Journal Detail Information

1

Cite

Share

Synergistic and protective effects of various combination of major components of YiQiJieDu (YQJD) on focal cerebral ischemia injury based on amino acid metabonomics

Junling WANG ; Yang YANG ; Jian GAO ; Qingying FANG ; Defeng LI ; Chuanhong WU ; Zhiying HUANG ; Gengliang YANG ; Shaojing LI

Chinese Pharmacological Bulletin.2014;(5):725-731. doi:10.3969/j.issn.1001-1978.2014.05.030

Aim To elucidate the therapeutic effect of ginsenosides, berberine and jasminoidin after given a-lone or treatment with combination on the focal cerebral ischemia rats and study the compatibility mechanism. Methods We determined 12 endogenous amino acids in serum of rats after cerebral ischemia over 12 hours with RRLC-QQQ to evaluate the integrated role of YQJD at the dosage of 25 mg·kg-1 and 5 mg·kg-1 . Generally accepted methods were used, including be-havior test, One-Way AVONA, PLS-DA, as well as PCA to evaluate the injury induced by focal cerebral is-chemia. Results The score of neurological deficits and the level of five amino acids, namely Glu, Asp, Met, Hcy, Phe in the combination of ginsenosides, berberine and jasminoidin group in the dosage of 25 mg ·kg-1 and 5 mg·kg-1 significantly decreased (P<0. 05, P<0. 01) compared to those of model group. For another, the largest contribution group in the three principal components of PC1 , PC3 , PC4 at the dosage of 25 mg/kg and the six principal components PC1 ~PC5, PC7 in 5 mg·kg-1 was the combination of gin-senosides, berberine, jasminoidin group. Conclusions The results suggest that the efficacy of the combina-tion of ginsenosides, berberine and jasminoidin is su-perior to the combination of two or any single compo-nent, which can significantly improve the metabolic disorder of the endogenous amino acid after cerebral is-chemia. And it could be speculated that ginsenosides may play a more important role than berberine and jas-minoidin in regulating the level of amino acid metabo-lism.

2

Cite

Share

Role and mechanism of autophagy in the arsenic trioxide-induced death of Burkitt lymphoma Raji cells

Caili LI ; Jing CHEN ; Bei WANG ; Feifei WANG ; Baoying TIAN ; Bei XIE ; Linlan FAN ; Hulai WEI

Chinese Pharmacological Bulletin.2014;(5):719-724. doi:10.3969/j.issn.1001-1978.2014.05.029

Aim To investigate the role of autophagy and its mechanism in Raji cell death induced by arse-nic trioxide. Methods Transmission electron micros-copy ( SEM) and MDC fluorescence staining were used to observe autophagy. MTT colorimetry was employed to assay the cellular proliferating activity. Cell apopto-sis and cell cycle analysis were performed using FITC-Annexin-V/PI double staining and flow cytometry ( FCM) . The expressions of LC3 and the conversion of LC3-I to LC3-II were measured by western bloting. The expression of bcl-2 mRNA and p53 mRNA were detected by reverse transcription-polymerase chain re-action ( RT-PCR ) . Results Arsenic trioxide could obviously inhibit the proliferation of Raji cells, arrest the cells at G2/M phase and induce apoptosis. Mean-while, arsenic trioxide markedly inhibited the expres-sion of bcl-2 mRNA and enhanced the expression of p53 mRNA in Raji cells. Arsenic trioxide also induced autophagy synchronously which paralleled with the in-duction of apoptosis in Raji cells, and 3-MA, an auto-phagy inhibitor, was able to reverse the arsenic triox-ide-activated autophagic activity, up-regulate bcl-2, down-regulated p53 expression and suppress the lethal effect of arsenic trioxide on Raji cells to reduce their sensitivity to arsenic trioxide. In contrast, the Rapamy-cin, an autophagy inducer, possessed the completely opposite effects on Raji cells compared with 3-MA. Conclusions The apoptosis and autophagic cell death are coexistent in arsenic trioxide-triggered death of Raji lymphoma cells, and Bcl-2 and p53 may play a key regulating role in this process.

