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Welcome to Chinese Journal of Clinical Pharmacology and Therapeutics,Today is Chinese

Table of Content

    Volume 14 Issue 10
    26 October 2009
    Personalized medicine in drug development
    ZHANG Wei, ZHOU Hong-hao
    2009, 14(10):  1081-1084. 
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    Pharmacogenomics has the potential to impact on the drug discovery and development process at many stages.Pharmacogenomic information helps researchers in drug discovery to better identify drug targets and the mechanisms of action of investigational New Chemical Entity (NCEs).Pharmacogenomics-related technology facilitates the removing of unfavorable products at preclinical stages of drug development.It also could guide companies in designing clinical trials that would more definitively confirm drug efficacy, consecutively decreasing the time, costs, and risks of drug development as well.
    Effect of Curcumin on proliferation inhibition induced by Urotensin-II in human lens epithelial cell and its mechanism of signal transduction
    QI Ming-xin, HUANG Xiu-rong, HU Jun, YANG Li-ying
    2009, 14(10):  1085-1090. 
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    AIM: To study the effect of Curcumin (Cur)on proliferation inhibition induced by urotensin-II in human lens epithelial cell (HLEC)and its signal transduction mechanism of [Ca2+] i, cAMP and cGMP. METHODS: The cultured HLEC were incubated with different concentrations of Cur and the HLEC activities were detected viaMTT assay.The proliferative cell nuclear antigen (PCNA)of HLEC were detected via flow cytometer(FCM).The concentration of intracellular free calcium ([Ca2+] i)of HLEC were determined by spectrofluoremeter.The intracellular contents of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP)of HLEC were detected by radioimmunoassay. RESULTS: The activity, expression of PCNA and the cGMP concentration of HLEC in U-II group were higher than those in control group, but they were significantly decreased in Cur group (P <0.01).Compared with control group, the [Ca2+] i concentration of HLEC in U-II group was increased, and the cAMP concentration in U-II group was decreased (P < 0.01).Compared with U-II group, the concentrations of cAMP and [Ca2+] i were increased (P <0.01). CONCLUSION: Cur can inhibit the proliferation of HLEC induced by urotensin- II.The signal transduction of [Ca2+], cAMP-PKA and cGMP-PKG may play an important role in it.Cur may become an effective drug of preventing and treating after-cataract.
    Inhibitory effect of aspirin-niacinamide-zinc complex on human gastric carcinoma cell line SGC-7901
    PU Qi-song, ZHENG Qian, ZHANG Jian-wu
    2009, 14(10):  1091-1094. 
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    AIM: To investigate the inhibitory effect of aspirin-niacinamide-zinc complex (Wuyisa, WUY) on human gastric carcinoma cell line SGC- 7901. METHODS: The inhibitory effect of WUY on SGC-7901 cells was evaluated by MTT analysis.The effect of WUY on SGC-7901 cell cycle was determined with flow cytometry. RESULTS: After treated with 2, 4, 8, 16 mmol/Lof WUY, the inhibition rates were 9.95 %, 19.28 %, 37.36 %, 63.47 % (P <0.05). The average IC50 of SGC-7901 cells was 11.06 mmol/L.The dose effect relationship and time effect relationship were described in the growth curve.The cell cycle distribution was changed in a concentrationdependent manner, after gastric cancer cell was treated for 24 hours with WUY by flow cytometry.Among phases of cell cycle, the G0 G1 phase ratio was decreased and the S and G0 M phase ratio were increased. CONCLUSION: WUY can obviously inhibit the growth of human gastric carcinoma cell line SGC- 7901 cells.It may be associated with the phases of cell cycle.
    Radiosensitizing effect of the selective cyclooxygenase-2 inhibitor celecoxib on esophageal carcinoma cell line ECA109
    WANG Zhao-xia, CHEN Yi-hong, HU Qin, TAN Wen-xia, JI Zhao-ning
    2009, 14(10):  1095-1100. 
