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1.
China Pharmacist ; (12): 743-744, 2016.
Artículo en Chino | WPRIM | ID: wpr-490879

RESUMEN

After the structural reform in the food and drug supervision system, the knowledge structure and the professional re-quirements of the supervisors is unmatched, which hinder the fulfillment of regulatory responsibilities and the performance of adminis-trative efficacy. Effective ways for team building are actively explored throughout the country. The paper introduced the adult corre-spondence education of the supervisors in Zhejiang Ningbo food and drug supervision system to provide a good example for training work throughout the country and some useful suggestions for the quality improvement of the supervision team.

2.
Acta Pharmaceutica Sinica ; (12): 1489-95, 2012.
Artículo en Chino | WPRIM | ID: wpr-433003

RESUMEN

This study aims to investigate the preventive role and potential mechanisms of blocking extracellular HMGB1 function on doxorubicin induced cardiac injury. Mice were treated with HMGB1 blocker glycyrrhizin 1 h before and one time every day (intraperitoneal, 10 mg per mouse) after doxorubicin injection, and sacrificed on the day 14 after doxorubicin challenge. Cardiac function was evaluated by echocardiography and hemodynamic measurement. Myocardial inflammation and collagen deposition were analyzed by immunohistochemistry and picrosirius red staining. The interaction of HMGB1 and TLR2 was assessed by co-immunoprecipitation and confocal microscopy. The protein contents of HMGB1, MyD88, p65NF-kappaB and phospho-p65NF-kappaB were measured by Immunoblot. Compared with mice treated with saline, doxorubicin treatment led to an upregulation in HMGB1 expression. Blocking HMGB1 activity with glycyrrhizin protected mice against cardiac dysfunction, inflammatory response, and cardiac fibrosis induced by doxorubicin challenge. Glycyrrhizin inhibited the interaction of HMGB1 and TLR2, and blocked the downstream signaling of TLR2. In conclusion, blocking HMGB1 protected against doxorubicin induced cardiac injury by inhibiting TLR2 signaling pathway.

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