Evaluation method of medicine nature of individual ginsenosides / 中国药理学通报

.Aim To establish the evaluation methods of the med¬icine nature of ginsenosides by eorrelation analysis between med¬icine nature and ginsenoside contents in five Panax herbs with different medicine nature and the measurement of their effects on Na + /K + -ATPase activities.Methods 'Hie contents of ginsen¬osides in Sanqi, red ginseng , ginseng , American ginseng and ginseng leaves in the existing literature were eolleeted.and the medicinal nature was assigned by vector methods.rI1ie medicine nature of ginsenosides and the contribution of ginsenoside to the medicine nature were evaluated through bivariate correlation a- nalysis and grey eorrelation degree respectively.'Hie effects of ginsenosides on the Na+ /K +-ATPase activities of L02 eells and in pig eerebral cortex were measured to evaluate the medicine na¬ture of ginsenosides.Results Correlation results indicated that the order of correlation coefficients of ginsenosides to the warm and hot medicine nature was Rf > R1 > Rg3 > Rg2 > Rbl > Ro, while the order of correlation coefficients of ginsenosides to the eool and eold medicine nature was Rb2 > Re > Rd > Fll.Grey eorrelation degree analysis showed that the contribution of ginsen¬oside to the medicine nature was F11 > Re > Kg2 > Rd > Rb2 >Rbl > Rgl > Rc > Rg3 > R1 > Rf > Ro.The effects of ginsen- osides on Na +/K +-ATPase activities showed that the substance basis of the warm medicine nature was ginsenoside Rbl, Rb3, Rc, Rf, Rg2, Rgl, Rhl, Rg3, R1 and Ro, which increased the activity of Na + /K + -ATPase.While the cold and cool medi- cine nature were ginsenoside Rh2, Rd, Rh2, Re and oleanolic acid, which inhibited the activity of Na+/K

Ursolic Acid Prevents Retinoic Acid-Induced Bone Loss in Rats / 中国结合医学杂志

OBJECTIVE@#To examine the effects of ursolic acid (UA) on mitigating retinoic acid (RA)-induced osteoporosis in rats.@*METHODS@#Fifty female Sprague-Dawley rats were randomly divided into the control group (n=10) and the osteoporosis group (n=40). The 40 osteoporosis rats were induced by 75 mg/(kg•d) RA once daily for 2 weeks, and then were randomly assigned to vehicle control (model), low-, middle-, and high-dose UA [(UA-L, UA-M, UA-H; 30, 60, 120 mg/(kg•d), respectively] groups (10 rats each). UA were administered once daily to the rats from the 3rd weeks for up to 4 weeks by gavage. Bone turnover markers [serum alkaline phosphatase (ALP), osteocalcin (OCN), urine deoxypyridinoline (DPD)] and other parameters, including serum calcium (S-Ca), serum phosphorus (S-P), urine calcium (U-Ca), urine phosphorus (U-P), and bone mineral density (BMD) of the femur, 4th lumbar vertebra and tibia, bone biomechanical properties and trabecular microarchitecture, were measured.@*RESULTS@#The osteoporosis in rats was successfully induced by RA. Compared with the model group, UA-M and UA-H significantly reversed the RA-induced changes in S-P, U-Ca, U-P, ALP, OCN and urine DPD ratio and markedly enhanced the BMD of right femur, 4th lumbar vertebra and tibia (Plt;0.05 or Plt;0.01). Further, biomechanical test and microcomputed tomography evaluation also showed that UA-H drastically improved biomechanical properties and trabecular microarchitecture (Plt;0.05 or Plt;0.01).@*CONCLUSION@#UA could promote bone formation, increase osteoblastic activity and reduce osteoclastic activity in rats, indicating that UA might be a potential therapeutic of RA-induced acute osteoporosis.