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    AIM: To investigete the radiosensitizing effect of celecoxib on esophageal carcinoma cell line CEA109. METHODS: The expression of COX-2 in CEA109 cells was detected by immunohistochemical staining.TheMTT assay and colony forming assay were performed to determine the influence of celecoxib on growth and proliferation of esophageal carcinoma cell line CEA109.The apoptosis of CEA109 cells was determined by flow cytometry. RESULTS: There were differences in colony forming, cell proliferation, and stage apoptosis among different dose levels of radiation and celecoxib concentrations (all P <0.05).And the inhibition of proliferation and induction of apoptosis in CEA109 cell line were depend on the dose levels of radiation and celecoxib concentrations.CEA109 cell survival rate was lower after treatment with the combination of radiation and celecoxib than that of radiation alone.The apoptosis rate of combined use of celecoxib (50 μmol/L) and radiation(4Gy) was significant different from the apoptosis rate of simple radiation group(P <0.05). CONCLUSION: Celecoxib can inhibit the proliferation and induce the apoptosis of ECA-109 cell line.Radiation combined with celecoxib has synergistic effect on ECA-109 cell line proliferation and apoptosis. Celecoxib can enhance the sensitivity of ECA-109 cell line to irradiation.
    Effects of carvedilol on the activities of IFN-γand IL-12 and oxygen free radical in murine model with coxsackievirus B3-induced viral myocarditis
    LI Yue-chun, CHEN Peng, GE Li-sha, REN Jiang-hua
    2009, 14(10):  1101-1105. 
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    AIM: The study was designed to examine the effects of carvedilol and metoprolol in a murine model of viral myocarditis induced by coxsackievirus B3 virus infection (CVB3). METHODS: BALB/C mice were intraperitoneally inoculated with CVB3, at the starting 24 h after infection carvedilol was administered orally in a dose of 10 mg°kg-1°d-1, and metoprolol was administered orally in a dose of 30 mg°kg-1°d-1 for 7 or 14 consective days.Virus infection group and normal group were used with same dose PBS.Mice were killed at day 7 and 14.Myocardial histopathology changes, the HW/BW ratio, the myocardial IFN-γand IL-12 production, the content of maleic dialdehyde (MDA) and superoxide dismutase (SOD) were detected. RESULTS: Carvedilol, but not metoprolol, markedly attenuated myocardial lesions and decreased HW/BW ratio.On day 7, carvedilol group, but not metoprolol group, increased the myocardial IFN-γand IL-12 production and decreased the content of MDA more significantly than virus infection group.On day 14, carvedilol group, but not metoprolol, markedly increased the content of SOD and manifested decreased the content of MDA than virus infection group. CONCLUSION: Carvedilol protects against CVB3-induced viral myocarditis in mice.Carvedilol exerts some of its beneficial effects by boosting the production of IFN-γ and IL-12 and inhibiting peroxidants.
    Experimental study on the protective effect of total glycosides of Zhizi for ulceration in pylorus ligature rats
    JU Jing
    2009, 14(10):  1106-1109. 
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    AIM: To investigate the antiulcer effect and concerned mechanism of total glycosides of Zhizi (TGZ) in pylorus ligature rats (Shay-rats). METHODS: Pylorus-ligation induced gastric ulceration in rats(Shay-rats model).Quantity determined the free acid, total acid contents and pepsase activity in gastric juice.The effect of TGZ on gastric mucosal lesion index in rats was also determined. RESULTS: TGZ 70 or 140 mg/kg injection gavage for five days versus shay model rats could significantly prevent gastric ulceration decreased free acid, total acid contents and pepsase activity of gastric juice. CONCLUSION: TGZ, through inhibiting gastric acid and pepsase activity evokes its anti-ulceration.
    Protection of ganoderan on methotrexate-induced intestinal damage in mice
    CHEN Li-hua, XIAO Xin-yu, ZENG Hui-lang, LIN Zhi bin, LI Wei-dong
    2009, 14(10):  1110-1114. 
