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Objective:To investigate the analgesic effect of neurotropin (NTP) on bone cancer pain (BCP) and its preliminary mechanisms in rats.Methods:(1) According to the random number table method, 72 Sprague-Dawley (SD) female rats were randomly and equally divided into 6 groups: normal control group, sham-operated group, BCP model group, BCP+low-dose NTP group, BCP+medium-dose NTP group, and BCP+high-dose NTP group ( n=12). The SHZ-88 breast cancer cells were inoculated into the tibias of rats in the latter 4 groups to establish BCP models. After 15-21 d of modeling, the rats of the latter 3 groups were intraperitoneally administered with 1.2, 2.4 and 3.6 unit NTP, respectively, once per d for 7 consecutive d. The mechanical withdrawal threshold (MWT) changes were measured in each group before BCP and 5, 7, 10, 14, 17, and 21 d after BCP. The number of 5-hydroxytryptamine 7 (5-HT7) positive cells and 5-HT7 protein expression in the ventrolateral periaqueductal gray (vlPAG) were detected by immunohistochemistry and Western blotting, respectively. (2) Twenty-four rats 21 d after BCP modeling were randomly divided into BCP group, BCP+high-dose NTP group (BCP rats with intraperitoneal injection of 3.6 unit NTP), BCP+NTP+SB-269970 group (BCP rats with pretreatment of specific 5-HT7 receptor antagonist SB-269970 in the vlPAG for 30 min, and then, with intraperitoneal injection of 3.6 unit NTP, n=8). The MWT changes were measured in each group before NTP and 15, 30, 45, 60 min after NTP. Results:(1) Seventeen and 21 d after modeling, the MWT values of the modeled hind limb of rats in BCP+low-dose NTP group, BCP+medium-dose NTP group, and BCP+high-dose NTP group were significantly higher than those in BCP group; those in the BCP+high-dose NTP group were significantly higher than those in BCP+low-dose NTP group and BCP+medium-dose NTP group; those in BCP+medium-dose NTP group were statistically higher than those in the BCP+low-dose NTP group ( P<0.05). Twenty-one d after modeling, the number of 5-HT7 receptor positive cells and protein expression in the vlPAG of rats in the BCP+low-dose NTP group, BCP+medium-dose NTP group, and BCP+high-dose NTP group were significantly larger/higher than those in BCP group; those in the BCP+high-dose NTP group were significantly larger/higher than those in BCP+low-dose NTP group and BCP+medium-dose NTP group; those in BCP+medium-dose NTP group were statistically larger/higher than those in the BCP+low-dose NTP group ( P<0.05). (2) At 15, 30, 45 and 60 min after injection of NTP, the MWT values of the modeled hind limb of rats in the BCP+high-dose NTP group and BCP+NTP+SB-269970 group increased gradually, enjoying statistical significance as compared with those in the BCP group at the same time point ( P<0.05); however, the MWT values of the BCP+NTP+SB-269970 group were significantly lower as compared with those in the BCP+high-dose NTP group at the same time point ( P<0.05). Conclusion:The activation of 5-HT7 receptor in the vlPAG is involved in the analgesic effect of NTP on BCP in rats.
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Objective To evaluate the role of P2X7 receptor in the ventrolateral periaqueductal gray (vlPAG) in tramadol-induced reduction of neuropathic pain (NP) in rats.Methods Fifty-four male clean-grade healthy Sprague-Dawley rats,aged 7 days,weighing 190-230 g,were studied.NP was induced by chronic constrictive injury (CCI) to sciatic nerve.Experiment Ⅰ Thirty-six rats were divided into 3 groups (n =12 each) using a random number table method:sham operation group (group S),group NP1 and NP plus tramadol group (group NP1 +T).Tramadol 15 mg/kg was intraperitoneally injected once a day from day 7 to day 14 after CCI in group NP1+T.The mechanical and thermal pain thresholds of the nerve-injured hindlimb were measured before CCI and on 1,5,7,10,12 and 14 days after CCI.Rats were sacrificed after measurement of pain threshold on day 14 after CCI,and the