RESUMO
<p><b>OBJECTIVE</b>To explore the effect of ricin temperature response gel on breast cancer and its regulatory effect on immune function in rats.</p><p><b>METHODS</b>Ricin was purified by chromatography and identified by immunoblotting. The rat subcutaneously transplanted breast cancer model was established. Forty model rats with a tumor diameter of about 3.0 cm were subjected to the study. They were randomized into four groups equally: the model group and three treated groups (blank gel, ricin, ricin-gel) were administered with blank gel, ricin, and ricin temperature response gel via percutaneous intratumor injection, respectively. The tumor was isolated 10 days later for the estimation of tumor inhibition rate (TIR) by weighing, pathologic examination, and detection of tumor apoptosis-associated genes bcl-2 and bax with semiquantitative RT-PCR. Also, peripheral blood was obtained to test T-lymphocyte subsets, the killing function of lymphocytes, and the contents of tumor necrosis factor-α (TNF-α) and interleukin-2 (IL-2). The outcomes were compared between groups.</p><p><b>RESULTS</b>The TIR in the ricin-gel group was 61.8%, with the pathologic examination showing extensive tumor tissue necrosis. Compared with the model group, after ricin temperature response gel treatment, bcl-2 expression was down-regulated, bax expression was up-regulated, CD4+ lymphocytes and CD4+/CD8+ ratio in peripheral blood were increased, the killing function of lymphocytes was enhanced, and the contents of TNF-α and IL-2 were elevated (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Intratumor injection of ricin temperature-responsive gel showed significant antitumor effect on breast cancer and could enhance the immune function in the tumor-bearing rat.</p>
Assuntos
Animais , Feminino , Ratos , Antineoplásicos , Apoptose , Relação CD4-CD8 , Modelos Animais de Doenças , Géis , Usos Terapêuticos , Imuno-Histoquímica , Imunomodulação , Injeções Intralesionais , Interleucina-2 , Alergia e Imunologia , Metabolismo , Neoplasias Mamárias Experimentais , Tratamento Farmacológico , Alergia e Imunologia , Patologia , Distribuição Aleatória , Ratos Wistar , Ricina , Sensibilidade e Especificidade , Temperatura , Fator de Necrose Tumoral alfa , Alergia e Imunologia , MetabolismoRESUMO
The biochemical mechanism of degrading keratins by S.fradiae var S-221 was primarily studied.The compounds (Na_ 2 SO_ 4 , Na_ 2 SO_ 3 and sulfdryl acohol), which respecitively enhance specific activity of keratinase, activate keratinase intensively and mainly act on the disulfide bonds reductase in the keratinase, Na_ 2 SO_ 3 activates intensively both disulfide bonds reductase and polypeptide hydrolytase at 0.01 mol/L, whereas Na_ 2 S_ 2 O_ 3 , which acts on the disulfide bonds reductase, inhibits keratinase.On the condition that substrate, keratins exists, S.fradiae var S-221 is induced to produce exo-keratinase, which is a multiproteinase, containing disulfide bonds reductase, which is a key enzyme degrading keratins, then, with polypeptidic, hydrolytase, graduately hydrolyzates denatured keratins into polypeptides, oligopeptides and free amino acids, so that keratins have been decomposed completely.Sulfur in the keratins was transferred into sulfhydryl compounds, H_ 2 S and sulfates in the course of keratinolysine.