3

Cite

Share

Inhibitory effect of mastoparan-like peptide from wasp (Vespa magnifica) venom on angiogenesis

Wenjun LIU ; Xueqing XU

Chinese Pharmacological Bulletin.2014;(5):715-718. doi:10.3969/j.issn.1001-1978.2014.05.028

Aim To investigate the anti-angiogenic effect of 12a, the mastoparan-like peptide from wasp ( Vespa magnifica ) venom. Methods The tube for-mation and proliferation of human umbilical vein endo-thelial cells ( HUVEC ) and chicken chorioallantoic membrane ( CAM) model were used to observe the an-ti-angiogenic effect of 12a in vitro and in vivo, respec-tively. Results In the CAM model, 0. 1 μg or 1 μg of 12 a could markedly inhibit angiogenesis induced by 0. 2 μg rh-bFGF with heavy loss of color, decreasing density and obscure frame of the vessels. The inhibi-tion rates of angiogenesis were 60 . 2 % for 0 . 1 μg and 90. 3 % for 1 μg, respectively. Accordingly, in HU-VEC culture experiment, the proliferation and angio-genesis of HUVEC treated by 1 mg·L-1 and 10 mg· L-1 of 12 a were decreased by 55. 4 %, 39. 3 % and 51. 6 %, 26. 7 %, respectively. Conclusion 12a has a significant anti-angiogenic effect in a concentra-tion-dependent manner.

4

Cite

Share

Influences of chrysophanol on immune function of lead poisoning mice

Ji ZHANG ; Chunlin YAN ; Yong HOU ; Shu WANG ; Danshen ZHANG ; Guiping XUE ; Xiaohua DONG

Chinese Pharmacological Bulletin.2014;(5):696-700. doi:10.3969/j.issn.1001-1978.2014.05.024

Aim To investigate the protective effects of chrysophanol( Chry) on immune function of lead poi-soning mice. Methods The lead poisoning model was established by peritoneally injecting mice with 7 mg · kg-1 lead acetate every day for 8 days. After Chry was ip injected for 14 days,spleen and thymus index, the white blood cell count, T, B lymphocyte proliferation, phagocytic function of macrophages, natural killer cell ( NK cell) activity were detected. The concentrations of IFN-γ,IL-2,IL-4,IL-10 in the lead poisoning mice ser-um were determined by enzyme-linked immunosorbent assay ( ELISA) . Results Intraperitoneal injection of 7 mg · kg-1 lead acetate for 8 consecutive days could cause an immunity decline in lead poisoning mice, Chry could significantly improve the immunity of lead poisoning mice. Compared with model group, Chry sig-nificantly improved growth rate, viscera index and white blood cell count of lead poisoning mice at differ-ent extent ( P<0 . 05 or P<0. 01 ) . Chry ( 1 . 0 ,10 . 0 mg·kg-1 ) significantly increased the B,T lymphocyte proliferation ( P<0 . 01 ) and the phagocytosis of macro-phage and NK cell activity ( P <0 . 01 ) . Compared with the control group, the concentrations of IFN-γ, IL-2 , IL-4 , IL-10 of lead poisoning mice serum were significantly reduced ( P <0 . 01 ) . Compared with the model group, Chry (1. 0、10. 0 mg·kg-1 ) significant-ly increased the concentrations of IFN-γ, IL-2 , IL-4 , IL-10 ( P <0. 01 ) , while there were no significant changes in (0. 1 mg·kg-1 ) concentrations of IFN-γ, IL-2 , IL-4 in Chry ( 0 . 1 mg · kg-1 ) treatment group ( P>0. 05 ) , only IL-10 was significantly increased in Chry ( 0 . 1 mg · kg-1 ) treatment group ( P<0 . 05 ) . Conclusion Chry can significantly improve the im-mune function of lead poisoning mice.

5

Cite

Share

Atorvastatin attenuates activation and injury of human microvascular endothelial cells induced by oxidized low density lipoprotein

Min LI ; Ling SUN ; Hongling LI ; Qianyun SUN

Chinese Pharmacological Bulletin.2014;(5):679-683. doi:10.3969/j.issn.1001-1978.2014.05.020

Aim To investigate the effects of atorvas-tatin ( ATV) on activation and injury of microvascular endothelial cells induced by oxidized low density lipo-protein ( ox-LDL) . Methods Cultured human micro-vascular endothelial cells were pre-incubated with ATV for 24 h prior to exposure of endothelial cells to ox-LDL. After exposure of endothelial cells to ox-LDL, the cell viability was measured by MTT method, LDH in supernatants was determined by enzyme activity as-say kit, ICAM-1 in supernatants was assayed by using ELISA method, phosphorylation of NF-κB p65 was de-tected by western blot analysis, transcriptional activity of NF-κB signal pathway was measured by employing dual-luciferase reporter assay system. Results Hu-man microvascular endothelial cells were activated and injured by ox-LDL. Inhibition of the cell viability, re-lease of LDH, expression of ICAM-1, phosphorylation of NF-κB p65 , and up-regulated transcriptional activity of NF-κB induced by ox-LDL were attenuated by ATV. Conclusion ATV can significantly inhibit the activa-tion and injury of human microvascular endothelial cells induced by ox-LDL, and that may be related to inhibition of phosphorylation and transcriptional activity of NF-κB.