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    AIM: To observe the protective effects of ganoderan on methotrexate (MTX) -induced intestinal damage in BALB/C mice. METHODS: The mouse model of intestinal damage was established by intraperitoneal injection of MTX once daily for two consecutive days, and this was to simulate clinical chemotherapyinduced intestinal injury.Intragastric administration of ganoderan was executed for 7 days before MTX injection, and the animals were sacrificed in 3 days after the last injection.The morphological and ultrastructural changes were observed to the jejunum segments by HE staining and electron microscope.The level of malondialdehyde(MDA) and the activity of total superoxide dismutase(T-SOD) were detected in intestinal homogenate supernatant. RESULTS: Compared with the normal group, the intestinal villus in the MTX group became shorter and fused, and the crypt cells were disappeared, the goblet cells were decreased.Ultrastructure showed that microvilli were irregularly arranged, variable short, and some were missing, and the nuclear membrane and mitochondria swelling.Morphological changes in the ganoderan group were smaller than those in MTX group.The T-SOD activity was decreased and the level of MDA was increased in MTX group, but the T-SOD activity was increased and the level of MDA was decreased in ganoderan group. CONCLUSION: The present study shows that ganoderan can protect the small intestine of mice from the MTX-induced damage.
    Oxidative lesions induced by medical SiO2 nanoparticles on normal human lung cells
    LI Ai-si, HUANG Yong-ping, LIU Jian-wen, LAN Min-bo, GAO Feng, XU Hao-liang, CHEN Ming-cang, XU Yi-chun
    2009, 14(10):  1115-1120. 
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    AIM: To investigate the medical SiO2 nanoparticles induced cytotoxicity and its mechanism on normal human lung cells (MRC-5 cells) in vitro. METHODS: The MRC-5 cells were exposed with different concentrations of SiO2 nanoparticles for 48 h. The cell survival rate was tested by MTT assay and the cell morphological changes were observed with HE staining.The activities of reactive oxygen species (ROS), glutathione (GSH) and superoxide dismutase (SOD) were determined to evaluate the oxidative damage after SiO2 exposure. RESULTS: Exposure with high concentrations above 0.4 mg/mL and 1.0 mg/mL of 21.6 nm and 48.6 nm SiO2 nanoparticles decreased the cell survival rate in a dose-dependent manner.The median inhibitory concentrations (IC50) were 0.8 mg/mL and 1.9 mg/mL respectively.Morphological observation revealed cell shrinkage and nuclear condensation after exposure.The reduced GSH content as well as SOD activity were decreased in SiO2 nanoparticles exposed cells than that of control. CONCLUSION: Medical SiO2 nanoparticles exposure resultes in a dosedependent cytotoxicity in cultured MRC-5 cells that was associated with increased oxidative stress.
    Proliferation inhibition and apoptosis induction in human ovarian cancer SKOV3 cells by Cpd5
    CHEN Li, HUO Guan-hua, LV Yao-feng, ZHANG Qin
    2009, 14(10):  1121-1127. 
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    AIM: To investigate the effect of Cpd5 on the proliferation inhibition and apoptosis induction in human ovarian cancer SKOV3 cells. METHODS: The growth inhibition of Cpd5 in SKOV3 cells was detected by MTT assay.AnnexinV PI staining was employed for quantifying apoptotic cells by fluorescence microscopy and flow cytometry.The apoptotic morphology was observed by Hoechst-33258 staining. RESULTS: After Cpd5 treatment at the concentrations of 5, 10, 20, 30, 40, 50 and 60 μmol/Lfor 48 h, the ratios of the cells growth inhibition were 2.77 %, 5.19 %, 10.61 %, 41.15 %, 71.37 %, 82.90 % and 89.81 %, respectively.The proliferation was inhibited after Cpd5 treatment at different times of 12, 24, 48 and 72 h, the cells were inhibited by Cpd5, in a dose-time-dependent manner.The apoptotic cells accounted for 9.25 %, 20.07 % and 56.16 %, after Cpd5 treatment by 30 μmol/Lfor 12, 24 and 48 h, respectively.The ratio of apoptotic cells in 50 μmol/Lgroup was significantly higher than that in 30 μmol/Lgroup.The morphological changes were emerged after Cpd5 treatment at the concent rations of 40, 50 and 60 μmol/Lfor 12 h.Compared with the control group, the ratios of the apoptotic cells were increased significantly in the groups induced by Cpd5 at different concentrations.The apoptotic cells were increased in the groups of Cpd5 treatment at 20 μmol/Lfor 24 h and 48 h by Hoechst-33258 staining.Furthermore, the ratios of apoptotic cells were increased significantly in the groups of Cpd5 treatment at 30, 40, 50 and 60 μmol/LCpd5 at different time-points. CONCLUSION: Cpd5 can induce proliferation inhibition and apoptosis in SKOV3 cells, in a dose-time-dependent manner.Our data reveal that Cpd5 is a novel anti-ovarian cancer compound.