expression of P2X7 receptor in vlPAG was detected by immunohistochemistry and Western blot assay.Experiment Ⅱ Eighteen rats were divided into 3 groups (n =6 each) using a random number table method:group NP2,NP plus tramadol group (group NP2+T) and NP plus tramadol plus a specific P2X7 receptor antagonist A-438079 group (group NP2+T+A).In NP2+T+A group,a catheter was implanted in vlPAG,and the NP model was established on 5th day after successful catheterization.Tramadol 15 mg/kg was intraperitoneally injected once a day from day 7 to day 14 after CCI in group NP2+T.In group NP2+T+A,tramadol 15 mg/kg was intraperitoneally injected once a day from day 7 to day 14 after CCI,followed by a microinjection of A-438079 100 pmol (0.3 μl) via vlPAG before giving tramadol on day 14.The mechanical and thermal pain thresholds were measured at the end of the last tramadol administration and within 1 h after the end of the last tramadol administration.Results Experiment Ⅰ Compared with group S,the mechanical and thermal pain thresholds were significantly decreased at each time point after CCI,the number of P2X7 receptor positive cells was increased,and the expression of P2X7 receptor was up-regulated in the other two groups (P＜0.01).Compared with group NP1,the mechanical and thermal pain thresholds were significantly increased at days 7-14 after CCI,the number of P2X7 receptor positive cells was increased,and the expression of P2X7 receptor was up-regulated in group NP1 +T (P＜0.01).Experiment Ⅱ Compared with group NP2,the mechanical and thermal pain threshold were significantly increased at each time point after CCI in NP2+T and NP2 +T+A groups (P＜0.01).Compared with group NP2 +T,the mechanical and thermal pain thresholds were significantly decreased at each time point after CCI in group NP2+T+A (P＜ 0.01).Conclusion The mechanism by which tramadol mitigates NP is partially related to enhanced function of P2X7 receptors in vlPAG of rats.
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Objective To observe the change of learning and memory and the expression change of GABAR1 and N-methyl-D-aspartate receptor 2B (NMDAR2B)in right frontal lobe of the brain of the aged rats after the inhalation of sevoflurane.Methods Fifty male SD rats were randomly divided into control group (group C,n=10)and experimental group (group T,n=40).The control group received air at room tempreture.Experimental groups were divided into two groups:group T1 (2 h)and group T2 (4 h)according to the time of inhalation of sevoflurane at 3% concentration.Ev-ery group was equally divided into two groups and Morris water maze was performed on day 1 and day 7 after sevoflurane inhalation.Then the right frontal lobe was gathered and the mRNA transcription and protein expression of GABAR1 and NMDAR2B were detected by Quantitative Real-time PCR and immunofluorescence technique.Results Compared with group C,the escape latency was prolonged in groups T1 and T2 after 1 day of inhalation of sevoflurane (P<0.05),and the times of space explora-tion reduced (P<0.05).mRNA transcriptional and protein content of GABAR1 were significantly upregulated in frontal lobes of groups T1 and T2,mRNA transcriptional and protein content of NMDAR2B were significantly down-regulated (P<0.05).After inhalation of sevoflurane for 7 days, the protein expression of NMDAR2B in the frontal lobe of group T1 was lower than that of group C (P<0.05).In group T2,the escape latency was prolonged (P<0.05),the number of space explo-ration traversals was decreased (P<0.05),the expression of GABAR1 protein in frontal lobe was up-regulated (P<0.05),and the expression of NMDAR2B protein was down-regulated (P<0.05), and the amplitude was higher than that in group T1 (P<0.05).Conclusion Continuous inhalation of sevoflurane can reduce the spatial memory ability of aged rats,and the effect of prolonged inhalation is greater and longer.This effect is related to the expression of neurotransmitter receptors such as GABAR1 and NMDAR2B in the frontal lobe.