6

Cite

Share

Effects of flavonoids from Prinsepia utilis Royle on the histomorphology of kidney in alloxan-induced diabetic mice

Cheng Lü ; Xiaolan WU ; Zhongqiong YIN ; Bo JING ; Zhengwen LI ; Shujun DAI

Chinese Pharmacological Bulletin.2014;(5):672-675. doi:10.3969/j.issn.1001-1978.2014.05.018

Aim To investigate the effect of flavonoids from Prinsepia utilis Royle( FPR) on the histomorphol-ogy of kidney in diabetic mice, and to investigate its protective mechanism. Methods Diabetic mice in-duced by alloxan were given FPR orally each day for four weeks. After the administration for two and four weeks, ten mice in each group were randomly sacri-ficed. The kidneys were removed and weighed. The extracted renal tissue was embedded with paraffin and sectioned, the sections were stained with Hematoxylin and Eosin(HE)、Periodic acid Schiff(PAS) and Go-mori, and then observed under the microscopy. 1mm3 of renal cortex fixed with glutaral in four centi-degree , and then the ultrastructure of each group was observed under the electron microscope respectively after four weeks′ treatment. Results Compared with the model control group, in the treatment group, observation un-der the microscopy showed that glomerular volume and mesangial cells reduced, FPR could relieve thickening of the glomerular basement membrane ( GBM ) , little inflammatory cells infiltrated in the interstitium,tubular epithelial cells almost became normal, renal tubule had little glucogen, fiber decreased in the interstitium of renal tubule. Observation under the electron micro-scope indicated that foot process in podocytes lined up in order, mitochondria of the renal tubule’ s epithelial cell almost recovered. Conclusion FPR can relieve the changes of renal pathology,improve renal function, and delay the progression of pathologic changes of kid-ney in diabetic mice partly through reducing the blood glucose and the blood lipid.

7

Cite

Share

Study on gallic acid induced human hepatoma SMMC-7721 cells apoptosis and its mechanism

Muhan LI ; Mingyan WANG ; Fengming ZHAO ; Haibin CHEN ; Hongguang ZHOU ; Qingchun ZHAO ; Wenting LI ; Mianhua WU

Chinese Pharmacological Bulletin.2014;(5):657-661. doi:10.3969/j.issn.1001-1978.2014.05.015

Aim To investigate the proliferative effect and the apoptosis of human hepatoma SMMC-7721 cells induced by gallic acid ( GA ) , and its underlying mechanism. Methods SMMC-7721 cells were cul-tured in vitro. MTT assay was used to observe the pro-liferation of SMMC-7721 cells induced on GA 24 , 48 , 72 h. The morphological and ultra structural changes of the SMMC-7721 cells were observed by inverted micro-scope and transmission electron microscope respective-ly. Annexin V-FITC/PI staining was used to quantify the percentages of apoptosis in the total cell popula-tion. The expression of p53 mRNA was investigated by RT-PCR. Western blot was used to determine the pro-tein expression of p53. Results GA(6. 25~50 μmol ·L-1 ) markedly inhibited the activity of proliferation and induced apoptosis of SMMC-7721 cells after 48 h in a dose-dependent manner. GA significantly induced cell nuclear condensation and fragmentation. RT-PCR and Western blot results showed that GA could improve the expression of p53 mRNA and protein. Conclusion GA can inhibit the proliferation of human hepatoma SMMC-7721 cells and induce cells apoptosis. The mechanism may be associated with improving tumor suppressor gene p53 expression.

8

Cite

Share

Effects of paeonol on lipopolysaccharide/adenosine 5′-triphosphate induced NLRP3 inflammasome activation in primary rat microglia

Wei WANG ; Min DAI ; Zhongdong XU

Chinese Pharmacological Bulletin.2014;(5):652-656. doi:10.3969/j.issn.1001-1978.2014.05.014

Aim To investigate the effects of paeonol on lipopolysaccharide ( LPS) and adenosine 5′-triphos-phate ( ATP) induced NLRP3 inflammasome activation in primary rat microglia and the mechanisms responsi-ble for this anti-inflammatory effects. Methods Pri-mary rat microglia were identified immunohistochemi-cally using the cluster of differentiation 11 b ( CD11 b ) antibody. Proinflammatory cytokine IL-1β was deter-mined by ELISA. Western blot was performed to ob-serve the protein expression of NLRP3 , ASC and caspase-1 in cultured primary rat microglia. The level of intracellular reactive oxygen species ( ROS) was mo-nitored by using the fluorescent probe 2′, 7′-dichlo-rofluorescein diacetate ( DCFH-DA ) . Results LPS (0. 5 mg · L-1 )/ATP ( 5 mmol · L-1 ) significantly increased intracellular ROS level and IL-1β secretion and upregulated NLRP3 , ASC and caspase-1 protein expression in primary rat microglia. Paeonol signifi-cantly decreased intracellular ROS level and IL-1β se-cretion, and inhibited LPS/ATP induced overexpres-sion of NLRP3 , ASC and caspase-1 in cultured primary rat microglia. Conclusion Paeonol can inhibit LPS/ATP induced NLRP3 inflammasome activation in pri-mary rat microglia, and this inhibitory effect may be through the suppression of intracellular ROS.