Ethanol extract of propolis protects vascular endothelial cells from oxidized low-density lipoprotein-induced apoptosis by inhibiting C/EBP homologous protein expression / 中国病理生理杂志

AIM:To investigate the inhibitory effect of ethanol extract of propolis (EEP) on oxidized low-density lipoprotein (ox-LDL)-induced vascular endothelial cell apoptosis and the underlying molecular mechanisms.METHODS:Human umbilical vein endothelial cells (HUVECs) were pretreated with EEP (7.5,15 and 30 mg/L) or 4-phenylbutyric acid (PBA,4 mmol/L) for 1 h and then treated with ox-LDL (100 mg/L) or tunicamycin (TM,4 mg/L) for 24 h.The cell viability and apoptosis were determined by MTT assay and Annexin V-FITC/PI double staining,respectively.The activities of lactic dehydrogenase (LDH) in the medium and caspase-3 in the HUVECs were measured.The protein and mRNA levels of C/EBP homologous protein (CHOP),a proapoptotic molecule under endoplasmic reticulum stress (ERS),and its downstream Bcl-2 were examined by Western blot and real-time PCR,respectively.RESULTS:Like PBA (an ERS inhibitor),EEP protected HUVECs from ox-LDL-induced injury in a dose-dependent manner,as assessed by the increased cell viability and the decreased LDH release,apoptotic rate and caspase-3 activation.The decrease in cell viability and the increases in LDH release,apoptotic rate and caspase-3 activation induced by TM,an ERS inducer,were also attenuated by EEP.Moreover,EEP suppressed ox-LDL-induced CHOP upregulation and Bcl-2 downregulation,and this effect was similar to that of PBA.Similarly,EEP significantly suppressed TM-induced CHOP upregulation both at the protein and mRNA levels.CONCLUSION:EEP may protect HUVECs from ox-LDL-induced apoptosis,and the mechanism is at least partially involved in suppressing CHOP-mediated ERS-associated apoptotic pathway.

Ethanol extract of propolis protects vascular endothelial cells from oxidized low-density lipoprotein-induced apoptosis by inhibiting C/EBP homologous protein expression / 中国病理生理杂志

AIM:To investigate the inhibitory effect of ethanol extract of propolis (EEP) on oxidized low-density lipoprotein (ox-LDL)-induced vascular endothelial cell apoptosis and the underlying molecular mechanisms.METHODS:Human umbilical vein endothelial cells (HUVECs) were pretreated with EEP (7.5,15 and 30 mg/L) or 4-phenylbutyric acid (PBA,4 mmol/L) for 1 h and then treated with ox-LDL (100 mg/L) or tunicamycin (TM,4 mg/L) for 24 h.The cell viability and apoptosis were determined by MTT assay and Annexin V-FITC/PI double staining,respectively.The activities of lactic dehydrogenase (LDH) in the medium and caspase-3 in the HUVECs were measured.The protein and mRNA levels of C/EBP homologous protein (CHOP),a proapoptotic molecule under endoplasmic reticulum stress (ERS),and its downstream Bcl-2 were examined by Western blot and real-time PCR,respectively.RESULTS:Like PBA (an ERS inhibitor),EEP protected HUVECs from ox-LDL-induced injury in a dose-dependent manner,as assessed by the increased cell viability and the decreased LDH release,apoptotic rate and caspase-3 activation.The decrease in cell viability and the increases in LDH release,apoptotic rate and caspase-3 activation induced by TM,an ERS inducer,were also attenuated by EEP.Moreover,EEP suppressed ox-LDL-induced CHOP upregulation and Bcl-2 downregulation,and this effect was similar to that of PBA.Similarly,EEP significantly suppressed TM-induced CHOP upregulation both at the protein and mRNA levels.CONCLUSION:EEP may protect HUVECs from ox-LDL-induced apoptosis,and the mechanism is at least partially involved in suppressing CHOP-mediated ERS-associated apoptotic pathway.