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Objective To investigate whether activation of the P2X7 receptor in the ventrolateral region of the midbrain periaqueductal gray (vlPAG) is involved in the analgesic mechanism of tramadol in rats with inflammation-induced pain.Methods One hundred and twelve male Sprague-Dawley (SD) rats were randomly divided into 7 groups (n=16 each):normal control (C group),normal saline group (NS group),formalin group (F group),formalin + low dose tramadol group (TL group),formalin +middle dose tramadol group (TM group),formalin + high tramadol dose group (TH group) and formalin +high dose tramadol + A-438079 group (TH+A-438079 group).The rat models of inflammatory pain were established by subcutaneous injection of 100 μL of 5％ formalin into the left thenar of the rats in F,TL,TM and TH groups.TL,TM and TH groups had an intrathecal injection of tramadol (5,15,25 μg/kg dissolved in 20 μL of normal saline,respectively) while F group had an intrathecal injection of equal amount of normal saline.A-438079 (100 pmol/0.3 μL),a selective P2X7 receptor antagonist,was microinjected into the vlPAG of the TH+A-438079 rats,and followed with the establishment of inflammatory pain rats which were then subjected to intrathecal injection of tramadol (25 μg/kg dissolved in 20 μL normal saline).The changes in pain behavior were observed for pain intensity scoring (PIS) at 5,10,15,25,35,40,50 and 60 min after formalin injection in each group.The number of P2X7 receptor positive cells and P2X7 protein expression levels in the vlPAG were detected by immunohistochemistry and Western blotting.Results (1) The PIS,the number of P2X7 receptor positive cells and the P2X7 receptor protein levels in the vlPAG in F group were significantly increased at all time points compared with C group (P＜0.05).(2) Compared with F group,the PIS scores in TM and TH groups were significantly decreased respectively at all time points from 25 and 15 min after formalin injection (P＜0.05);the expression and protein levels of P2X7 receptor in the vlPAG were further significantly up-regulated (P＜0.05).(3) Compared with TM group,the PIS scores in TH group were significantly decreased at all time points from 15 min after formalin injection (P＜0.05);the expression and protein levels of P2X7 receptor in the vlPAG were further significantly up-regulated (P＜0.05).(4) Compared with TH group,microinjection of P2X7 receptor antagonist A-438079 in the vlPAG in TH+A-438079 group significantly raised the PIS scores at all time points from 15 min after formalin injection (P＜0.05).Conclusion Intrathecal injection of tramadol may induce analgesic effect on inflammatory rats by promoting the expression of P2X7 receptor in vlPAG.
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Heart dominating mind is one of the main contents in the visceral manifestation theory of tradi-tional Chinese medicine ( TCM ) theory . This article summed up documents , clinical studies , basic experimental studies , and modern scientific researches to review the research results of the relationship between heart and emotion . The connotation of heart dominating mind theory in modern biology was interpreted . And the scien-tificity of TCM theory was explained .
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BACKGROUND:Cerebral ischemia often occurs in underlying pathological conditions, such as hypertension, hyperlipidemia and diabetes. Therefore, it is of great significance to construct a cerebral ischemia rat model with hyperlipidemia and to study the effect of basic pathological changes on the cerebral ischemia. OBJECTIVE:To observe the brain tissue pathological changes of rat models with coexistence of hyperlipidemia and cerebral ischemia, and the effect of hyperlipidmia on cerebral ischemia. METHODS:The rats were fed with high-fat diet to establish the hyperlipidmia models, and then focal cerebral ischemia models were prepared with suture method. At 3 and 7 days after modeling, the 2,3,5-triphenyltetrazolium chloride staining was used to observe the volume of brain tissue ischemia, and hematoxylin-eosin staining was performed to observe pathological change of the margin of the brain tissue ischemia zone. RESULTS AND CONCLUSION:2,3,5-Triphenyltetrazolium chloride staining staining results showed that the volume of cerebral ischemia was significantly reduced in the hyperlipidemia+cerebral ischemia 7 day group. Hematoxylin-eosin staining results showed there was typical ischemic changes in al the cerebral ischemia models, and the number of microglial cel s after cerebral ischemia for 7 days was significantly smal er than that after cerebral ischemia for 3 days, and the changes were more obvious in the hyperlipidemia+7-day cerebral ischemia group when compared with the hyperlipidemia+3-day cerebral ischemia group. Ultrastructure showed there were neuronal and glial nuclear membrane shrinkage in al the cerebral ischemia models, mitochondria cristae was disappeared completely, endothelial cel mitochondria was decreased, most of the synaptic vesicles of nerve synapse were dissolved;the damages above were improved after ischemia for 7 days, especial y hyperlipidemia+cerebral ischemia for 7 days, the neuronal degeneration and necrosis were reduced, the mitochondrial damage was repaired, the number of mitochondrial cristae was increased significantly, and the synaptic vesicles of nerve synapse were recovered significantly. The results indicate that hyperlipidemia can promote the recovery of cerebral ischemic injury, probably because the hyperlipidemia factors can activate the protection mechanism.
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Objective To investigate the protective effects of insulin like growth factor 1(IGF-1) on cortical neurons under condition of hypoxia and the possible mechanism. Methods Cerebral cortical neurons from newborn rats were cultured under the condition of oxygen and glucose deprivation (OGD) . On day 7, neurons were treated with IGF-1 or IGF-1 plus LY294002 or PD98059 under condition of OGD or normal condition. MTT assay was used to analyze the viability of neurons in each group. The expression of total Akt and p-Akt were analyzed by Western blot. Results Compared with the control, the neuron viability was significantly higher in IGF-1 treated group under normal or OGD condition (P＜0.05). The protective effects of IGF-1 were attenuated in the presence of LY294002 but not PD98059. The result of Western blot showed IGF-1 upregulated the expression of p-Akt, which was inhibited by LY294002. Conclusion PI3K pathway may play an important role in neuroprotection afforded by IGF-1.
