3.Prostaglandin E2 receptor 1 antagonist attenuates mesangial cell lesion induced by TGF-β1 in mice through inhibiting ERK signal pathway
Zhi QIU ; Xiaolan CHEN ; Yuyin XU ; Tianyi PAN ; Wen MA ; Yaping FAN
Chinese Journal of Nephrology 2014;30(8):598-603
Objective To explore the effects and mechanisms of prostaglandin E2 (PGE2) receptor 1 antagonist (SC-19220) on proliferation,prostaglandin synthase and extracellular regulated protein kinases (ERK) signal pathway induced by transforming growth factor β1(TGF-β1) in glomerular mesangial cells.Methods Mouse glomerular mesangial cells (GMCs) were divided into 5 groups:control group,TGF-β1 (10 μg/L) group,TGF-β1 (10 μg/L) plus SC-19220 group (0.1,0.5,1.0 μmol/L).The proliferation of GMCs was measured by CCK-8.The PGE2 in supernatant was measured by ELISA.The expression of connective tissue growth factor (CTGF),laminin (LN),cyclooxygenase 2(COX2),membrane-bound prostaglandin E2 synthase 1 (mPGES1) protein and mRNA was examined by Westem blotting and real-time quantitative PCR,ERK1/2 or phospho-ERK1/2 was measured by Western blotting as well.Results TGF-β1 induced the proliferation of GMCs and increased the secretion of PGE2.Besides,TGF-β1 significantly up-regulated the expression of CTGF,LN,COX2 and mPGES1 mRNA and protein (P < 0.05),and increased the expression of phospho-ERK1/2 protein (P < 0.05).However,SC-19220 significantly attenuated the changes of above-mentioned parameters and their activities (P < 0.05).All the effects of SC-19220 were in dose-dependent manner.Conclusions SC19220 may reduce TGF-β1-induced cell damage by suppressing the activity of ERK1/2,and feedback inhibition of COX2,mPGES1 and PGE2,thus decreases the expression of LN and CTGF.
4.Investigation of the carotid intima-media thickness in 221 individuals with metabolic syndrome
Wen-Sheng JIN ; Chang-Yu PAN ; Ju-Ming LU ; Guang ZHI ; Bo YANG ;
Chinese Journal of Endocrinology and Metabolism 1986;0(03):-
Metabolic abnormalities were identified and carotid intima-media-thickness(IMT)was measured in 221 individuals at risk for metabolic syndrome(MS).The results indicated that IMT was significantly thicker in MS individuals than that in non-MS individuals(P<0.01).And there was a tendency of progressive increase in IMT with increasing components of metabolic syndrome.
5.Study on cytokines and dendritic cells involving immunologic inhibition of rat high-risk corneal transplantation induced by SEB
Xiao-Bo TAN ; Zhi-Qiang PAN ; Yu CHEN ; Ying JIE ; Wen-Hua ZHANG ; Yu-Ying WU ;
Ophthalmology in China 1993;0(03):-
objective To explore the role of cytokines and dendritic cells (DCs) in rat high-risk corneal allograft survival pro- longed by superantigen Staphylococcal Enterotoxin B (SEB) and to compare the different effects between SEB and glucocorticoid. Design Experimental study.Participants Fisher 344 and Lewis rats.Methods The Fisher 344 and Lewis inbred rats were used for high-risk penetrating keratoplasty model.All of the Lewis rat recipients were divided into three groups by blinded fashion.GroupⅠand GroupⅡrats were injected intraperitoneally with 0.2ml saline buffer or SEB (75?g/ml) respectively at 4-day intervals on three occasions before transplantation.GroupⅢrats were injected subconjunctivally with 0.1ml dexamethasone (1mg/ml) daily from the first day after surgery for 2 weeks.The allograft survival was examined under slit-lamp.The concentration of interleukin IL-1?,IL-2,IL-4,IL-5,IL-6, IL-10,TNF-?in rat aqueous humor and peripheral blood were measured by liquichip and the cytokine and CD11c,CD80,MHC-Ⅱex- pression in corneal grafts were examined by immunohistochemestry staining.Main Octcome Measures Mean survival time of the allo- grafts,the level of cytokines in aqueous humor,peripheral blood and corneal grafts.Results Compared with group control,the grafts mean survival time was delayed about 3.8d in group SEB (P=0.00) and 7.1d in group dexamethasone(P=0.01).But there was no signifi- cant difference between group SEB and dexamethone (P=0.26).Liquichip test showed that the level of IL-1?in aqueous humor was re- duced and IL-4,IL-6 and IFN-?,ascended.Only IFN-?,and IL-6 could be found in peripheral blood,and the changing shift of them was similar to that in aqueous humor.The immunohistochemistry staining showed that the expression of IL-2 in rat corneal grafts was signif- icantly decreased but IL-4,IL-6 and IL-10 elevated.The expression of DCs in group SEB was similar to that in group control,which was elevated after keratoplasty,but the phenotype of DCs was not the same.There were predominantly mature DCs in group control while immature DCs in group SEB.Conclusions The immunological inhibiting effect of SEB is same to glucocorticoid,but the mecha- nism is different.SEB can modulate immune response,which might induce immune inhibition via the local production of cytokines and effect on DCs maturation involving corneal graft rejection prevention.