    Inducible nitric oxide synthase expression in lung tissue and neutrophil of asthmatic rats and the effects of dexamethasone on them
    CHEN Cun-guo, JIN Hai-hua, LI Shao-bo, JIN Xiao-hong, CHEN Bao-guo, TONG Xia-sheng, YE Hui
    2009, 14(10):  1128-1132. 
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    AIM: To observe the expression of inducible nitric oxide synthase (iNOS)in neutrophils and lung tissues and explore the roles of peripheral blood neutrophils in the pathogenesis of asthmatic inflammation in asthmatic rats. METHODS: Experimental rats were randomly divided into asthma, control and dexamethasone treated groups.Peripheral blood neutrophils were isolated and the expression of iNOS was detected by immunohistochemistry.The nitric oxide (NO)concentration of bronchoalveolar lavage fluids (BALF)was also determined. RESULTS: iNOS protein of PMN in asthmatic rats (0.122 ±0.017 Optical density)was significantly higher than that in control group (0.076 ±0.014, P <0.01).iNOS protein of PMN in dexamethasone treated group (0.089 ±0.013)was markedly lower than that in asthma group (P <0.01), but there was no statistically significant for the PMN iNOS expression between the dexamethasone treated group and control group.Furthermore, iNOS of bronchial wall in asthma group (0.243 ±0.039)was dramatically higher than that in control group (0.119 ±0.016, P <0.01).iNOS in dexamethasone treated group (0.164 ±0.016)was significantly lower than that in asthma group, but was higher than that in control group (P <0.01, respectively).NO concentration of BALF in asthma group (8.59 ±1.07)ng/mL was significantly higher than control group (3.69 ±1.00 ng/mL, P <0.01).NO concentration of BALF in dexamethasone treated group (4.28 ±0.89)ng/mL was significantly lower than that in asthma group, while no significance was observed between the indexamethasone treated and control group.Moreover, iNOS protein expression of PMN was highly correlated with NO concentration of BALF (n =29, r =0.770, P <0.01), and a similar strong association was established between the bronchial wall iNOS and NO concentration of BALF (n =29, r =0.802,P <0.01). CONCLUSION: iNOS of PMN was elevated in asthmatic rats, which could be partly inhibited by dexamethasone.Our study indicated that an increased iNOS expression of PMN may involved in the pathogenesis of asthma in rats.
    Protection effect and mechanism of Doxycycline on lipopolysaccharideinduced acute lung in mice
    LIU Yong-ping, ZENG Zhi-ping
    2009, 14(10):  1133-1136. 
