OBJECTIVE:To study the protective effect of tanshinoneⅡA(TSⅡA)sulfonate injection against vancomycin(VAN)-induced renal injury model rats and its mechanism. METHODS:72 rats were randomly divided into blank group,model group, positive control group(amifostine,1 mg/kg)and TSⅡA sulfonate injection low-dose,medium-dose and high-dose groups(15,30, 60 μg/kg),with 12 rats in each group. Except for blank group,those groups were given VAN(200 mg/kg)intravenously via tail vein to induce renal injury rat model;after modeling,each drug group was given relevant medicine intraperitoneally once a day, and blank group and model group were given normal saline intragastrically for consecutive 10 days. The levels of 24 h protein, NAG and KIM-1 in urine were determined,and those of Cys C,Scr and BUN in serum and those of SOD,MDA,GSH-Px and NO in renal homogenate were also determined;the pathological change of renal tissue was observed. RESULTS:Compared with blank group,the levels of Cys C,Scr and BUN in serum,those of 24 h protein,NAG and KIM-1 in urine and those of MDA and NO in renal tissue increased significantly in model group,while the levels of SOD and GSH-Px decreased significantly(P<0.01);the pathological slice indicated that model group suffered from renal injury such as kidney tubules albuminoid degeneration,brush border abscission,renal tubular epithelial cell disintegration and abscission. Compared with model group,the levels of Cys C,Scr and BUN in serum,those of 24 h protein,NAG and KIM-1 in urine and those of MDA and NO in renal tissue decreased signifi-cantly in treatment groups,while the levels of SOD and GSH-Px in renal tissue increased significantly(P<0.05 or P<0.01);path-ological changes of renal tissue were relieved significantly. CONCLUSIONS:TSⅡ A sulfonate injection can effectively relieve VAN-induced renal injury in rats,and its mechanism may be associated with inhibiting the oxidative reaction of rats in vivo.

Objective:To study the effects of panax notoginsenosides on the proliferation and oxidation indices of cisplatin-induced nephroxicity in HK-2 cells. Methods:HK-2 cells were cultured in vitro till the number was up to 1 × 106/ml. The cells were inoculated in 96-well culture plate and randomly divided into six groups:normal saline ( NS) group,the model group, the positive control group and the high dose group , medium dose group and low dose group of panax notoginsenosides ( PNS) . The nephroxicity model was dupli-cated with the addition of cisplatin (the final concentration was 6. 25μg·L-1). The model group, positive control group and the three panax notoginsenosides groups was treated with saline solutions, amifostine, panax notoginsenosides at the dose of 100,50 and 25 mg· L-1 , respectively. The cell viability was detected with an MTT method, the content of MDA and the activity of SOD, GSH-PX and LDH were measured and the cell structure was observed. DCFH-DA was used as the fluorescence probe to detect the level of ROS by a fluorescence microplate reader. Results:Compared with those in the model group, the cell viability and the activity of SOD and GSH-PX in the three PNS groups and the positive control group significantly increased (P<0. 05);the content of MDA, the level of ROS and the activity of LDH significantly decreased (P<0. 05); the cell structure was significantly improved. Conclusion: PNS can pro-mote the proliferation of HK-2 cells in vitro, and improve the biochemical parameters and enzyme levels. The results suggest that PNS has a protective effect on HK-2 cell,and the protective mechanisms may be related with its antioxidant effect.

OBJECTIVETo investigate the relationship between miR-144 and Toll-like receptor 2 (TLR2).

METHODSRT-qPCR was used to determine the expression of TLR2 and its downstream inflammatory cytokine TNF-α in rat macrophage cell line NR8383 transfected by a mimic miR-144 or miR-144 inhibitor. The fragments of 3'UTR region of rat TLR2 mRNA including wild or mutant miR-144 binding site obtained by PCR using rat liver cDNA were ligated to pmirGLO report gene vector digested with SacI and XbaI to construct the recombinant vectors of pmir-TLR2-3'UTR and pmir-mutant-TLR2-3'UTR. The miR-144 targeting TLR2 was further determined by dual luciferase reporter assay and miR-144 mimics.