6.Study on the Optimum Culture for Growth of Bacillus Subtilis B115 andthe Antibacterial Effect of B115 on Aeromonas
Zhi-Hua SHEN ; Jin-Yu SHEN ; Wen-Lin YIN ; Xiao-Yi PAN ; Ying-Lei WU ;
Microbiology 1992;0(04):-
The essential medium of B115 composed of 1% tryptone, 0.25% yeast extract and 0.5% sodium chloride was determined by using an orthogonal design. The orthogonal design was also employed in testing the optimum additions. It was composed of 0.1%(NH_(4))_(2)SO_(4),1.4%K_(2)HPO_(4), 0.6% KH_(2)PO_(4) and 0.1% (Na_(3)C_(6)H_(5)O_(7)). The yield of B115 cultured in optimum medium was compared with the one in essential medium. Statistic analysis showed that the growth of B115 was most significantly improved by adding K~(+)、NH~+_(4) and (Na_(3)C_(6)H_(5)O_(7)) to essential medium. The antibacterial effect of Bacillus subtilis strain B115 on pathogenic Aeromonas was studied. The results showed different antibacterial effects of B115 on different aeromonads. There were obvious antibacterial effects on BSK-10 and CL990920, while no effect on the growth of TL970424.
7.Association between unique nucleotide polymorphism of 2350G→A in angiotensin converting enzyme and myocardial infarction in Han nationality
Min PAN ; Wen-Ping JIANG ; Zhi-Hua LIU ; Xiang-Jun YANG ; Zhi-Chu CUI ; Dong-Lei ZHANG ; Jian-Hua ZHU ;
Chinese Journal of Emergency Medicine 2006;0(05):-
0.05).Conclusions SNP of 2350G→A in ACE gene is associated with MI,AA genotype is probably a genetic marker of MI in Han nationality.
8.Effects of Rb1 and Rg1 on the expression of Bcl-2, Bax in apoptosis of HK-2 cells induced by the serum of kidney ischemia/reperfusion.
Min-Xia ZHU ; Bing RAN ; Zhi-Qiang FENG ; Qiang-Wen PAN
Chinese Journal of Applied Physiology 2009;25(4):496-499
AIMTo explore effects of Ginsenosides (Rb1, Rg1) on the expression of Bcl-2, Bax in the serum of kidney ischemia/reperfusion inducing apoptosis of HK-2 cells.
METHODSThe serum of rabbits with renal ischemia/reperfusion (SIR) and the control serum of rabbits (SC) were acquired and cultured with HK-2 cells. Detected apoptosis with TUNEL assay. The experiment was designed as: control group,ischemia/ reperfusion group, Rb1 blocking group and Rg1 blocking group. To detect the expression of Bcl-2, Bax with immunocytochemistry after 24 hours' cultured.
RESULTSThe expression of Bax in Rb1 blocking group and Rg1 blocking group were significantly decreased (P < 0.01), the ratios of Bcl-2/Bax were increased as compared with ischemia/reperfusion group.
CONCLUSIONRb1 and Rg1 have protective effects on apoptosis of HK-2 cells induced by serum of kidney ischemia/reperfusion.
Animals ; Apoptosis ; drug effects ; Cell Line ; Female ; Ginsenosides ; pharmacology ; Ischemia ; blood ; Kidney ; blood supply ; Kidney Tubules, Proximal ; cytology ; Male ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Rabbits ; Reperfusion Injury ; blood ; Serum ; physiology ; bcl-2-Associated X Protein ; genetics ; metabolism
9.Effect of different pacing sites on ventricular synchrony evaluated by gated blood pool SPECT
Xue, GONG ; Yan-gang, SU ; Wen-zhi, PAN ; Shu-guang, CHEN ; Hong-cheng, SHI ; Xian-hong, SHU ; Jun-bo, GE
Chinese Journal of Nuclear Medicine 2010;30(5):307-311
Objective To compare the effect of right ventricular outflow tract (RVOT) and right ventricular apex (RVA) pacing on ventricular systolic synchrony using gated blood pool SPECT (GBPS).Methods A total of 50 patients implanted with pacemaker due to high degree or complete atria-ventricular block were enrolled in the study. Twenty-three patients were RVOT paced ( Group A, n = 23) and 27 were RVA paced (Group B, n=27). Twenty-four patients with malignancy, normal echocardiographic findings and no history of cardiac diseases were scheduled for pre-chemotherapy evaluation of cardiac structure and function and were enrolled as control group ( Group C, n = 24). All patients underwent GBPS imaging and the values of phase angle (PS), mean phase of each wall, standard deviation (SD) of mean phase of each wall, lateral-septal motion delay of left ventricle ( LV Sep-Lat Delay), septal-right ventricular (RV) delay of LV ( LV Sep-RV Delay) and LV-RV Delay were acquired. The parameters of ventricular systolic synchrony among the three groups were compared using one-way ANOVA. Results The mean phase of LV lateral wall in Groups A and B were significantly higher than that in Group C: Group A (120.50 ±40.58) ms; Group B (103.23±28.34) ms; Group C (84.63 ±22.38) ms (F=7.72, P <0.05). There was no significant difference between Groups A and B ( t = 1.30, P > 0.05 ). The mean phase of RV in Group A was significantly larger than those in Groups B and C: Group A ( 137.05 ± 39.27) ms, Group B ( 100.85 ± 23.79) ms,Group C (59. 