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<p><b>OBJECTIVE</b>To investigate the influence of Dureping injection to the murinal celiac macrophage Ana-1 on TIR signal pathway.</p><p><b>METHOD</b>Ana-1 cell line was infected by influenza virus FM1 strain and treated with the Dureping injection in different concentrations (10.1 mg x L(-1) group) for 12 h and 24 h. Then we collected the cells, extracted mRNA and measured the expressions of TLR7, MyD88, IRAK4, TRAF6 and NF-kappaB p65 respectively by RT-PCR.</p><p><b>RESULT</b>Dureping injection down-regulated the expression of TLR7, MyD88, IRAK4, TRAF6 and NF-kappaB p65 mRNA in Ana-1 cell line infected by influenza virus, in a dose-dependent manner significantly.</p><p><b>CONCLUSION</b>Dureping injection has an obvious effect against influenza virus FM1 strain by regulating the TIR signal pathway.</p>
Subject(s)
Animals , Mice , Adaptor Proteins, Signal Transducing , Cells , Cells, Cultured , Epithelial Cells , Metabolism , Interleukin-1 Receptor-Associated Kinases , Genetics , Macrophages , Metabolism , Myeloid Differentiation Factor 88 , Genetics , Metabolism , NF-kappa B , Metabolism , RNA, Messenger , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Signal Transduction , TNF Receptor-Associated Factor 6 , Genetics , Metabolism , Transcription Factor RelA , Metabolism摘要
To establish an ischemia-reperfusion injury model of rat cerebral microvascular endothelial cells (MVECs) in vitro, and to explore the relationship between nuclear factor-kappa B (NF-kappaB) and the protective effects of Qingkailing effective components (hyocholic acid, taurocholic acid, baicalin, jasminoidin, Pinctada martensii) on MVECs.
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OBJECTIVE: Using the method of lactate dehydrogenase (LDH) assay, to observe the activities of rat cerebral microvascular endothelial cells (CMECs) intervened by Tongluo Jiunao Injection (TLJNI), a traditional Chinese compound drug removing toxin to dredge brain collaterals, and then further study the effects of different kinds of conditioned mediums (CMECs-CM) of cerebral microvascular endothelial cells on ischemia and ischemia/reperfusion cerebral cortex cells, and to probe into the drug pharmacological mechanisms of CMECs in modulating the neurons. METHODS: Three kinds of CMECs (normal, ischemic and ischemic/reperfusional) were all treated by TLJNI previously, and then the three pairs of CMECs-CM without serum were collected respectively for LDH assay. Rat cerebral cortex neurons were also primarily cultured and then divided into similar three groups (normal, ischemic and ischemic/reperfusional). The neuron responses caused by CMECs-CM at different concentrations were observed by using LDH transudation rate assay. RESULTS: The LDH release values of ischemic and ischemic/reperfusional CMECs with TLJNI treatment were obviously reduced (P<0.01) compared with the same kinds of CMECs untreated. For ischemic neurons, both conditioned medium of ischemic CMECs (Is-CM) and conditioned medium of ischemic CMECs with drug treatment (IsT-CM) in high concentration of 100% increased the LDH transudation rate (P<0.01), while in low concentration of 10%, IsT-CM reduced the transudation rate (P<0.05). For ischemia/reperfusion neurons, all kinds of CMECs-CM reduced the transudation rate respectively (P<0.05 or P<0.01). As far as each group concentration was concerned, 10% or 50% showed relatively stronger effects, and both conditioned medium of normal CMECs (N-CM) group and conditioned medium of ischemic/reperfusional CMECs (Rp-CM) group had statistical significance (P<0.05 or P<0.01). For normal neurons, all kinds of CMECs-CM increased the transudation rate respectively (P<0.05 or P<0.01). As far as each group concentration was concerned, only conditioned medium of normal CMECs (N-CM) had statistical significance (P<0.05 or P<0.01). CONCLUSION: The study shows that TLJNI is capable of preventing the damage of CMECs from both ischemia and ischemia/reperfusion states. Chinese drug can restrain the brain ischemia and ischemia/reperfusion damage by the media that CMECs modulate the neurons, demonstrating the pharmacological mechanisms of TLJNI. This work also indicates that there exist some active substances against ischemia/reperfusion injury secreted from CMECs-CM with TLJNI treatment.