Allicin attenuates macrophage-derived foam cell apoptosis by inhibiting caspase-12 / 中国病理生理杂志

AIM:To investigate the inhibitory effect of allicin on apoptosis and caspase-12 activation of macro-phage-derived foam cells,and to elucidate the underlying molecular mechanisms. METHODS:RAW264.7 macrophages were pretreated with allicin (12.5,25 and 50 mg/L) or 4-phenylbutyric acid(PBA,4 mmol/L) for 1 h and then treated with oxidized low-density lipoprotein(ox-LDL,100 mg/L) or tunicamycin(TM,4 mg/L) for 24 h. The cell viability and apoptosis were examined by MTT assay and flow cytometry with Annexin V-FITC/PI staining,respectively. The activities of caspase-3 in the cells and lactic dehydrogenase (LDH) in the medium were measured. The protein levels of caspase-12 were determined by Western blot. The intracellular lipid accumulation was measured with oil red O staining and the content of intracellular total cholesterol was determined by enzymatic colorimetry. RESULTS:Similar to the endoplasmic reticulum stress (ERS) inhibitor PBA, allicin inhibited ox-LDL-induced injury of RAW264.7 macrophages in a concentration-de-pendent manner,as determined by the increased cell viability and the decreased LDH leakage,apoptosis and caspase-3 ac-tivity. The decrease in cell viability and increases in LDH leakage and apoptosis induced by TM (an ERS inducer) were also suppressed by allicin. Moreover, similar to PBA, allicin remarkably inhibited ox-LDL- or TM-induced activation of caspase-12. Furthermore, allicin remarkably attenuated ox-LDL-induced lipid accumulation in the RAW264.7 cells and foam cells formation in a concentration-dependent manner. CONCLUSION:Allicin may inhibit macrophage-derived foam cell apoptosis induced by ox-LDL,and the mechanism is partially related to suppressing the activation of caspase-12.

The synergism and mechanism of action of rClone30-hDR5 in combination with TRAIL on HCC / 药学学报

To investigate the cell-killing effect and its possible mechanism of rClone30-hDR5 in combination with TRAIL on human hepatic carcinoma (HCC) cell line, first of all, recombinant plasmid pee12.4-hDR5 was introduced into HepG2 cells by liposome transfection. After five rounds of screening by flow cytometry, HepG2 cells expressing high levels of DR5 on cell surface were isolated. The cytotoxicity of TRAIL to selected cells was higher than that of TRAIL to HepG2 cells by MTT method (P < 0.01). The result suggested that the cloned hDR5 gene had biological activity. MTT assay showed that, rClone30- hDR5 in combination with TRAIL more efficiently inhibited the tumor growth of HepG2 cells compared to rClone30-hDR5 or TRAIL in vitro. The results of Annexin V-FITC/PI staining and Quantitative Real-time PCR indicated that rClone30-hDR5 in combination with TRAIL significantly increased the mRNA levels of caspase 3 and caspase 8, and induced the apoptosis of tumor cells. HepG2 cells were infected with rClone30-hDR5 or rClone30 at MOI of 1. The expression of hDR5 on tumor surface increased significantly by rClone30-hDR5 compared to that by rClone30, which contributed to the sensitivity to TRAIL. In conclusion, rClone30-hDR5 in combination with TRAIL has potential application value in cancer treatment.

Determination of the content of phloridzin using reversed-phase high-performance liquid chromatography / 南方医科大学学报

<p><b>OBJECTIVE</b>To establish a reversed-phase high-performance liquid chromatographic (RP-HPLC) method for determination of phloridzin content.</p><p><b>METHODS</b>A RP-HPLC method was established for determination of phloridzin using an Inertsil ODS-3 (4.6×150 mm, 5 µm) column with the detection wavelength of 288 nm, flow rate of 1.0 ml/min, and column temperature of 25 degrees celsius;.</p><p><b>RESULTS</b>The result showed that the phloridzin had a good linear relationship when its concentration ranged between 0.5988 and 89.72 µg/ml. The regression equation was Y=46.370 X-0.6728 (r=0.9999, n=3). The average recovery of phloridzin was 99.40% with the relative standard deviations (RSD) of 0.67%.</p><p><b>CONCLUSION</b>This method is simple, quick and accurate for determination of phloridzin content.</p>

Advance in the pharmacological research on matrine / 中国中药杂志

<p><b>OBJECTIVE</b>The progress in the research on matrine was involved to provide references for the exploitation and utilization of the matrine.</p><p><b>METHOD</b>Pharmacological functions and mechanism were reviewed according to related experimental studies.</p><p><b>RESULT</b>Matrine has various pharmacological activities.</p><p><b>CONCLUSION</b>Matrine has extensive applied prospect and will be developed further.</p>