Novel Antihypertension Mechanism of β-Glucan by Corin and ANP-Mediated Natriuresis in Mice

Many of the β-glucans are known to have antihypertensive activities, but, except for angiotensin-converting enzyme II inhibition, the underlying mechanisms remain unclear. Corin is an atrial natriuretic peptide (ANP)-converting enzyme. Activated corin cleaves pro-ANP to ANP, which regulates water–sodium balance and lowers blood pressure. Here, we reported a novel antihypertensive mechanism of β-glucans, involved with corin and ANP in mice. We showed that multiple oral administrations of β-glucan induced the expression of corin and ANP, and also increased natriuresis in mice. Microarray analysis showed that corin gene expression was only upregulated in mice liver by multiple, not single, oral administrations of the β-glucan fraction of Phellinus baumii (BGF). Corin was induced in liver and kidney tissues by the β-glucans from zymosan and barley, as well as by BGF. In addition to P. baumii, β-glucans from two other mushrooms, Phellinus linteus and Ganoderma lucidum, also induced corin mRNA expression in mouse liver. ELISA immunoassays showed that ANP production was increased in liver tissue by all the β-glucans tested, but not in the heart and kidney. Urinary sodium excretion was significantly increased by treatment with β-glucans in the order of BGF, zymosan, and barley, both in 1% normal and 10% high-sodium diets. In conclusion, we found that the oral administration of β-glucans could induce corin expression, ANP production, and sodium excretion in mice. Our findings will be helpful for investigations of β-glucans in corin and ANP-related fields, including blood pressure, salt–water balance, and circulation.

Effects and Mechanisms of Taurine as a Therapeutic Agent

Taurine is an abundant, β-amino acid with diverse cytoprotective activity. In some species, taurine is an essential nutrient but in man it is considered a semi-essential nutrient, although cells lacking taurine show major pathology. These findings have spurred interest in the potential use of taurine as a therapeutic agent. The discovery that taurine is an effective therapy against congestive heart failure led to the study of taurine as a therapeutic agent against other disease conditions. Today, taurine has been approved for the treatment of congestive heart failure in Japan and shows promise in the treatment of several other diseases. The present review summarizes studies supporting a role of taurine in the treatment of diseases of muscle, the central nervous system, and the cardiovascular system. In addition, taurine is extremely effective in the treatment of the mitochondrial disease, mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and offers a new approach for the treatment of metabolic diseases, such as diabetes, and inflammatory diseases, such as arthritis. The review also addresses the functions of taurine (regulation of antioxidation, energy metabolism, gene expression, ER stress, neuromodulation, quality control and calcium homeostasis) underlying these therapeutic actions.

Potentiation of Innate Immunity by beta-Glucans

beta-Glucans have been known to exhibit antitumor activities by potentiating host immunity by an unknown mechanism. The C-type lectin dectin-1, a beta-glucan receptor, is found on the macrophage and can recognize various beta-glucans. Previously, we demonstrated the presence of beta-glucan receptor, dectin-1, on the Raw 264.7 cells as well as on murine mucosal organs, such as the thymus, the lung, and the spleen. In order to investigate immunopotentiation of innate immunity by beta-glucan, we stimulated a murine macrophage Raw 264.7 cell line with beta-glucans from Pleurotus ostreatus, Saccharomyces cerevisiae, and Laminaria digitata. Then, we analyzed cytokines such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 by reverse transcription-polymerase chain reaction (RT-PCR). In addition we analyzed gene expression patterns in beta-glucan-treated Raw 264.7 cells by applying total mRNA to cDNA microarray to investigate the expression of 7,000 known genes. When stimulated with beta-glucans, the macrophage cells increased TNF-alpha expression. When co-stimulation of the cells with beta-glucan and lipopolysaccharide (LPS), a synergy effect was observed by increased TNF-alpha expression. In IL-6 expression, any of the beta-glucans tested could not induce IL-6 expression by itself. However, when co-stimulation occurred with beta-glucan and LPS, the cells showed strong synergistic effects by increased IL-6 expression. Chip analysis showed that beta-glucan of P. ostreatus increased gene expressions of immunomodulating gene families such as kinases, lectin associated genes and TNF-related genes in the macrophage cell line. Induction of TNF receptor expression by FACS analysis was synergized only when co-stimulated with beta-glucan and LPS, not with beta-glucan alone. From these data, beta-glucan increased expressions of immunomodulating genes and showed synergistic effect with LPS.

