4.HPLC Determination of Ketoconazole and Desamethasone Acetate in Ketoconazole Spraying Film Simultaneously
Xuemei YI ; Wenji WANG ; Chun ZHANG ; Jianhua WU ; Hai WEN
China Pharmacy 2001;0(11):-
OBJECTIVE:To establish an approach to determination of ketoconazole and desamethasone acetate in novel ketoconazole spraying film.METHODS:Chromatography was performed using a Waters Symmetry C 18 .The mobile phase consisted of methyl-monopotassium phosphate(4∶1).Detection wave was at239nm.The flowing rate was0.6ml/min.RESUL_ TS:Excellent linear correlations were showed when the concentrations of ketoconazole and desamethasone acetate were in the ranges of0.2~2mg/ml and0.02~0.2mg/ml respectively.The mean recoveries of ketoconazole and desamethasone acetate were98.41%(RSD=2.29%,n=6)and97.84%(RSD=2.60%,n=6)respectively.CONCLUSION:The established approach is precise,reliable and therefore applicable to the quality control of novel ketoconazole spraying film.
5.Studies on antineoplastic constituents from chinese marine mollusc sea hare(Ⅰ)
Houwen LIN ; Chun ZHANG ; Yanghua YI ; Al ET ;
Chinese Journal of Marine Drugs 1994;0(03):-
Two active compounds were isolated from chinese marine mollusc sea hare (Notarchus leachii cirrosus) by bioassay guided method with conidia of Pyricularia oryzae , and by a combination of extraction and purification with suitable solvent as well as multiple column chromatographies. Their structures were elucidated as (7 E) 1 acetoxy 8 chloro 7 (dichloromethyl) 3 methyoct 7 en 4 one (Ⅰ), (7 Z) 1 acetoxy 8 chloro 7 (dichloromethy l) 3 methyoct 7 en 4 one (Ⅱ). All compounds were obtained for the first time from this specimen and showed significant antineoplastic activities in vitro .
6.Research about the expression changes of CNTF and CGRP in the rabbits' model of neuroma-in-continuity
Chun-Hui SONG ; Tong-Yi CHEN ; Feng ZHANG ; Jian ZHANG ; Zhong-Wei CHEN ;
Chinese Journal of Microsurgery 2000;0(03):-
Objective In view of being short of the mammalian model in neuroma-in-continuity,the experiment injured the part of peroneal nerve to the formation of the neuroma-in-continuity and was applied to the foundation of farther research.Methods Twelve New Zeland rabbits were selected as experimental sub- jects randomly.One lateral peroneal nerves of twelve rabbits were resected,the damaged nervous tissues' slice were showed to the typical pathological changes of neuroma by the stain of HE,luxol fast blue after six weeks. As compared with the health sides of six model rabbits,the methods of real-time PCR and Western blot were used to evaluate the expression of CNTF,CGRP mRNA and protein in injured nerves and L_7、S_1 dorsal root ganglions respectively.Results The injured nerve formed the typical pathological changes of neuroma at six weeks.Compared with hea|thg side the expression of CNTF mRNA and protein was down-graded at the lateral of neuroma(P<0.05),and the expression of CGRP mRNA and protein was up-graded(P<0.05).Con- clusion The method of partly injuring the peroneal nerve could effectively set up the model of the neuroma-in- continuity,furthermore,resulted to the expression changes of the CNTF,CGRP mRNA and protein.
7.Detection of early glial responses in the retina,optic nerve and optic chiasm in acute ocular hypertension rat model
Shao-dan, ZHANG ; Wei-yi, LI ; Wen-qian, WANG ; Ping, HUANG ; Ning-li, WANG ; Chun, ZHANG
Chinese Journal of Experimental Ophthalmology 2012;30(8):704-708
Background Glial cells perform specialized function in many aspects of the development,homeostasis,and function of neurons.Retinal ganglion cells (RGCs)and glia interactions are critically important in glaucomatous neurodegeneration.However,the precise mechanisms of glial activation and ganglion cells damage are still remained unclear. Objective This study was to assess the early responses of glial cells in the retina,optic nerve and optic chiasm in rat models of acute high intraocular pressure (IOP),and to examine the expression of nestin,a neuronal progenitor marker,in the reactive glias. Methods Acute high IOP of 110 mmHg was induced in the right eyes of 6 clean adult female Wistar rats by infusing normal saline solution into the anterior chamber for 60 minutes.Three normal matched Wistar rats were used as controls.The rats were sacrificed by overanaesthesia and sections of retina,optic nerve and optic chiasm were collected on 3 days and 7 days after the injection.Rat retina was examined by Nissl staining to illustrate the gross structure changes.Loss of axons of RGCs in the optic nerve was assessed by immunostaining of β Ⅲ-tubulin.Double labeling of glia] fibrillary acidic protein (GFAP) and nestin was performed in sections of retina,optic nerve and optic chiasm to evaluate the glial responses.The use of the animals complied with Statement of Animal Ethic Committee of Peking University Third Hospital. Results In control rats,GFAP-positive glial cells were observed in the retina,optic nerve and optic chiasm,where only weak positive response for nestin was noticed.Three days after acute IOP elevation,thickness of inner plexus form layer was significantlydecreased in comparison with the control rats.A loss of 46% RGCs was found in the rats with ocular hypertension.Obvious increase of GFAP expression was displayed in the retina,and processes of GFAP-positive glia cells extended into outer retina accompanied with significant up regulation of nestin.Axons in the optic nerve demonstrated a tendency of degeneration.Nestin expression increased significantly in the GFAP-positive glias in the optic nerve.Cross-sectional area of optic chiasm corresponding to the injured retina decreased relative to its countcrpart.Astrocyte like GFAP and nestin-colabeled glials were observed in this part of optic chiasm.The pathological changes of the retina,optic nerve and optic chiasm in hypertensive eyes aggravated on 7 days. Conclusions Acute ocular hypertension induce early onset of RGCs loss and axon degeneration.Neuronal injury is accompanied with glial reaction.Reactive glial cells express neuronal progenitor markers.The structural changes of the optic nerve and optic chiasm occur simultaneously with the high IOP.
