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Hypoxia-ischemia induces an inflammatory and immune response in the nervous system that may be important for development of brain injury. Recent data implicate that cytokines, chemokines, adhesion molecules，are involved in the recruitment of inflammatory-immune cells. A cytokines which promote emigration of leukocytes from the vascular lumen into the injured brain tissue are produced at the site of incipient cerebral infarction. The expression of mRNA for alpha- and beta-chemokines preceded the appearance of immune cells suggesting that these molecules may have a role in the inflammatory response to insults. The humoral and cell-medated immunity under the conditions of focal brain ischemia was discussed. These results together indicate that cell-cell interaction by adhesion molecules and cytokines is an important component in the pathogenesis of ischemic cerebral diseases, especially at the acute phase.Recently accumulated data show that depleting the amount of circulating leukocytes or administering anti-inflammatory chemicals such as cytokine blocking agents, anti-adhesion molecule antibodies, and immunosuppressants effectively minimize the size of ischemia induced cerebral infarction.
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OBJECTIVE:To observe the protective effect of total flavone of Abelmoschl Manihot L medic(TFA)on acute myocardial ischemic and anoxic injury in mice.METHODS:Acute myocardial ischemic model induced by subcutaneous injection of Isoproterenol was adopted to observe the effects of TFA on the abnormal ST segment in lead II and T wave on ECG,my?ocardial water content(MWC)and myocardial index(MI);Moreover the effect of TFA on myocardial anoxic tolerance was ob?served in trachea clamping mice.RESULTS:TFA could remarkably ameliorate the abnormal changes of ECG and significantly inhibit the increase of MWC and MI of model group.It was found that the ECG lasting time was much longer in the groups pretreated with TFA.CONCLUSION:TFA plays a protective role in myocardial ischemia and anoxic injury in mice.
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AIM To investigate the effect of paclitaxel and cisplatin on apoptosis of MCF 7 and its mechanism. METHODS The apoptotic cells were detected by TUNEL method and the expression of Bcl 2 and bax were examined using immunohistochemistry S P method in different time. RESULTS Cisplatin resulted in the death of MCF 7, but did not cause the apoptois of MCF 7. Paclitaxel caused time dependent and concentration dependent increases in the apoptotic cells. Treatment of MCF 7 cells with paclitaxel resulted in time and concentration dependent decreases in bcl 2 and increased in bax proteins. CONCLUSION The apoptosis induced by paclitaxel is related to the increase of bax protein and the decrease of bcl 2 protein.
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Aim To observe the protective effect and possible mechanisms of Total Flavone of Abelmoschus Manihot L medic(TFA) on myocardial reperfusion injury in rabbits,when it was given as a preconditioning inducer.Method Different doses of TFA were perfused intravenously lasting for 5 min,followed by a 10 min break before 30 min ischemia and 60 min reperfusion in rabbits.Using this preconditioning method,we observed the histo-pathological changes of myocardium,the content of MDA,the activities of SOD and GSH-PX in plasma,and also,the expression of ICAM-1 in myocardium.Results TFA(16,8 and 4 mg?kg~(-1)) significantly ameliorated myocardium ischemical reperfusion injury.The activities of SOD and GSH-PX in plasma were enhanced,while the MDA level was decreased.Meanwhile,the expression of ICAM-1 mRNA in myocardium was down-regulated.Conclusion Pharmacological preconditioning of TFA could protects myocardial ischemic reperfusion injury in rabbits by inhibiting lipid peroxidation and myocardium inflammatory reaction.
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Aim To study the antidepressant effects of bioactive compounds from entomogenous fungi(BCEF) in mouse models of depression. Methods The antidepressant effects of Bioactive compounds from entomogenous fungi was examined on the chronic unpredictable stress test, yohimbine induced lethality test, and 5-HTP induced head-twitches test. Results BCEF(50 mg?kg~-1 , ig, qd?21 d)could significantly increase the crossing and rearing score in open-field test. After administration yohimbine 1 h, BCEF 100 mg?kg~-1 group mice mortality rate rising rapidly; BCEF(50,100 mg?kg~-1 ) could distinctly increase the head-twitch number in the 5-HTP induced head-twitches test. Conclusion BCEF has antidepressant effects in depression mouse models. The mechanisms of its antidepressant effects may be related with the reinforcement of central monoamine neurotransmitter especially to 5-HT and NE nerves system.
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AIM To observe the protective effect of total flavone of Abelmoschl Manihot L medic(TFA) on myocardial ischemia reperfusion injury(IRI) in the rat heart in vitro. METHODS We adopted the method of in vivo perfusion set up by Langendorff to observe the changes of some markers, such as MDA,SOD,CPK,LDH,etc in the myocardial homogenate in the rat heart following ischemia and reperfusion. RESULTS TFA( 100,50,25 mg?L -1) can significantly reduce the lipid peroxidation product malondialdehyde(MDA), increase the activity of myocardium superoxide dismutase(SOD), decrease the transudation of creatine phosphokinase(CPK) and lactate dehydrogenase (LDH) from cardiomyocyte. And also, TFA caused an improvement of nitric oxide (NO) and its synthase, NOS. CONCLUSION TFA play a protective role on myocardial reperfusion injury in the rat in vitro via inhibition of lipid peroxidation, enhancement of anti-oxidation and relaxing of coronary artery.