The Influence of Admission Characteristics on Premedical School Achievement at a Medical School / 한국의학교육

PURPOSE: This study examined the relationship between the achievement of premedical students and admission characteristics at University of Ulsan College of Medicine: high school types and majors, gender, admission assessment method and interval from the high school graduation to the entrance of premedical school. METHODS:: Admission characteristics and demographic informations was obtained for students who entered from 1999 to 2001. Academic achievement was measured according to the results of grade point average(GPA) of total subjects and science subjects and each subject's grades. Admission characteristics and the GPA's and grades were analysed. Multiple linear regression was used to examine the relationship between admission variables and academic achievement. RESULTS: 1. For the first year of premedical school students who studied natural science at ordinary high school, or who graduated science high school showed better achievement than others. 2. Students entered by general selection method also got significantly higher GPA's than other students in the first year. 3. Female students got significantly higher GPA's than male students in two consecutive semesters(1-2 and 2-1). 4. Students qualified by the national highschool graduation examination showed significantly lower achievement than other students in the first semester of the second year. 5. There were no relationships between achievement and other characteristics. CONCLUSION: Students who have academic difficulties in the first year of the premedical course is those who were not exposed to the natural science subjects. It seemed that the premedical course worked as a buffer absorbing differences from the students of various academic backgrounds in their high school period. For the second year, high school majors did not influence the academic achievement.

Inhibition of Interleukin-1 Signal by Annexin-1 in Phorbol Myristate Acetate Stimulated Lymphocytes / 대한면역학회지

Annexin-1 (ANX1) is a 37 kDa protein that is induced and secreted by glucocorticosteroid hormone. The secreted ANX1 has been believed to exert its function by binding to its putative rnembrane receptor. In this report we demonstrate that ANXl receptor (ANX1R) signal blocks the interleukin-1B (IL-1B) receptor signal pathway in human peripheral blood mononuclear cells (PBMCs). When PBMCs were treated with both IL-1B (100 ng/ml) and PMA (10 ng/ml) in the absence or presence of dexamethasone for 5 days, dexamethasone (100 nM) suppressed lymphocyte proliferation to 24% of the control. However addition of anti-ANX1 polyclonal antibody of 1:200 and 1:1,000 dilution to this system induced recovery of proliferation to 80% and 40%, respectively, when compared to the control. In the mixed lymphocyte reaction, dexamethasone suppressed lymphocyte proliferation to 9% of that of control when stimulated with IL-1B (100 ng/ml) and phorbol myristate acetate (10 ng/ml). Addition of anti-ANX1 polyclonal antibody (1:1,000) to this system also recovered the proliferation to 20% of that of the control system. In the ANX1 receptor induction experiment using flow cytometry, ANX1 receptor expression on lymphocytes, CD4+ T cells, CD8+ T cells and monocytes increased depending on the externally added IL-1B ranging from 10 to 1,000 ng/ml. From these results, it is evident that dexamethasone induces ANX1 secretion into the culture medium and anti-ANX1 polyclonal antibody abolishes the effects of dexamethasone. Furthermore these results imply that extracellular ANX1 exerts its effects by binding to the receptor on the cell membrane and the activated signal(s) of ANX1R block IL-1B receptor signal in the lymphocytes.

Immunological studies on collyban of collybia confluens / 대한암학회지

No abstract available.