ABSTRACT
<p><b>OBJECTIVE</b>To study the neuro-endocrine adjustment effects of Herba Epimedii and Fructus Ligustrilucidi on the asthmatic rats.</p><p><b>METHOD</b>Rat asthma model was duplicated by OVA (ovalbumin) through sensitizing and challenging. Fifty male rats were randomly divided into normal group, model group, adjustment group of Herba Epimedii and Fructus Ligustrilucidi, Peibenfang group and Asimei capsule group. Investigating levels of ET (Endothelin), NO, iNOS (inducible NOS ), and cNOS (constitutive NOS) in blood serum and BALF (bronchoalveolar lavage fluid ), CORT (corticotrophin) in serum, ACTH (adrenocorticotropin hormone) in plasma, CHR (corticotropin release hormone) in hypothalamus, protein expression of GCR (glucocorticoid receptor) in lung tissue.</p><p><b>RESULT</b>The adjustment of Herba Epimedii and Fructus Ligustrilucidi could inhibit ET and NO content in BALF (all P < 0.05), decrease the level of iNOS in serum and BALF (P < 0.01 or P < 0.05), and increase the level of cNOS in serum and BALF (P < 0.01 or P < 0.05), raise the concentration of serum CORT (P < 0.01), enhance the protein expression of GCR in lung tissue (P < 0.05).</p><p><b>CONCLUSION</b>The preventive and therapeutic effect of Herba Epimedii and Fructus Ligustrilucidi on asthma relates to their adjustment effect on ET/NO and HPA axis.</p>
Subject(s)
Animals , Humans , Male , Rats , Asthma , Blood , Drug Therapy , Metabolism , Bronchoalveolar Lavage Fluid , Chemistry , Disease Models, Animal , Endothelins , Blood , Hypothalamo-Hypophyseal System , Lung , Metabolism , Nitric Oxide , Blood , Nitric Oxide Synthase Type II , Blood , Pituitary-Adrenal System , Metabolism , Plant Extracts , Random Allocation , Rats, Sprague-Dawley , Receptors, Glucocorticoid , MetabolismABSTRACT
EBP50(ERM-binding phosphoprotein-50),a multifunctional adapter protein with 358 amino acids and two PDZ domains, regulates cell growth and migration. Lines of evidences indicate that it is a potential cancer suppressor protein. Loss of heterozygosity (LOH) and intragenic mutation of the ebp50 gene have been found in both primary breast tumors and breast cancer cell lines. EBP50 suppresses the breast cancer cell proliferation via its interaction with many tumor suppressor protein including PTEN, SYK, MERLIN, etc. Here the molecular structure of EBP50, signal pathway regulated by EBP50, and the relationship between breast cancer development and EBP50 are discussed.