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    AIM: To investigate the potential role and of Doxycycline in lipopolysaccharide-induced acute lung injury in mice and its possible mechanism. METHODS: Kunming mice were treated with Doxycycline (20 mg/kg)or saline an hour before LPS administration (10 mg/kg)by intraperitoneal injection and were decapitated 24 h after LPS challenge.The bronchoalveolar lavage fluid (BALF)samples were analyzed for total protein concentrateion and white blood cell (WBC)count.The lung samples were taken for histopathological evaluation and for determination of lung wet-to-dry weight ratio (W D).The changes of tumor necrosis factor α(TNF-α), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1)levels in the pulmonary tissues were detected by ELISA. RESULTS: LPS-induced increases in total protein concentration, WBC number in BALF and W D levels of lung tissues, were significantly attenuated in Doxycycline-treated mice (P <0.01).Doxycycline treatment also resulted in a significant protection of lung tissues against LPS-induced acute lung injury via decreasing TNF-αand MMP-9(P <0.01).However, TIMP-1 levels were slightly higher in Doxycycline-treated group than those in LPS group.Histological examination revealed that doxycycline treatment resulted in reduced hemorrhage, intra-alveolar edema and neutrophilic infiltration. CONCLUSION: It suggest that Doxycycline plays a protective role in attenuating LPSinduced acute lung injury in mice, which may be the mechanism through regulating the balance of MMP-9 TIMP-1 and inhibiting the pro-inflammatory factor (TNF-α).
    Effect of extracellular signal-regulated kinase on apoptosis of pneumocyte during lung ischemic and reperfusion injury in rats
    HONG Jia-lin, ZHENG Yan-rong, SHI Lu, JIA Xu-guang, WANG Wan-tie
    2009, 14(10):  1137-1141. 
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    AIM: To explore the effect of extracellular signal-regulated kinase (ERK) on apoptosis of pneumocyte during lung ischemic and reperfusion injury in rats. METHODS: 30 rats were randomly divided into three groups:control group(Group C), lung ischemia- reperfusion injury group(Group I R) and PD98059 group(Group P).The content of MDA in serum, the activity of SOD, cell apoptosis index and the p-ERK protein expression were detected by immunohistochemistry, and the ultrastruction changes of lung were observed by electron microscope. RESULTS: Compared with Group C, the content of MDA was increased, the content of SOD was decreased remarkably (all P < 0.01), the expression of p-ERK protein was increased remarkably (P <0.01), and the apoptosis index (AI) was increased in Group I R (P <0.01), abnormal changes of the lung tissue in morphology were observed in Group I R.After PD98059 treatment, the content of MDA was increased (P <0.01), the content of SOD was decreased (P <0.05), the expression of p-ERK protein was decreased(P <0.01), the value of AI was increased(P <0.01), the abnormal changes of the lung tissue in morphology were aggravated markedly. CONCLUSION: The ERK signal transduction pathway maybe protect the lung from the injury caused by ischemia and reperfusion through lessening apoptosis of lung cells in rats.
    Study on the hypoglycemic mechanism of the fusion protein HSP65 -6 ×P277 in NOD mice
    JIN Liang, WANG Yu, ZHU Ai-hua, LIU Jing-jing
    2009, 14(10):  1142-1150. 
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    AIM: To evaluate the hypoglycemic mechanism of the fusion protein HSP65 -6 ×P277 in NOD mice. METHODS: The fusion protein was used to immunize 4-week old female NOD mice with three i. n.inoculations in the absence of adjuvants.The effects of HSP65 -6 ×P277 on NOD mice were investigated by observing the change of blood glucose, cytokine levels, antibody types and degree of insulitis. RESULTS: The sera collected from HSP65 -6 ×P277 treated mice, contained relatively high levels of interleukin IL-4 but low levels of IL-2, and the antibody types were almost exclusively of the IgGl and IgG2b subclass, but at very low levels of IgG2a.T cells from HSP65 -6 ×P277 treated mice when incubated with HSP-peptide conjugate showed an increase in IL-10 secretion and a decrease in interferon (IFN)-γsecretion. HSP65 -6 ×P277 treatment reduced insulitis and T1DM incidence. CONCLUSION: The hypoglycemic mechanism of the fusion protein HSP65 -6 ×P277 is related to its inducing Th2 responses.
    Effects of erythromycin on the expressions of P38 and Th2 Cytokines in rats with asthma
    ZHANG Jin-bo, WU Cheng-yun, LI Zhi-qiang, DAI Yuan-rong
    2009, 14(10):  1151-1155. 