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Objective To investigate the protective effect of Tanreqing injection on the mice infected with influenza virus FM 1 . Methods The experiment includes protection of Tanreqing injection to the mice infected with influenza virus FM1, and effect of Tanreqing injection to the viral titers, pathology and lung index of mice with influenza virus FM 1 . Results Tanreqing injection can reduce the mortality of the mice with influenza virus FM 1 infected. And Tanreqing injection can improve viral titers, pathology, and lung index of the mice infected with influenza virus FM1. Conclusions Tanreqing injection can protect the mice infected with influenza virus FM 1 by resisting the influenza virus and meliorating the lung pathology of the mice infected with influenza virus FM 1 .
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<p><b>OBJECTIVE</b>To investigate the effect of New Qingkailing injection (NQKLI) on cerebral edema following intracerebral hemorrhage (ICH) induced by collagenase VII in rats.</p><p><b>METHODS</b>After being established into ICH model by collagenase VII, rats were treated with NQKLI by intraperitoneal injection. Forty-eight hrs later, brain contents of water was detected with wet and dry method, calcium content in brain was detected by atomic spectrophotometer, tumor necrosis factor-alpha (TNF-alpha) in brain tissue was determined by liquid competitive ibhibitory immunoassay, and serum matrix metalloproteinase-9 (MMP-9) were detected with enzyme-linked immunosorbent assay (ELISA) respectively.</p><p><b>RESULTS</b>NQKLI reduced the contents of water, calcium and TNF-alpha content of brain tissue and serum MMP-9 in rats with ICH.</p><p><b>CONCLUSION</b>NQKLI could alleviate both vasogenic and cytotoxic cerebral edema by prohibiting calcium over-load, protecting basilar membrane and eliminating inflammation.</p>
Subject(s)
Animals , Male , Rats , Brain Edema , Metabolism , Therapeutics , Cerebral Hemorrhage , Collagenases , Drugs, Chinese Herbal , Injections , Matrix Metalloproteinase 9 , Blood , Neuroprotective Agents , Phytotherapy , Random Allocation , Rats, Wistar , Tumor Necrosis Factor-alpha , Metabolism摘要
Objective: To observe the effect of Tongluo Jiunao oral solution on learning and memory and the expression of AChE in hippocampus of AD rats induced by ?-amyloid1-40.Methods: 140 SD rats were divided into blank control group(normal group),pseudo-operation control group,negtive control group(model group),positive control group and experiment group(48、24、12mg?kg-1?d-1)at random.The model of AD were established by injecting ?-amyloid1-40 into bilateral hippocampus.After 4 weeks,Morris Water Maze was used to determine the ability of learning and memory.Immunohistochemical method and image analysis techniques were used to determine the expression of AChE in Hippocampus.Results: Compared with normal group,in place navigation test,the mean escape latencies of the model group increased obviously,and in spatial probe test,the frequency of passing through the platform of the model group decreased obviously(P
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Objective: To observe the effects of new Qingkailing injection on the toxic substances accumulation post-hematencephalon.Methods: Using VII-type collagenase inducing rat hematencephalon,the contents of TNF-?,IL-1? and sICAM-1 of brain homogenate were detected by ELISA;the contents of SOD and MDA were determined separately by xanthine oxidase method and thio-barbituric acid method; brain water content was detected by dry-wet weight method;serum NSE content was determined by liquid phase competition method.Results: Inflammatory reaction was fierce 48 h after hematencephalon in rat,and that new Qingkailing injection could effectually lower the contents of the inflammatory factors,MDA,brain water content and NSE,and could heighten the content of SOD.Conclusion: New Qingkailing injection has favorable heat-clearing and detoxicating effects on the pathologic state of flourishing toxic heat post-hematencephalon.
