Objectives : The aims of this study were to exploring the therapeutic effect of Imperatae Rhizoma Extract(IRE) on Asthma. Methods : To investigate biological modulation activities of IRE, we conducted the cell-based assay whether IRE could regulate T helper 2 cells activity with EL4 T cells and mouse splenocytes, and followed animal study to conform the efficacy of their therapeutic potential on OVA-induced asthmatic mouse. Results : In cell study, IRE suppress the nuclear translocation of GATA binding protein-3 protein in phorbol 12-myristate 13-acetate/Ionomycin-stimulated EL4 T cells and Interleukine(IL)-4, IL-5 and IL-13 production in splenocytes at concentration dependent manner. In animal study, IRE-treated groups both 100mg/ml and 200mg/ml improve airway hypersensitibility reaction(AHR) response to methacholine about 30% and 40% with positive control group. Peritoneal blood analysis reveal that eosinophil number and ovalbumin-specific IgE is reduced by IRE treatment. Cell number of eosinophil is also reduced in bronchoalveolar lavage of IRE group like to peritoneal cell and real time-polymerase chain reaction data show that expression levels of IL-4, IL-5 and IL-13 were down regulated in lung tissue. Finally, histological analysis indicate that IRE protect the bronchial tissue damages through the accumulation of inflammatory cells and collagen, and these effect may be cause by interfering Th2 cells activity. Conclusions : Our data represent that IRE potentiates therapeutic activities to the allergic diseases such as asthma by regulating Th2 cells differentiation.
Cortex mori (Morus alba L.), the root bark of mulberry tree, has been used as an antiphlogistic, diuretic, and expectorant in herbal medicine. The purpose of this study was to determine whether Cortex mori could inhibit the ovalbumin (OA) -induced late asthmatic reaction in guinea pigs. Guinea pigs were sensitized by two exposures to an aerosol of OA(1.0%) and then challenged with aerosolized antigen(2.0%), The animals were pretreated by three inhalations of the aerosoled Cortex mori either before antigen sensitization or cahllenge. Bronchoalveolar lavage fluid(BALF) and peripheral blood were collected at 17 hours after OA challenge. The cell populations in BALF and peripheral blood were examined to determine the changes of the relative proportions of eosinophils,neutrophils and mononuclear cells etc. Beta-glucuronidase activity in BALF was measured to evaluate the alveolar macrophage activation. OA-induced histamine release from guinea pig peritoneal fluid cells was measured by radioisotope enzymatic asssay. Results were as follows. The number of eosinophils, neutriphils and lymphocytes recovered in BALF were significantly increased in the 17h following aerosol challenge with OA. Among them, eosinophil and neutriphils were decreased remarkably in group that had been preinhalated with Cortex mori. The number of lymphocytes in BALF were not decreased in group pretreated with CM before sensitization but decreased in Group pretreated with CM before challenge. After OA challenge, the number of eosinophils in peripheral blood were markedly increased, but Cortex mori inhibited significantly the OA-induced eosinophilia. Beta-glucuronidase activity in the supernatants of BALF were significantly increased in the 17h following aerosol challenge with OA, however, pretreatment of Cortex mori had no influence on Beta-glucuronidase activity, suggesting that Cortex mori had no inhibitory effect on OA-induced alveolar macrophage activation. Cortex mori inhibited the OA-induced histamine release from guinea pig peritoneal fluid cells. From the above results, it is suggested that Cortex mori contains some substances with an activity to inhibit the the OA-induced late phase reaction of the bronchial asthma in guinea pigs.
Objectives: To investigate the anti-inflammatory effects of cultivated wild ginseng pharmacopuncture in lipopolysaccharide (LPS)-induced inflammatory rat model. Methods: Sprague-Dawley rats were divided into 4 groups; LPS control (n=6), LPS+cultivated wild ginseng pharmacopuncture at CV4 (n=6), LPS+cultivated wild ginseng pharmacopuncture at CV17 (n=6), and LPS+cultivated wild ginseng pharmacopuncture at Ex-HN1 (n=6). Pharmacopuncture (0.1 ml) was given every two days for 4 weeks followed by inflammation induction by peritoneal LPS injection (5 mg/kg). Blood, liver tissue, and peritoneal lavage fluid were taken and proinflammatory cytokines and other related factors were analysed. Results: Compared with the control group, CV4 and Ex-HN1 pharmacopuncture groups significantly attenuated plasma IL-$1{\beta}$, IL-6, and TNF-$\alpha$ increase at 2h and 5h after LPS injection (P<0.05). A significant difference from control group emerged at 5 h for plasma IL10 (P<0.05). For liver cytokines analyzed at 5 h after LPS injection, only CV4 pharmacopuncture group showed significant difference in TNF-$\alpha$ and IL-10 (P<0.05). Blood CD4/CD8 ratio and the phagocytic activities of polymorphonuclear neutrophils were not different from those of control group in all pharmacopuncture groups (P>0.05). CV4 pharmacopuncture significantly attenuated increase of plasma ${NO_3}^-/{NO_2}^-$, Intracellular adhesion molecule-1 (ICAM-1), cytokine-induced neutrophil chemoattractant-1 (CINC-1), and prostaglandin $E_2$ ($PGE_2$) compared with the control group (P<0.05). Monocyte chemoattractant protein-1, $PGE_2$, and CINC-1 level of CV4 pharmacopuncture group was significantly different from those from the control group (P<0.05). Conclusions: These results indicate that cultivated wild ginseng pharmacopuncture at CV4 may have a potent anti-inflammatory effect in an LPS-induced inflammatory rat model.