RESULTSTLR2 and TNF-α in NR8383 cells were decreased after transfection with 100 nmol/L mimic miR-144 for 24 h and increased after transfection with 100 nmol/L miR-144 inhibitor. PCR and double-enzyme digestion with SacI and XbaI confirmed successful insertion of the target fragments. Dual luciferase reporter assay suggested the binding of miR-144 to the 3'UTR of rat TLR2 mRNA.

CONCLUSIONmiR-144 negatively regulates the expression of TLR2 and its down-stream cytokine TNF-α by targeting TLR2 in NR8383 cells.

3' Untranslated Regions ; Animals ; Binding Sites ; Cell Line ; Genetic Vectors ; Luciferases ; Macrophages ; metabolism ; MicroRNAs ; metabolism ; RNA, Messenger ; Rats ; Real-Time Polymerase Chain Reaction ; Toll-Like Receptor 2 ; metabolism ; Transfection ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVE： To study improvement effects of Panax notoginsenoside（PNS） on cisplatin-induced renal injury model rats and its effects on related factors. METHODS： Totally 72 SD rats were randomly divided into blank group， model group， positive drug group and PNS low-dose， medium-dose， high-dose groups， with 12 rats in each group. Except for blank group， other groups were given cisplatin via tail vein （3 mg/kg×4 times） to establish renal injury model. Since the first day after the first injection of cisplatin， positive group was given anfostine solution intraperitoneally （1.0 mg/kg）； PNS groups were given PNS solution intraperitoneally （15.63， 31.35， 62.70 mg/kg）； blank group and model groups were given constant volume of normal saline 0.2 mL， for consecutive 60 d. The 24 h urine of rats was collected； the contents of β-N-acetylaminoglycosidase（NAG） and 24 h urine protein （Upro/24 h） were detected； the serum contents of Scr and BUN were detected. mRNA and protein expression of CTGF， TGF-β1， Col-1， TIMP-1 and PAI-1 in renal tissue were determined by RT-PCR and immunohistochemistry respectively. RESULTS： Compared with blank group， the contents of NAG and Upro/24 h in urine， serum contents of Scr and BUN， mRNA and protein expression levels of CTGF， TGF-β1， Col-1， TIMP-1 and PAI-1 in renal tissue were increased significantly （P＜0.05）. Compared with model group， the contents of above urine and serum biochemical indicators were decreased significantly in PNS groups； mRNA expression of CTGF and TGF-β1 and protein expression of CTGF， TGF-β1， Col-1 and TIMP-1 in renal tissue of rats in PNS groups， mRNA expression of Col-1 in PNS high-dose group， and mRNA expression of TIMP-1 and protein expression of PAI-1 in PNS medium-dose and high-dose groups were decreased significantly （P＜0.05）. Compared with positive group， the contents of NAG and Upro/24 h in urine were decreased significantly in PNS medium-dose and high-dose groups （P＜0.05）. CONCLUSIONS： PNS can effectively improve the renal function of cisplatin-induced renal injury model rats， and relieve cisplatin-induced renal fibrosis by decreasing the expression of renal fibrosis related factors as CTGF， TGF-β1， Col-1， TIMP-1 and PAI-1 in renal tissue.

