ABSTRACT
Aim To investigate the angiogenic promoting effect of Morinda officinalis How oligosaccharides(MOO) in the ischemic myocardium of rats after acute myocardial infarction(AMI).Methods 40 male Wistar rats were established into AMI model successfully and were randomly divided into 5 groups equally, i. e. the low, medium and high doses of MOO groups, the Shexiangbaoxin group and the model group. They were treated with different doses of the water fraction of the ethanolic extract of Radix morinda officinalis (0.7, 1.4, 2.8 mg·kg~(-1) ·d~(-1)), suspension liquid of Shexiangbaoxin Pill(30 mg·kg~(-1) ·d~(-1)) and distilled water with the same volume respectively.Besides, a sham operated group with 10 rats was set up for control. All rats were sacrificed after 6-week-treatment.The Ⅷ coagulation factor, vascular endothelial growth factor(VEGF) and basic fibroblast growth factor(bFGF) protein in ischemic myocardium of rats in each group were detected by immunohistochemistry assay.The microvessel density(MVD) was calculated. Gray values of protein expression of VEGF and bFGF in ischemic myocardium were calculated and analyzed by image analysis system.Results The MVD, the gray values of VGF and bFGF were higher in the medium and high doses of MOO groups than those in the model group(P <0.05), but still lower than those in the Shexiangbaoxin group(P <0.05). The MVD and the gray values of VEGF among 3 doses of MOO groups showed significant differences (P <0.05).Significant differences of gray value of bFGF were observed between small and middle doses of MOO groups, also between small and large doses of groups(P <0.05).Conclusion MOO can obviously promote angiogenesis in the ischemic myocardium of the rats after AMI.And up-regulating expressions of VEGF and bFGF protein in the ischemic myocardium may act as one of its angiogenic promoting mechanisms.
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Aim To study the function of VR1 in chronic pain, to construct VR1 siRNA expression vectors and to study their silencing effect in the DRG neurons of rats were detected.Methods The hairpin sequences of siRNAs targeting VR1 gene of rat were designed, and two pairs of oligonucleotide sequence were synthesized. The annealed oligonucleotide fragments were cloned into linearized pRNAT-U6.2/Lenti expression vector and identified by PCR and DNA sequencing.Then, they were co-transfected by lipofectamine into 293T cells.The silencing effects of the lentivector-mediated VR1 siRNAs on the expression of VR1 mRNA were determined by RT-PCR after intrathecal injection in rats.Results DNA sequencing showed that the oligonucleotide fragments were correctly cloned into linearized pRNAT-U6.2/Lenti expression vector and the expression of VR1 mRNA in L4-L6 DRG neurons was inhibited significantly by pRNAT-U6.2/Lenti-siVR1 after intrathecal injection in rats.Conclusion The lentivector-mediated siRNAs are successfully constructed and they inhibit the expression of VR1 mRNA in the DRG neurons of rats, which may provide a potential tool for the further study and treatment of chronic pain.
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Aim To study the effects of amitriptyline(Ami)on focal cerebral ischemia-reperfusion injury in rats.Methods An animal model of focal cerebral ischemia-reperfusion injury was induced by the middle cerebral artery occlusion(MCAO) by reversibly inserting a nylon thread method.The rats were decapitated after ischemia for 1 hour and reperfusion for 2 hours.The infarct volumes were determined using a 2,3,5-tri-phenyl tetrazolium chloride(TTC) staining and assessed by image analysis system.The neurologic deficit status were evaluated on 0~5 grade scale.The levels of dopamine(DA),norepinephrine(NE),serotonin(5-HT) and its metabolic product~hydroxyindole acetic acid(5-HIAA) in cortex and striatum were measured by fluoro-spectrophotometry.Results Ami treatment exhibited a remarkable reduction in infarct volume and neurologic deficit scores.The monoamines content of cortex and striatum had a significant increase compared with ischemia-reperfusion group.Conclusion Amitriptyline has protective effect on cerebral ischemia-reperfusion injury in rats.The mechanism might be related to reducing the release of NE,DA and 5-HT during cerebral ischemia-reperfusion,attenuating or inhibiting of the neurotoxic effects of monoamine neurotransmitters.
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AIM To study the effects of matrine (Ma) on the action potential and contractile force in guinea pig papillary muscles. METHODS Conventional microelectrode technique was used to record the fast action potentials (FAP) and slow action potentials (SAP) induced by histamine and BaCl_2 of guinea pig papillary muscles. RESULTS Ma 10,25,50 ?mol?L -1 dose-dependently prolonged the action potential duration at 50%, 90% repolarization (APD_ 50 , APD_ 90 ) and effective refractory period (ERP) of FAP, and lengthened the APD_ 50 , APD_ 90 of SAP induced by histamine and BaCl_2 when perfused with KCl 25 mmol?L -1 Tyrode's solution. The maximal upstroke velocity (V_ max ) of FAP, SAP and contractile force (Fc) were not affected by matrine 10,25,50 ?mol?L -1 . CONCLUSION It was suggested that Matrine could block K + channels in the myocardium.-