8.Verification and Evaluation on Microbial Limit Test of Methodology for Changyanning Tablets in ChP 2015
Xuping LIU ; Wenting ZHANG ; Luyao YI ; Jun XIONG ; Chunhua ZHANG ; Chun XIAO
China Pharmacist 2017;20(5):946-948
Objective: To provide a method of microbial limit test for Changyanning tablets and carry out the verification of the mothod.Methods: A plate method was used in the total aerobic microbial count and the concentration of the test liquid was 1∶100.A plate method was used in the total yeast and mold count while the concentration of the test liquid was 1∶10.The direct inoculation method was used for the detection of Escherichia coli,bile-tolerant gram-negative bacteria and Salmonella enterica subsp.Results: The recoveries of the five strains were from 0.5 to 2.0.Conclusion: The method is suitable for the microbial limit examination of Changyanning tablets.
9.Ischemia-induced release of cytochrome c from mitochondria and up-regulation of Bcl-2 expression in rat hippocampus.
Chun-Yi ZHANG ; Wan-Hua SHEN ; Guang-Yi ZHANG
Acta Physiologica Sinica 2004;56(2):147-152
To evaluate the effects of different antagonists on the release of cytochrome c from mitochondria to cytosol and the expression of Bcl-2 in mitochondria in rat hippocampus after ischemia, we examined Bcl-2 and cytochrome c expression by immunoblotting using 4-vessel occlusion (4-VO) as brain ischemia model. The results showed that after 24 h ischemia/reperfusion (I/R) cytochrome c decreased markedly in mitochondria, which was correspondingly increased in the cytosolic fraction. Bcl-2 expression was time-dependent, reaching its peak level after 6 h I/R. In all those samples, there were no alterations in the subcellular distribution of cytochrome oxidase, a mitochondrial respiratory chain protein. The decreases in Bcl-2 and cytochrome c in mitochondria were restored by pretreatment with non-competitive NMDA receptor antagonist ketamine or L-type voltage-gated Ca(2+) channel (L-VGCC) antagonist nifedipine at 20 min prior to ischemia. The results demonstrate that the release of cytochrome c from mitochondria to cytosol and the up-regulation of Bcl-2 are possibly mediated by NMDA receptors or L-VGCC following brain ischemia. Cytochrome c release may be injurious while Bcl-2 up-regulation may be protective to ischemic hippocampus.
Animals
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Brain Ischemia
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metabolism
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Calcium Channel Blockers
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pharmacology
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Calcium Channels, L-Type
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drug effects
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Cytochromes c
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metabolism
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Cytosol
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Hippocampus
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metabolism
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Ketamine
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pharmacology
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Male
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Mitochondria
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metabolism
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Nifedipine
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pharmacology
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Proto-Oncogene Proteins c-bcl-2
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biosynthesis
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genetics
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Rats
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Rats, Sprague-Dawley
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Receptors, N-Methyl-D-Aspartate
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antagonists & inhibitors
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Up-Regulation
10.Proteomics Study of Benzene Metabolite Hydroquinone Induced Hematotoxicity in K562 Cells
Shan Yi JIN ; Chun Zong YI ; Jing Yu ZHANG ; Long RONG ; Hong Chun YU
Biomedical and Environmental Sciences 2024;37(4):341-353
Objective Hydroquinone(HQ),one of the phenolic metabolites of benzene,is widely recognized as an important participant in benzene-induced hematotoxicity.However,there are few relevant proteomics in HQ-induced hematotoxicity and the mechanism hasn't been fully understood yet. Methods In this study,we treated K562 cells with 40 μmol/L HQ for 72 h,examined and validated protein expression changes by Label-free proteomic analysis and Parallel reaction monitoring(PRM),and performed bioinformatics analysis to identify interaction networks. Results One hundred and eighty-seven upregulated differentially expressed proteins(DEPs)and 279 downregulated DEPs were identified in HQ-exposed K562 cells,which were involved in neutrophil-mediated immunity,blood microparticle,and other GO terms,as well as the lysosome,metabolic,cell cycle,and cellular senescence-related pathways.Focusing on the 23 DEGs and 5 DEPs in erythroid differentiation-related pathways,we constructed the network of protein interactions and determined 6 DEPs(STAT1,STAT3,CASP3,KIT,STAT5B,and VEGFA)as main hub proteins with the most interactions,among which STATs made a central impact and may be potential biomarkers of HQ-induced hematotoxicity. Conclusion Our work reinforced the use of proteomics and bioinformatic approaches to advance knowledge on molecular mechanisms of HQ-induced hematotoxicity at the protein level and provide a valuable basis for further clarification.