Objective To investigate the relationship between miR-144 and Toll-like receptor 2 (TLR2). Methods RT-qPCR was used to determine the expression of TLR2 and its downstream inflammatory cytokine TNF-α in rat macrophage cell line NR8383 transfected by a mimic miR-144 or miR-144 inhibitor. The fragments of 3'UTR region of rat TLR2 mRNA including wild or mutant miR-144 binding site obtained by PCR using rat liver cDNA were ligated to pmirGLO report gene vector digested with SacI and XbaI to construct the recombinant vectors of pmir-TLR2-3'UTR and pmir-mutant-TLR2-3'UTR. The miR-144 targeting TLR2 was further determined by dual luciferase reporter assay and miR-144 mimics. Results TLR2 and TNF-αin NR8383 cells were decreased after transfection with 100 nmol/L mimic miR-144 for 24 h and increased after transfection with 100 nmol/L miR-144 inhibitor. PCR and double-enzyme digestion with SacI and XbaI confirmed successful insertion of the target fragments. Dual luciferase reporter assay suggested the binding of miR-144 to the 3'UTR of rat TLR2 mRNA. Conclusion miR-144 negatively regulates the expression of TLR2 and its down-stream cytokine TNF-αby targeting TLR2 in NR8383 cells.

Objective To investigate the relationship between miR-144 and Toll-like receptor 2 (TLR2). Methods RT-qPCR was used to determine the expression of TLR2 and its downstream inflammatory cytokine TNF-α in rat macrophage cell line NR8383 transfected by a mimic miR-144 or miR-144 inhibitor. The fragments of 3'UTR region of rat TLR2 mRNA including wild or mutant miR-144 binding site obtained by PCR using rat liver cDNA were ligated to pmirGLO report gene vector digested with SacI and XbaI to construct the recombinant vectors of pmir-TLR2-3'UTR and pmir-mutant-TLR2-3'UTR. The miR-144 targeting TLR2 was further determined by dual luciferase reporter assay and miR-144 mimics. Results TLR2 and TNF-αin NR8383 cells were decreased after transfection with 100 nmol/L mimic miR-144 for 24 h and increased after transfection with 100 nmol/L miR-144 inhibitor. PCR and double-enzyme digestion with SacI and XbaI confirmed successful insertion of the target fragments. Dual luciferase reporter assay suggested the binding of miR-144 to the 3'UTR of rat TLR2 mRNA. Conclusion miR-144 negatively regulates the expression of TLR2 and its down-stream cytokine TNF-αby targeting TLR2 in NR8383 cells.

OBJECTIVE： To provide reference for improving the level of pharmaceutical care in medical institution， and realizing the precision of pharmaceutical care. METHODS： A sampling survey of third grade class A hospitals in Guangxi was conducted on the basis of Guangxi Hospital Pharmaceutical Administration Quality Control Center. Based on the results of literature analysis and international standard， by using Delphi method， the expert consultation form was issued by E-mail and field investigation； the results of four rounds of expert consultation were analyzed and summarized. Pharmaceutical care quality control index system was established in medical institutions. RESULTS & CONCLUSIONS： All experts （100％） agreed that pharmaceutical care in medical institutions was very important and required a quality control index system. Finally， 5 first-level indicators （including the construction of pharmaceutical care management organizational framework， rational drug use management， pharmaceutical care professional capacity management， pharmaceutical care monitoring management and characteristic pharmaceutical care management） and 26 second-level indicators were fitted according to results of expert consultation. Among first-level indicators， the indicators of “the construction of pharmaceutical care management organizational framework”， “rational drug use management” and “pharmaceutical care professional competence management” were generally considered as important quality control indicators by experts； the proportion of “very important” and “important” were 96.65％， 100％ and 100％. Among second- level indicators， the indicators of “organization construction”“system construction”“prescription drug use management”“hospitalization medical order review”“adverse drug reaction monitoring”“medicine knowledge”“clinical knowledge” were generally considered as important quality control indicators by experts； the proportion of “very important” and “important” were 95.65％， 95.65％， 100％， 95.66％， 96.65％， 100％ and 91.30％. The quality control index system of pharmaceutical care in medical institutions fitted by this research institute is authoritative. Now， 15 medical institutions in Guangxi Zhuang Autonomous Region have been pilot implemented after audited and finalised by Guangxi  Hospital Pharmaceutical Administration Quality Control Center.

