Objective: To determine the content of sanguinarine and chelerythrine in Macleaya microcarpa(Maxim) Fedde. Methods: RP-HPLC was adopted, kromasil C 18 column (150mm?4.6mm.5?m) with a mobile phase acetonitrile-0.1%(V/V) phosphoric acid solution(25∶75) by UV detector at 270nm. Results: The average recoveries of chelerythrine and sanguinarine were 90.2%,92.8%,RSD were 1.5%,2.4% respectively. Conclusion: A simple, rapid and sensitive method with good precision was established.

[Objective]This study was designed to investigate the genetic evolution of the neuraminidase(NA)gene of seasonal A/H1N1 and 2009 novel A/H1N1 inflilenza virus,and discuss the genetic variation of influenza A virus.[Methods]The virus strains were separately isolated from the clinical samples collected in 2006 and 2009,and then identified as seasonal A/H1N1 and novel A/H1N1.The full length of the NA gene of these strains was amplified by RT-PCR.Then the genetic evolution and mutations of important functional sites were analyzed.[Results]The homology of NA gene between the 2009 novel A/H1N1 isolates and 2006 seasonal A/H1N1 isolates was low(77.9%～78.8%),so was the homology of NA gene between the 2009 novel A/H1N1 isolates and representative strains of different periods and 1979-2001 WHO recommended vaccine strains(78.1%～79.3%).But compared with the WHO recommended vaccine strains of 2009 novel A/H1N1,the homology reached more than 99%.The genetic evolution analysis revealed that NA gene of 2009 novel A/H1N1 had the closest genetic relationship with the swine influenza A virus(A/swine/Belgium/1/1983)from Eurasian Iineage,and some of the antigenic sites and neuraminidase active sites of NA gene of seasonal A/H1N1 were mutated after 2005.[Conclusion]The NA gene of 2009 novel A/H1N1 may originate from Eurasian Iineage of swine influenza virus.The variation of NA gene of seasonal A/H1N1 has occurred in a certain degree.Hence,it is very necessary to continuously monitor the variant of influenza A virus.

Objective To evaluate the effect of cardiopulmonary bypass (CPB) on the expression of hypothalamic nerve growth factor precursor (proNGF) and the influence of hypothalamic proNGF on the sympathetic output of paraventrucular nucleus. Methods Forty-two male SD rats, aged 3-4 months, weighing 350-500 g, were divided into control group, CPB group and ischemia reperfusion (IR) group. At the end of CPB for 110 min, hypothalamus and dorsal root ganglion (DRG) were taken to measure the levels of proNGF mRNA and hypothalamic proNGF protein. Mini pipe was put into bilateral paraventrucular nucleus (PVN) and human recombination proNGF protein was injected into PVN for 7 d before the local field potentials (LFP) of RVLM was recoreded. Human recombination proNGF protein was administrated into lateral ventricle, the prior-administration-LFP of PVN and post-administration-LFP were recorded and compared. At the end of the experiment, hypothalamus was taken to measure the levels of glutamate and gammer amino butyric acid (GABA). Results Hypothalamic proNGF protein in CPB group and IR group was higher than that in the control group (P ＜ 0.05); NGF mRNA of hypothalamus and DRG in CPB and IR group were higher than those of control group (P ＜ 0.05). In PVN and RVLM, after the administration of proNGF protein, the power of delta band significantly decreased and other bands increased (P ＜ 0.05). The hypothalamic GABA level decreased (P ＜ 0.05) with no change of hypothalamic glutamate after proNGF was injected into lateral ventricle. Conclusion CPB increases the expression of proNGF in the hypothalamus contributing to the changes of hypothalamic sympathetic output.

OBJECTIVE: To investigate the effect of acute cardiac injury on the activation of interleukin-1 beta (IL-1 beta) signaling in the spinal cord. METHODS: Acute cardiac injury rat model was established by intra-myocardial injection of formalin through diaphragm. IL-1 beta expression was determined by Western blot, immunohistochemistry and in situ hybridization. The DNA binding activities of 2 IL-1 beta transcription factors, activator protein (AP)-1 and nuclear factor kB (NF-kappaB) were measured by electrophoretic mobility shift assay (EMSA). RESULTS: After cardiac injury, the IL-1 beta protein level was dramatically upregulated in the spinal cord. The upregulated IL-1 beta was mainly expressed in the neurons in the lamina II approximately IV of the spinal cord. In response to cardiac injury, the DNA binding activities of NF-kappaB and AP-1 were greatly activated. CONCLUSION Acute cardiac injury could activate the spinal IL-1 beta signaling, which, in turn, may be involved in the progression of heart failure after injury.
Animals ; Interleukin-1beta ; genetics ; metabolism ; Male ; Myocardial Reperfusion Injury ; chemically induced ; metabolism ; pathology ; Myocardium ; metabolism ; pathology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Signal Transduction ; Spinal Cord ; metabolism