About 8 year-old castrated male Yorkshire terrier was presented for evaluation of dysuria, stranguria, hemtauria, and pollakiuria. On history taking, dysuria first was observed three months ago and these signs were waxed and waned. Physical examination revealed mild left perineal swelling. On routine laboratory examination, no significant findings were identified. Positive contrast urogram identified peritoneal herniation of urinary bladder. Urinalysis showed proteinuria and hematuria. Urine sediment revealed epithelial cells, white blood cells and rod-shaped bacteria. Pseudomonas aeroginosa was isolated from urine obtained through cystocentesis, and had resistance against fourteen antibiotics. Cystitis caused by P. aeruginosa concurrent with cystolithiasis and perineal hernia was diagnosed. Cystotomy, herniorrhaphy and EDTA-Tris solution lavage of bladder were performed. The patient was recovered to normal condition 2 days after treatment. Two weeks later, bacterial culture of urine was negative and any abnormality in ultrasonogram and urinalysis was not observed except calcium oxalate dihydrate crystals.
Liquid biopsy, a minimally invasive procedure that causes minimal pain and complication risks to patients, has been extensively studied for cancer diagnosis and treatment. Moreover, it facilitates comprehensive quantification and serial assessment of the whole-body tumor burden. Several biosources obtained through liquid biopsy have been studied as important biomarkers for establishing early diagnosis, monitoring minimal residual disease, and predicting the prognosis and response to treatment in patients with cancer. Although the clinical application of liquid biopsy in gastric cancer is not as robust as that in other cancers, biomarker studies using liquid biopsy are being actively conducted in patients with gastric cancer. Herein, we aimed to review the role of various biosources that can be obtained from patients with gastric cancer through liquid biopsies, such as blood, saliva, gastric juice, urine, stool, peritoneal lavage fluid, and ascites, by dividing them into cellular and acellular components. In addition, we reviewed previous studies on the diagnostic, prognostic, and predictive biomarkers for gastric cancer using liquid biopsy and discussed the limitations of liquid biopsy and the challenges to overcome these limitations in patients with gastric cancer.
Purpose: Despite the great advances in laparoscopic techniques, most active general surgeons do not apply laparoscopic surgery in the treatment of duodenal ulcer perforation when facing a real-life emergency. Therefore, our study was designed to evaluate the feasibility of laparoscopic surgery in duodenal ulcer perforation, and provide a step-by-step protocol with tips and recommendations for less experienced surgeons. Materials and Methods: Between March, 2011 and May, 2012, 21 patients presenting with duodenal ulcer perforation underwent laparoscopic primary repair with omentopexy. There were no contraindications to perform laparoscopic surgery, and the choice of primary repair was decided according to the size of the perforation. The procedure for laparoscopic primary repair with omentopexy consisted of peritoneal lavage, primary suture, and omentopexy using a knot pusher. Results: During the operation, no conversion to open surgery or intra-operative events occurred. The median operation time was 45.0 minutes (20~80 minutes). Median day of commencement of a soft diet was day 6 (4~17 days). After surgery, the median hospital stay was 8.0 days (5~27 days). Postoperative complications occurred in one patient, which included a minor leakage. This complication was resolved by conservative management. Conclusions: Although our study was carried out on a small number of patients at a single institution, we conclude that laparoscopic primary repair can be an effective surgical method in the treatment of duodenal ulcer perforation. We believe that the detailed explanation of our procedure will help beginners to perform laparoscopic primary repair more easily.
Objective : In vitro proapoptotic effect of Hangbaek-Tang (HBT) has been documented by one of us. In the present study, we aimed to demonstrate in vivo effect of HBT on tumor growth. Methods : In vitro selective cytotoxicity of HBT was examined by enumeration of viable cell numbers using BC3A mouse leukemic cells and normal spleen cells. In vivo effect of HBT (25 and 50 mg/mouse) on tumor growth was assayed using BC3A cells innoculated subcutaneously in the flank. Annexin-V apoptosis assay and PI staining was performed to determine the effective serum factor in HBT-treated mice. Leukocyte recruitment into peritoneum were analyzed by microscopy with a stained cytosmear of peritoneal lavage fluid. Results : HBT exhibited in vitro selective cytotoxicity to leukemic cells and did not show any toxicity on immune organs. In vivo i.p. administration of HBT induced significant reduction in tumor growth but not complete regression. Sera obtained from HBT-treated mice strongly inhibited BC3A cell growth in vitro and were revealed to markedly enhance apoptosis and accompanying cell death, when compared to those from PBS-treated mice. Abundant extravasation of leukocytes, especially neutrophils, into peritoneum was observed in HBT-treated mice. Conclusions : HBT causes leukemic, BC3A cell death in vivo via apoptosis as well as in vitro, for which functional involvement of leukocytes is suggested.