ObjectiveTo observe the effect of Sanhuang Tangshenkang on the Wnt/β-catenin signaling pathway in the bone tissue of diabetic rats. MethodA high-sugar and high-fat diet was administered for 4 weeks， along with intraperitoneal injection of freshly prepared 2% streptozotocin （pH 4.5） at 30 mg·kg^-1 body weight to induce a diabetes model in rats. The rats with diabetes were randomly divided into model group， low- and high-dose Sanhuang Tangshenkang groups （12.8， 38.4 g·kg^-1）， and Gushukang group （1.8 g·kg^-1） according to the blood glucose level. Rats of the same age were fed on a regular diet and assigned to the control group. After 12 weeks of respective treatments with drugs or physiological saline， the fasting blood glucose （FBG） levels of the rats were measured using an automated biochemical analyzer. Enzyme-linked immunosorbent assay （ELISA） was used to detect fasting serum insulin （FINS）， bone-specific alkaline phosphatase （BALP）， and tartrate-resistant acid phosphatase （TRAP） levels. Micro-computed tomography （Micro-CT） was used to scan the femurs of rats to observe bone tissue microstructure and measure bone mineral density （BMD）. Hematoxylin-eosin （HE） staining and safranin O/fast green staining were performed to observe pathological changes in the femoral bone tissue. Immunohistochemistry （IHC） and Western blot were used to detect the expression of Wnt3a， low-density lipoprotein receptor-related protein 5 （LRP-5）， and β-catenin proteins. ResultCompared with the control group， the model group showed a significant increase in FBG， FINS， and TRAP levels （P<0.01）， a significant decrease in BALP level （P<0.01）， a significant decrease in BMD （P<0.01）， and disorganized， elongated， and sparse bone trabecular structures with fractures and increased lipid droplets. Additionally， the expression of Wnt3a， LRP-5， and β-catenin proteins decreased （P<0.05， P<0.01）. Compared with the model group， the low- and high-dose Sanhuang Tangshenkang groups showed a reduction in FBG and an increase in BALP （P<0.05）. The low-dose Sanhuang Tangshenkang group also exhibited a decrease in FINS （P<0.05）. All treatment groups showed a significant decrease in TRAP （P<0.01）， varying degrees of improvement in BMD （P<0.05， P<0.01））， increased and denser bone trabeculae with more regular arrangements and reduced lipid droplets， and improved bone microstructure morphology. The average optical density values of Wnt3a， LRP-5， and β-catenin proteins were significantly increased in all drug-treated groups （P<0.05， P<0.01）， and the expression of Wnt3a， LRP-5， and β-catenin proteins was elevated （P<0.05， P<0.01）. ConclusionSanhuang Tangshenkang may regulate the imbalance of the Wnt/β-catenin signaling pathway by increasing the expression of Wnt3a， LRP-5， and β-catenin proteins in bone tissue， which may promote bone formation， reduce bone resorption， and lower blood glucose levels， thereby achieving the effect of preventing and treating diabetic osteoporosis.

Antineoplastic drugs refer to the drugs that act at the cellular and molecular levels to inhibit tumor growth or eliminate tumors through pathways such as cell killing,immune regulation,and endocrine regulation.Antineoplastic drugs generally including chemotherapeutic drugs,molecular targeted therapeutic drugs,immunotherapeutic drugs,and endocrine therapeutic drugs.The management and rational application of antineoplastic drugs in medical institutions are related to the safety of patient treatment.The standard for management of antineoplastic drugs use in clinical is compiled by the Pharmaceutical Affairs Committee of China Hospital Association,which specification requirements 18 key elements in the organizational management and system,medication management,drug monitoring and evaluation of antineoplastic drug management in healthcare institutions.This standard is applicable to all levels and types of healthcare institutions carrying out oncology diagnosis and treatment.This paper describes the methodology and basic content of the standard,hoping to providing a reference for medical institutions to carry out relevant work.

Humans ; Severe Acute Respiratory Syndrome ; diagnosis ; therapy