13 ±30.52) ms (F=35.55, P<0.05). PS, SD and LV Sep-Lat Delay in Groups A and B were significantly higher than those in Group C: (85.73 ± 12.00)°vs (89.85 ± 15.61 )°vs (58.95 ±9.87)°, (27.68±10.66) ms vs (26.15 ±13.02) ms vs (15.63 ±8.35) ms, (25.06±34.23) ms vs (2. 62 ± 60. 31 ) ms vs ( - 23.66 ± 31.39) ms, F = 41.54,8.55,6.81, all P < 0.01 ), however, there was no significant difference between Groups A and B ( t = 0. 68, 0.68, 1.30, all P > 0.05 ). LV Sep-RV Delay and LV-RV Delay were significantly different among the three groups ( LV Sep-RV Delay: Group A (57.60 ±56.77) ms, Group B (6.36 ±61.88) ms, Group C ( -41.89 ±35.78) ms; LV-RV Delay:Group A (47.36 ±42.59) ms, Group B ( 3.08 ± 38.81 ) ms Group C ( - 26.50 ± 20.99 ) ms, F = 20. 32,25.38, both P < 0.01 ). Conclusion Both RVA and RVOT pacing increase the segmental phases detected by GBPS, causing inter- and intra- ventricular asynchrony compared with patients without pacemakers.
10.Stimulation of endothelial non-neuronal muscarinic receptor attenuates the progression of atherosclerosis via inhibiting endothelial cells activation.
Jing-Hong ZHOU ; Zhi-Yuan PAN ; Yan-Fang ZHANG ; Wen-Yu CUI ; Chao-Liang LONG ; Hai WANG
Chinese Journal of Applied Physiology 2014;30(6):549-559
OBJECTIVETo investigate the effects of non-neuronal muscarinic receptors (NNMR) stimulation on atherosclerosis and endothelial cells activation.
METHODSAtherosclerosis model was established in ApoE-/- mice by a high fat diet for 7 weeks. During the experimental periods, animals were received a low (7 mg/kg/d) or a high (21 mg/kg/d) dose of arecoline by gavage. At the termination of the treatments, serum total cholesterol and NO levels were measured, and the aorta morphology was analyzed by hematoxylin and eosin staining. The gene expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in the thoracic aortas was determined by RT-PCR, and the MCP-1 protein expression and NF-κB activity were detected by Western blot analysis. NO production, MCP-1 secretion in cultured rat aortic endothelial cells (RAECs), and monocyte-endothelium adhesion assay were also performed after arecoline treatments.
RESULTSArecoline efficiently decreased atherosclerotic plaque areas, increased serum nitric oxide (NO) content, suppressed the mRNA and protein expression of MCP-1, and modulated the IκB-α degradation and P65 phosphorylation in the aortae of ApoE-/- mice. Furthermore, arecoline promoted NO production and suppressed MCP-1 secretion in cultured RAECs after ox-LDL exposure, and either atropine or NG-nitro-L-arginine methylester could abrogate these effects. Arecoline also significantly inhibited the adherence of U937 monocytes to the ox-LDL injured human umbilical vein endothelial cells, which could be abolished by atropine.
CONCLUSIONOur results indicate that arecoline attenuates the progression of atherosclerosis and inhibits endothelial cells activation and adherence by stimulating endothelial NNMR. These effects, at least in part, are due to its modulation on NF-κB activity.
Animals ; Aorta ; cytology ; Apolipoproteins E ; Arecoline ; pharmacology ; Atherosclerosis ; physiopathology ; prevention & control ; Cell Adhesion Molecules ; metabolism ; Chemokine CCL2 ; metabolism ; Cholesterol ; blood ; Disease Progression ; Endothelial Cells ; cytology ; drug effects ; Endothelium, Vascular ; Human Umbilical Vein Endothelial Cells ; cytology ; Humans ; I-kappa B Proteins ; metabolism ; Lipoproteins, LDL ; Mice ; Mice, Knockout ; Monocytes ; cytology ; NF-KappaB Inhibitor alpha ; Nitric Oxide ; blood ; Nitroarginine ; pharmacology ; Rats ; Receptors, Muscarinic ; physiology ; Transcription Factor RelA ; metabolism