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    AIM: The purpose of this study is to explore the effects of erythromycin on the expressions of phosphorylation P38 and Th2 cytokines in asthmatic rats. METHODS: Thirty male Sprague-Dawley adult rats were randomly divided into normal, asthma and erythromycin-treated group (n =10 for each group). Peripheral blood monouclear cells(PBMCs) of rats were collected and cultured in each group.The concentrations of IL-4, IL-5 and IL-13 in cell supernatant were detected by ELISA.The mRNA and phosphor protein of P38 in PBMCs were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting (WB), respectively. RESULTS: The expression of mRNA and phosphor protein of P38 in PBMCs and the concentrations of IL-4, IL-5 and IL-13 in cell supernatant were higher in asthmatic group than those in normal group (P <0.05).Compared with the asthmatic group, the above indexes were significantly decreased in erythromycin-treated group (P <0.05). There were positive correlations between the expression of phosphor-P38 in PBMCs and the concentrations of IL-4, IL-5 and IL-13 in cell supernatant (r =0.75, 0.82 and 0.70, all P <0.05). CONCLUSION: The P38 may be involved in the pathogenesis of bronchial asthma.Erythromycin playing its role in the treatment of asthma may be achieved by acting on the P38.
    Intervention study on compliance of aspirin in clinical practice
    SUN An-xiu, LIU Yang-chen, GU Ling, LV Jian-feng, FAN Hui, SHI Ai-ping, WANG Lin
    2009, 14(10):  1156-1159. 
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    AIM: To examine the effect of clinical pharmacists' intervention on compliance of aspirin. METHODS: 262 cardiovascular patients with hypertension, diabetes, coronary heart disease, stroke or hyperlipemia were randomly chosen.Clinical pharmacists gave the patients four lessons about aspirin, such as the effect of aspirin to prevent and cure cardiovascular diseases, the canonical dosage, usage and course, the skill how to reduce adverse reactions of aspirin et. Blooding time, clotting time, routine blood test, liver function and kidney function were examined before and after the intervention. RESULTS: After four lessons about aspirin given, all the patients gained more confidence in aspirin to prevent cardiovascular disease.IPSs of the four measurement indicators of the compliance (the number, the dosage, the time, and long-term medication by doctors) were excellent than before the lessons.The occurrence rates of gastrointestinal reactions, bleeding tendency, thrombophilia, abnormal liver function were reduced significantly, the rates of abnormal kidney function, nervous system reactions and coagulopathy were reduced too.The compliance after intervention (68.3 %) was higher than the compliance before intervention (23.3 %) dramatically and the difference was statistically significant(P <0.05). CONCLUSION: Clinical pharmacists can improve medication compliance of aspirin by active intervention such as give lessons.
    Changes of endodermis cell NO, ET and VEGF levels of stable angina patients and the effect of Salvianolate intervention
    CHEN Shu, ZHANG Jing, YAN Feng-di, YAN Jian-feng, YUAN Bing, HE Sheng-hu
    2009, 14(10):  1160-1163. 
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    AIM: To observe the changes of endodermis of stable angina patients and the effect of Salvianolate injection intervention. METHODS: 82 stable angina patients were chosen and randomly divided into two groups:one group was given conventional therapy, the other was added to Salvianolate injection in the base of conventional therapy.The treatment course was two weeks.The levels of NO, ET and VEGF were observed before and after treament. RESULTS: The anginal symptom of both two group patients were relieved.ET value was significantly decreased and the NO, VEGF value significantly increased in Salvianolate injection group more than before treament. CONCLUSION: Stable angina patients exist endodermis function damage.Salvianolate injection can effectually improve the endothelial function and relieve the anginal attack.
    Observation of terlipressin in management of patients with hepatorenal syndrome
    YU Zhe, YE Jiang-hong, WANG Che, RU Ren-ping
    2009, 14(10):  1164-1167. 
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    AIM: To observe the effect of terlipressin in the management of patients with hepatorenal syndrome. METHODS: 60 patients were divided into two groups.In Group A, terlipressine was used and Group B was control group.The clinical manifestation, laboratory examination, turnover were observed during treatment. RESULTS: Compared with Group B, the effective power, the mean arterial pressure and the total urine output were increased significantly, the serum creatinine level was decreased remarkably. CONCLUSION: Terlipressin is safe and effective on hepatorenal syndrome with minute adverse reaction.