9

Cite

Share

Effects of glycyrrhizic acid on glomerular mesangial cells and ECM expression induced by AGEs

Shaozhang HOU ; Fangfang ZHENG ; Yuan LI ; Ling GAO

Chinese Pharmacological Bulletin.2014;(5):642-645. doi:10.3969/j.issn.1001-1978.2014.05.012

Aim To investigate the influence of gly-cyrrhizic acid( GA) on cell proliferation and cell cycle and secretion of extracellular matrix ( ECM) , the level of fibronection ( FN) , type Ⅳ collagen ( C-Ⅳ) in the rats′ glomerular mesangial cells ( HBZY-1 ) cultured with advanced glycation endproducts ( AGEs ) . Meth-ods HBZY-1 were incubated in culture medium con-taining AGEs in the presence of GA and treated for 48 h. At the same time, the normal and control groups were established. Methylthiazoletetrazolium ( MTT) as-say was used to measure cell proliferation;cell cycle a-nalysis was performed using a flow cytometry; FN and C-Ⅳwere analyzed by enzyme-linked immunosorbent assay ( ELISA ) . Results Cell counts increased markedly in AGEs group. Cell cycle analysis showed that cell percentage of S phase increased, G1 reduced and PI increased from 35. 01% ± 4. 21% to 44. 93%± 0. 25% ( P <0. 05 ) . FN and C-Ⅳ secretion in-creased ( P <0. 05 ) . Whereas GA was added, cell counts decreased, and the percentage of S phase also decreased and G1 increased, PI decreased from 44. 93% ± 0. 25% to 42. 16% ± 1. 04% ( P<0. 05 ) . In addition, the secretion of FN and C-Ⅳ decreased ( P<0. 05 ) . Conclusion GA could prevent AGEs-induced HBZY-1 . GA may protect HBZY-1 from in-hibiting the abnormal cell proliferation, changing the cell cycle. GA can reduce the synthesis of FN and C-Ⅳ.

10

Cite

Share

Signaling mechanisms in endothelial monocyte-activating polypeptide-Ⅱ-enhanced permeability of the blood-tumor barrier

Zhen LI ; Xiaobai LIU ; Yunhui LIU ; Yixue XUE ; Ping WANG ; Libo LIU

Chinese Pharmacological Bulletin.2014;(5):632-637. doi:10.3969/j.issn.1001-1978.2014.05.010

Aim To investigate the signaling mecha-nisms in endothelial monocyte-activating polypeptide-Ⅱ( EMAP-Ⅱ)-induced increase in blood-tumor barri-er ( BTB ) permeability. Methods Relatively pure cerebral microvessel fragments were obtained from the cortex of 3-5 days old Wistar rats by using careful dis-section, enzyme digestion, and dextran centrifugation. Then, these fragments were seeded on dishes and cul-tured primarily. In vitro BTB models were constructed by co-cultivation of rat brain microvascular endothelial cells ( BMECs) with C6 glioma cells. Confluent mono-layers of co-cultured BMECs were divided randomly in-to 5 groups ( each n=6 ): control, EMAP-Ⅱ, H7 +EMAP-Ⅱ, C3 exoenzyme + EMAP-Ⅱ, and C3 ex-oenzyme + H7 + EMAP-Ⅱ groups. Transendothelial electric resistance values and horseradish peroxidase flux were measured to evaluate changes in the BTB permeability . The expression levels of tight junction-re-lated protein occludin and ZO-1 in BMECs were meas-ured by Western blot. Immunofluorescence was used to identify the expression and distribution of occludin and ZO-1 in BMECs. Also, Western blot were used to de-tect the expression levels of myosin light chain ( MLC) and phosphomyosin light chain ( pMLC ) in BMECs. Results Compared with control group, the BTB per-meability of EMAP-Ⅱ group was increased significant-ly. The expression levels of occludin and ZO-1 in BMECs were significantly decreased, accompanied with marked increase in the expression level of pMLC. These above-mentioned effects of EMAP-Ⅱ were sig-nificantly inhibited by pretreatment with H7 ( an inhib-itor of PKC ) or/and C3 exoenzyme ( an inhibitor of RhoA ) . Conclusion Signaling molecules PKC and RhoA play important roles in EMAP-Ⅱ-induced in-crease in BTB permeability; signaling pathways PKC-pMLC and RhoA-pMLC are involved in this process.

DISPLAY OPTIONS

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share