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Objective: To study the influence of conditioned medium of rat brain microvascular endothelial cells on the activity of cortical neurons and the protective effect of Tong Luo Jiu Nao Injection.Methods: We collected the conditioned media from 4 different cultured endothelial cell groups,which were normal endothelial cells,the normal ones and treated with Tong Luo Jiu Nao Injection,the injured ones damaged by simulated cerebral ischemia,as well as the injured ones and treated with Tong Luo Jiu Nao Injection,respectively(N-CM,NT-CM,I-CM,IT-CM).Then,the conditioned medium was added into the cultures of the normal neurons and the damage ones which are injured by simulated cerebral ischemia as well,respectively.The effect of each type of conditioned medium on the activities of neurons was determined through the measurement of MTT and the transduction rate of LDH.Results:(1) N-CM has no obvious effect on the normal neurons,but does show some protective effect on the injured ones by increasing its activity significantly;(2) I-CM could decrease the activity of the normal neurons as well as aggravate the damage on the injured ones,while this injury effect can be reversed remarkably by IT-CM.Conclusion: The paracrine secretion of the brain microvascular endothelial cells might be one of the vital mechanisms in cerebral ischemic injury,indicating that the brain microvascular endothelial cells could be the therapeutic targets of Chinese medicine,which are not able to permeate through the Blood-Brain Barrier.
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Objective: To observe the protective effects of Gastrodine on the cultivated rat brain microvessel endothelial cells damage by mimic cerebral ischemia.Methods: The endothelial cells activity,survival rate,the change in NO content,and the effects of Gastrodine were observed in the cultivated rat brain microvessel endothelial cells(BMEC) damaged by mimic cerebral ischemia.Results: The activity and survival rate of BMEC in the ischemia groups are obviously lower than that in the normal groups;compared with the normal groups,the activity,survival rate and NO content of BMEC in the Gastrodin groups have the increasing tendency;comparing to the ischemia groups,the activity of BMEC in the Gastrodin groups obviously increasing(P
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Objective: To observe the expression of cell adhesion molecules ICAM-1 and VCAM-1of cultured rat brain microvascular endothelial cells(MVEC),expecting to explore the mechanisms of new QingKaiLing injection protecting brain from injury of inflammatory cascade in cerebral ischemia diseases.Methods: Rat cerebral MVEC were extracted by separating microvessel sections and collagenase enzymatic digesting,an in vitro ischemia reperfusion model was established(Kreb,95%N2+5%CO2),the protein and mRNA expression of ICAM-1 and VCAM-1 were detected by using immunocytochemical stain and RT-PCR method.Results:The expression of adhesion molecules of model group were significantly higher than those of noral group(P
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Objective: To investigate the mechanism of Glytan lowering portal pressure induced by biliary liver fibrosis. Methods: SD male rats, 240-260g weight around, were randomly divided into sham-operation group, model group, propranolol group, Glytan high-dose, middle-dose and low-dose group according to the weight. Portal hypertension was induced by common bile duct ligation in rats. After two and four weeks, measured the portal pressure(PP) of each group, observed the histological changes of liver by HE staining, tested liver function and the concentration of endothelin-1 in systemic circulation and mesenteric circulation radioimmnuoassay. Results: After two and four weeks, portal pressure of model group rats increased significantly. Both Glytan and propranolol can decrease PP after two and four weeks, and the pressure-relief effect was similar between the two drugs. HE staining showed that Glytan can significantly inhibit the formation of collagen, promote the recovery of liver tissue structure; liver function indicated a significant decrease in serum AST, ALT, TBIL and Na+ concentration. In addition, Glytan decreased the concentration of endothelin -1 in systemic circulation, increased it in mesenteric circulation after two weeks. Conclusion: Glytan decrease PP by improving liver function and microcirculation, inhibiting collagen formation and water-sodium retention after long-term therapy, ameliorating hyperdynamic circulation at the early stage.
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Objective:To survey the effect of the Dureping Injection on the kinetic change of nitrous oxide(NO) in macrophage infected by the influenza virus FM1 strain.Methods:The murinal celiac macrophage(Ana-1) was infected by the virus,add the different concentration of the drug in the supernatant of the macrophage for 6 h,12 h,24 h and 36 h.The level of the NO in the supernatant was measured by the method of traditional Griess.Ana-1 cell line was infected by influenza virus FM1 strain,then treated with Dureping Injection 1 ?g/ml for 24 h.The cells were then collected,mRNA was extracted and the expression of NF-?B p65 was measured by RT-PCR;The nuclear protein was extracted and the expression of NF-?B p65 measured by Western blot.Results:60 ?g/ml,30 ?g/ml,10 ?g/ml and 1 ?g/ml group of Dureping Injection down-regulated amount of NO secreted by the Ana-1 cells infected by virus,and it was showed in dose relationship significantly;1 ?g/ml group of Dureping Injection down-regulated the expression of the NF-?B p65 mRNA and protein.Conclusion:Dureping Injection has an obvious effect against influenza virus FM1 strain by depressing the activity of NF-?B,which prevents the production of NO secreted by Ana-1 cells infected by the virus.