    Advances on the causes and strategies of clopidogrel resistance
    YU Chang-yong, ZHANG Yong, ZOU Jian-jun, YAN Xiang, MA Hai-tao, NI Bin, ZHU Yu-bing, FAN Hong-we, HE Chun-hui
    2009, 14(10):  1168-1173. 
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    As we all know, platelets play a key role in the formation of arterial thrombosis and antiplatelet therapy has become the cornerstone for the prevention and treatment of arterial thrombosis in patients with acute coronary syndrome.Clopidogrel is a new antiplatelet drug, which has been confirmed as an important adjuvant therapy of cardiovascular disease.However, Many studies have found that about 11 %-44 %of patients show low response even non-response to clopidogrel, which is defined as clopidogrel resistance.The causes, which lead to this resistance phenomenon, may be due to inadequate doses of clopidogrel administration, the individual gene polymorphism, drug interactions and so on.The main strategies of clopidogrel resistance include increasing doses of clopidogrel administration, combining with other antiplatelet drugs, reducing adverse drug interactions and using of new drugs.
    Progress on anti-cancer mechanisms of natural coumarins
    WU Long-huo, LI Pei, DIAO Yong, XU Rui-an
    2009, 14(10):  1174-1177. 
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    Many literatures on anti-cancer activities of natural occurring coumarins are available.The anti-cancer mechanisms of coumarins are related to the physiological modulations in the living body.This paper is aimed to review the anti-cancer mechanisms of coumarins from different aspects such as influences on cell cycles, induction of cell apoptosis, SAPK JNK p38MAP signaling pathways and the system of glutathione S-transferases (GST) NADPH quinine oxidoreductase (NQO).
    Advances in the studies on the anti-tumor effect and mechanism of baicalein
    MAO Jie, XU Shan-shui, SHEN Li-li, WANG Xuan-zhi
    2009, 14(10):  1178-1182. 
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    Baicalein is applidied in clinic as Qing Re traditional Chinese herb.The recent research indicate that baicalein in scutellaria has anti-tumor effect by regulating arachidonic acid (AA)metabolites, inducing cancer cell cycle arrest and apoptosis, restraining tumor new angiogenesis, inhibiting cancer cell invasion and aversion, and enhancing cancer cell sensitiveness to chemotherapeutics.This article reviews the development of its anti-tumor effect and mechanism and provides theoretical evidence for clinical application.
    Progress and research in the effect of itraconazole on pharmacokinetic drug-drug interactions
    MIAO Cai-yun, CHEN Yi, CHEN Jiang-fei
    2009, 14(10):  1183-1192. 
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    Itraconazole, as one of the broad-spectrum antifungal drugs, is an inhibitor of CYP3A4 and P-glycoprotein and was widely used in clinic.CYP3A4 and P-glycoprotein with extensive substrate have present at high levels in gastrointestinal tract, the primary site of absorption for orally administrated drugs, and share a significant overlap in substrate specificity, thus resulting in widely pharmacokinetic interaction by itraconazole, part of which has clinical importance.In this article, the effect of itraconazole on pharmacokinetic drug-drug interactions is reviewed and discussed in order to promote its safe usage.
    Research development and clinical significance of genetic polymorphism of CYP450
    LI Na, SHI Xiao-jin
    2009, 14(10):  1193-1200. 
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    Cytochrome P450 is the very most important enzyme of drug metabolism.It involves in biotransformation of various endogenous and exogenous compounds, especially for clinical drugs.There are many polymorphisms of gene and phenotype, resulting in significant individual variability of different kinds of compounds.This article reviews the genetic polymorphisms of CYP, the characters and clinical meanings of diverse subgroups that relevant to drug metabolism in recent years.The major object of this article is reasonably explaining and predicting the interaction of clinical drugs and the drug adverse reaction in order to providing scientific evidences for the individual administration in clinic.