This study measured the plasma and liver concentrations of cytokines, the distribution of blood lymphocyte subpopulations (CD4 and CD8), plasma levels of nitrite (NO3–) and nitrate (NO2–), intercellular adhesion molecule 1 (ICAM-1), cytokine-induced neutrophil chemoattractant 1 (CINC-1), prostaglandin E2 (PGE2), and peritoneal lavage fluid (PLF) levels of monocyte chemotactic protein 1 (MCP-1) and CINC-1 in order to examine the anti-inflammatory activity of the cinnamon extract in lipopolysaccharide (LPS)-exposed rats. The plasma concentrations of interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNF-α) were lower in the cinnamon extract groups than in the control group at both 2 and 5 h after LPS injection. Furthermore, the liver concentrations of IL-1β, IL-6, and TNF-α were lower in the cinnamon extract groups than in the control group at 5 h after LPS injection. Plasma IL-10 concentrations were higher in the cinnamon extract groups than in the control group at both 2 and 5 h after LPS injection, and liver concentrations of IL-10 did not differ significantly among all treatment groups at 5 h after LPS injection. The distribution of CD4 tended to increase, and that of CD8 tended to decrease in the cinnamon extract groups. The CD4/CD8 ratio was increased in the cinnamon extract groups. The plasma concentrations of NO3–/NO2–, ICAM-1, CINC-1, and PGE2 and the PLF concentrations of MCP-1 and CINC-1 exhibited a tendency to decrease in the cinnamon extract groups. These results indicate that cinnamon extract can exert functional anti-inflammatory effects.
Park, Donghwan;Ro, MyungJa;Lee, A-Jin;Kwak, Dong-Wook;Chung, Yunro;Kim, Jae-Hong
Molecules and Cells
/
제44권12호
/
pp.893-899
/
2021
BLT2 is a low-affinity receptor for leukotriene B4, a potent lipid mediator of inflammation generated from arachidonic acid via the 5-lipoxygenase pathway. The aim of this study was to investigate whether BLT2 plays any role in sepsis, a systemic inflammatory response syndrome caused by infection. A murine model of cecal ligation and puncture (CLP)-induced sepsis was used to evaluate the role of BLT2 in septic inflammation. In the present study, we observed that the levels of ligands for BLT2 (LTB4 [leukotriene B4] and 12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid]) were significantly increased in the peritoneal lavage fluid and serum from mice with CLP-induced sepsis. We also observed that the levels of BLT2 as well as 5-lipoxygenase (5-LO) and 12-LO, which are synthesizing enzymes for LTB4 and 12(S)-HETE, were significantly increased in lung and liver tissues in the CLP mouse model. Blockade of BLT2 markedly suppressed the production of sepsis-associated cytokines (IL-6 [interleukin-6], TNF-α [tumor necrosis factor alpha], and IL-1β [interleukin-β] as well as IL-17 [interleukin-17]) and alleviated lung inflammation in the CLP group. Taken together, our results suggest that BLT2 cascade contributes to lung inflammation in CLP-induced sepsis by mediating the production of inflammatory cytokines. These findings suggest that BLT2 may be a potential therapeutic target for sepsis patients.
Acinetobacter baumannii is known for its multidrug antibiotic resistance. New approaches to treating drug-resistant bacterial infections are urgently required. Cathelicidin-related antimicrobial peptide (CRAMP) is a murine antimicrobial peptide that exerts diverse immune functions, including both direct bacterial cell killing and immunomodulatory effects. In this study, we sought to identify the role of CRAMP in the host immune response to multidrug-resistant Acinetobacter baumannii. Wild-type (WT) and CRAMP knockout mice were infected intranasally with the bacteria. CRAMP-/- mice exhibited increased bacterial colony-forming units (CFUs) in bronchoalveolar lavage (BAL) fluid after A. baumannii infection compared to WT mice. The loss of CRAMP expression resulted in a significant decrease in the recruitment of immune cells, primarily neutrophils. The levels of IL-6 and CXCL1 were lower, whereas the levels of IL-10 were significantly higher in the BAL fluid of CRAMP-/- mice compared to WT mice 1 day after infection. In an in vitro assay using thioglycollate-induced peritoneal neutrophils, the ability of bacterial phagocytosis and killing was impaired in CRAMP-/- neutrophils compared to the WT cells. CRAMP was also essential for the production of cytokines and chemokines in response to A. baumannii in neutrophils. In addition, the A. baumannii-induced inhibitor of κB-α degradation and phosphorylation of p38 MAPK were impaired in CRAMP-/- neutrophils, whereas ERK and JNK phosphorylation was upregulated. Our results indicate that CRAMP plays an important role in the host defense against pulmonary infection with A. baumannii by promoting the antibacterial activity of neutrophils and regulating the innate immune responses.
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