. However, the motility of glycyrrhizin-exposed planarians recovered than nicotineexposed planarians. In the assessment of seizure-like behavioral pattern, planarians exposed to nicotine showed head-bop or c-like type rather than screw-like or snake-like patterns. However, planarians exposed to glycyrrhizin showed no seizure-like behavior. To examine the oxidative stress response, planarians were cultured in fresh water containing 1 mM nicotine for 1 day. Planarians were homogenized and extracted to assay the contents of reactive oxygen species (ROS), lipid hydroperoxides (LH), glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). The result showed that a significantly higher level of ROS, LH indicated in planarians exposed to nicotine, on the other hand, glycyrrhizin-exposed planarians were significantly decreased ROS, LH levels. In conclusion, the motility decreased when planarians were exposed to nicotine, in a dose-dependent manner, whereas seizurelike behavior increased. Nicotine induced behavioral disturbances and cell toxicity in planarians were recovered by glycyrrhizin, suggesting a candidate substance for nicotine addiction treatment.
The occurrence of allergic disease has increased harmfully in the last few decades. Atopic dermatitis (AD) is an allergic inflammation disorder characterized by itchy, red, swollen, cracked skin. Although the pathogenesis of AD is not fully understood, it is assumed that deregulation of T-helper 1 (Th1) and T-helper 2 (Th2) immune responses, a predominance of allergen-specific IgE, and interrupted epidermal barrier function are keys to the pathogenic mechanism. Activated T helper 2 (Th2) immune function is hallmark of various allergic diseases. Oxidative stress implicated in cutaneous damage in various inflammatory skin diseases.
We investigated the effect of fermented soybean (SCGB1) on the improvement of AD. Soybean fermentation was carried out using B. amyloliquefaciense SCGB1 (KCCM11964P), which is known to produce of natural antibiotics. And then, we experiment of SCGB1 and soybean powder (NC) in DNCB-induced AD model. Mice were respectively oral administration of variety dose for 14 days. As a results, it was confirmed that serum Immunoglobulin E (IgE) expression was dose-dependently decreased in SCGB1 and NC compared to negative control, and it was reduced the skin pruritus inducing factor that Interleukin-31 (IL-31) mRNA level. In addition, the inflammatory cells were infiltration in skin for histological analysis. As a result, it reduced that epidermal hyperplasia, cancellation and aveolarization compared to negative control. These results suggest that SCGB1 may be effective for prevention and treatment of AD.
This study investigated the prokinetic effect of metoclopramide and mirtazapine on gastric transit time (GTT), small bowel transit time (SBTT) and gastrointestinal transit time (GITT) during capsule endoscopy in four healthy beagle dogs. Four beagle dogs participated in the experiment as four groups at intervals of more than three days as the following: Control group 1 (capsule alone), Control group 2 (capsule alone), Metoclopramide administered group (metoclopramide + capsule) and Mirtazapine administered group (mirtazapine + capsule). The results of this study demonstrated there was no significant difference in GTT ([min] control group 1: 105 ± 90, control group 2: 172.5 ± 102 vs metoclopramide administered group: 247.5 ± 93, p = 0.07, 0.10) and SBTT ([min] control group 1: 120 ± 88, control group 2: 75 ± 39 vs metoclopramide administered group: 37.5 ± 15, p = 0.20, 0.18) for capsule only administered groups (control group 1 & 2) compared to metoclopramide administered group. In addition, there was no significant difference in GTT ([min] control group 1: 105 ± 90, control group 2: 172.5 ± 102 vs mirtazapine administered group: 127.5 ± 45, p = 0.56, 0.36) and SBTT ([min] control group 1: 120 ± 88, control group 2: 75 ± 39 vs mirtazapine administered group: 157.5 ± 38, p = 0.29, 0.07) between capsule only administered groups (control group 1 & 2) and mirtazapine administered group. In this study, the fact that metoclopramide might be ineffective and administration of mirtazapine might be inadequate in dogs were confirmed.
Acute myocardial infarction (AMI) is considered the major cause of mortality in the world. Tremendous animal studies are performed to develop novel therapeutics, and this study aimed to induce porcine myocardial infarction model by using polyethylene terephthalate (PET). Coronary guidewire was placed in left anterior descending artery (LAD). The balloon angioplasty catheter was inserted at the back of the PET. The balloon catheter was carefully pushed forward, until the balloon marker was located in mid-LAD. Coronary angiography was performed pre- and post-occlusion at 28 days by C-arm. Histologic analysis of heart tissue was performed 28 days after inducing AMI. Thirty three pigs were anesthetized and underwent percutaneous coronary catheterization. All pigs were successfully embolized in mid-LAD by PET. Fifteen pigs died due to ventricular fibrillation during post-anesthetic recovery time, and overall experiment mortality was 45.5%. In 2,3,5- triphenyl tetrazolium chloride staining, gross finding of the ischemic heart lesion showed firm and white area of infarction associated with the apex and left ventricular posterior wall. Infarct on H&E-stained sections demonstrated a region without myocytes and rich with cardiomyocyte with atypical nuclei. Successful induction of AMI by using PET may provide the pathophysiological information of ischemic heart disease and improvement of therapy development for AMI.