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OBJECTIVE：To explore high-alert drug management mode of our hospital ，and to provide reference for the management and utilization of this category in medical institutions. METHODS ：According to High-alert Drug Catalog （2019 edition）issued by Hospital Pharmacy Committee of Chinese Pharmaceutical Association ，the high-alert drug catalog of our hospital and their risk points were formulated. Relevant training and assessment were conducted for physicians ，pharmacists and nurses throughout the hospital. Using qualification rate of high-alert drug management and utilization as index ，the effectiveness of high-alert drug management and utilization were compared before and after optimization. RESULTS ：In our hospital ，the risk of high-alert drugs was controlled by establishing inspection and supervision group ，pharmacist education ，information management ， prescription review and individualized administration ，medication guidance ，prescription review and medication error reporting and other measures and with continuous optimization. Compared with before optimization ，qulification rate of high-alert drug management and utilization increased from 37.3％ to 80.1％ in clinical departments （P＜0.01），and that increased from 59.2％ to 85.0％ in pharmacy department （P＜0.01）. There were still some problems ，such as the inconsistency of high-alert drugs accounts and materials ，the failure to report all medication errors in time ，the imperfect establishment of prescription review software rules ， the insufficient medication guidance ，and the lack of individual medication varieties. CONCLUSIONS ：By optimizing the management of high-alert drugs ，the management and utlization of this category is improved effectively in clinical departments and pharmacy departments of our hospital.
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OBJECTIVE：To provide method reference for scientifically eva luating the rationality of the use of saxagliptin . METHODS：Based on the drug instructions ，clinical guidelines ，clinical pathways ，related references ，clinical endocrinology department and pharmaceutical experts of a hospital jointly discussed and formulated the evaluation criteria for the rationality of the use of saxagliptin. AHP method was used to assign weights to various indexes of evaluation criteria ；TOPSIS method was used to analyze the use of saxagliptin of 106 cases in the hospital during Nov. 2018-Apr. 2019 retrospectively and evaluate rational drug use. RESULTS ：A total of 6 primary indicators and 12 secondary indicators were established. The first three indicators with a relatively high index weight were indications （with a weight of 0.25），dose and adjustment of administration （with a weight of 0.21）and frequency of administration （with a weight of 0.15）. Among 106 cases，39.6％ of drug use were reasonable ，51.0％ were basically reasonable and 9.4％ were unreasonable. Evaluation results made by weighted TOPSIS were consistent with the actual situation. CONCLUSIONS ：TOPSIS method weighted by AHP is reasonable and feasible for evaluating the rationality of saxagliptin use.
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Aim To investigate the renoprotective effect of berberine in diabetic nephropathy rat model. Methods The rat model of DN was induced by intra-peritoneal injection of streptozotocin ( STZ ) after fed with high sugar and high fat diet for six weeks. The rats were divided into 5 groups randomly, i. e. normal control group, model group, BBR ( 50 mg · kg-1 ) , BBR ( 100 mg · kg-1 ) and BBR ( 200 mg · kg-1 ) treatment group. The fasting blood glucose ( FBG) was evaluated at 2, 4, 6,8 week respectively. The patho-logical changes in the kidney were determined by PAS staining. The expression of vascular endothelial growth factor ( VEGF) was detected by immunohistochemistry and Western blot respectively. Results Compared with normal control group, the value of FBG, SCr, BUN and UTP of model group were sharply increased. Compared with model group, the value of FBG in ber-berine different dosage treatment groups were signifi-cantly decreased to various degrees, and berberine dif-ferent dosage treatment could decrease the levels of SCr, BUN and UTP in different degree. Berberine could surpress the alterations of pathological changes in the kidneys and downregulate the expression levels of VEGF in the kidney of diabetic rats with nephropathy. Conclusion Berberine could significantly ameliorate the biochemical indicators and renal injury of the model rats through affecting the abnormal expression levels of VEGF in the kidney.
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Aim To investigate the effect of berberine on the expression of nephrin, podocin and intergrinα3β1 in diabetic nephropathy ( DN ) rat model, and further probe in to the renoprotective effects of berber-ine and its potential mechanisms. Methods The rat model of DN was induced by intraperitoneal injection of streptozotocin ( STZ ) after fed with high-sugar and high-fat diet for six weeks. The rats were assigned into 6 groups randomly: normal control group, DN model group, BBR (50,100 and 200 mg·kg-1 ) treatment group and enalaprilat positive control group ( 1 mg · kg-1 ) . The distribution and expression of kidney podocyte related proteins nephrin, podocin and interg-rinα3β1 were detected by immunohistochemical meth-od following electron microscopy observation ( × 1000 ) and high magnification observation( × 400) and West-ern blot. Results The podocyte related protein neph-rin, podocin and intergrin α3β1 were mainly distribu-ted in podocyte, but slightly different. Compared with normal control group, the expresion of podocyte related protein nephrin, podocin and intergrin α3β1 was de-creased obviously; compared with model group, BBR (100 and 200 mg·kg-1 ) treatment group could sig-nificantly suppress the abnormalities of pathological changes of the kidney and upregulate the expression levels of podocyte specific protein nephrin, podocin and intergrin α3β1 in the kidney of diabetic rats with nephropathy. Conclusions Berberine could alleviate the abnormalities of kidney pathological changes and proteinuria production in the DN model rats, which may be related to the upregulation of the expression of the podocyte proteins nephrin, podocin and intergrinα3β1.