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The studies on pharmacoki-netics of Quercetin in rabbits were carried out by UV-spectrophotometry. The experimental results were shown that after 10mg ? kg-1 of Quercetin iv administration in rabbits, the curve of plasma concentration - time was shown to fit an open two compartment model. The pharmacokinetic parameters were as follow:T1/2 (?) = 2. 91 ? 1. 36min,T1/2(?) = 183. 78?82. 67min,Vd=0. 624?0. 225L ???kg-1,CL = 3. 15 ?2. llml ? kg-1 ? min-1. The bioavailability (F) of Quercetin after 10mg ? kg-1 ig in rabbits was 42.7% and Cpk was 10. 9mg ? L, tpk was 60min.After 10mg ? kg-1 iv administration in rabbits,Quercetin was rapidly eliminated from the blood. The compound and its metabolites were exereten by kidney and bile.
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After icv administration, the analgesic action of Hyp was found on the tail-flick and hot-plate tests. The analgesic action potency of icv Hyp was approximately equal to 1 ~20 of morphine and was about 100 times as potent as sc administration. No effect was seen on the analgesic action of Hyp after ip naloxone, the analgesic action of Hyp was no concern of L-enkephalin contents in discrete regions of rat brain either. But icv EGTA markedly enhanced while icv CaCl2 antagonized the analgesic action of Hyp. It was also found that calcium ion content in mice brain markedly reduced when the analgesic action of Hyp appeared. These results suggest that Hyp have significant central analgesic action and the central analgesic action of Hyp may relate to reducing of calcium ion in brain.
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AIM To study the inhibitory effect of bioactive compounds from entomogenous fungi(BCEF0083) on monoamine oxidase. METHODS Spectrofluorometer was used to detect the activity of MAO in mouse and rat brain mitochondria; Dose effect and time effect relationship of BCEF in inhibition of MAO were studied in vivo and in vitro in mice and rats; Method of Lineweaver Burk was used to assay the Km of MAO. RESULTS The antagoning action of BCEF0083 on MAO( BCEF 500 mg?kg -1 , 0 5, 1, 2, 4, 8, 16, 24, 48, 72 h after ig; 500, 400, 200, 100, 50, 25 mg?kg -1 , 2 h after ig)showed some extent of dose effect and time effect relationship. BCEF0083 in vitro inhibited the activity of MAO A,B in a dose dependent manner with IC 50 (95% of confidence limits)of 128 88(82 70～200 86),184 14(156 17～217 11) ?g?ml -1 in rats. The antagonism type of BCEF0083 on MAOA, B were both mixed type, their Km were 11 97, 8 13 ?mol?L -1 . CONCLUSION The results suggest that BCEF0083 could obviously inhibite the activity of MAO on brain remitochondria in mice and rats.
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AIM To investigate actions of total paeony glycoside(TPG) on learning and memory capacity and related products of metabolism of senile mice induced by D galactose. METHODS The subacute senile mouse models induced by injection of D galactose subcutaneously were used. RESULTS TPG could improve the learning and memory capacity of model mice in shuttle test and enhance spatial resolution in water maze test. TPG not only reduced the content of monoamine oxidase(MAO) and inhibited the decrease of cholinesterase(CHE) significantly, but also lessened the level of malondialdehyde(MDA) and inhibited the decrease of superoxide dismutase(SOD) in cerebrum of model mice. TPG still promoted the recovery of lobar atrophy and hypoimmunity of senile mice remarkedly. CONCLUSION TPG possesses obvious effects of improvement on learning, spatial resolution and delaying senility.
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AIM To study the protective and mechanism of Tfa (total flavone of the flowers of Abelmoschl Manihot L. Medic). METHODS The rats were injected Iso and then the T wave movement value observed. The rats anterior descenging bracnch of left artery were occluded for 48 hours the results of CPK, LDH and disscoate fatty acid of serum and infarct area of myocardium observed. RESULTS Tfa 100,200 mg?kg -1 ,ip depressed the T wave rise by injection of Iso in rats. Tfa 100 mg?kg -1 ?d -1 ?3,ip inhibited the serum CPK and LDH disscoate fatty acid in myocardium induced by coronary artery occluded in rats;also markedly depressed the infarct area in myocardial infarct rats. Tfa 0 03 mg?kg -1 ?d -1 ?3,ip obviously reduced the MDA contents,increased SOD and GSHPx activities in the mitochondria in mice. CONCLUSION Tfa shows a protective effect against myocardial injury. The mechanism may be via against oxygen free radicals and lipid peroxidation,also stabilize the mitochondria function.
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Following ageing, memory and learning attenuate apparently. Mechanisms responsible for the aging related memory and learning deficit may involve in synaptic morphology and fanction deterioration in hippocampas, changes of central neurotransmitter systems、 brain intracellular calcium ions concentration、 gene expression and neurotrophasthemic etc. The mechanisms of aging related attenuation in memory and learning is summarized.
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AIM To study the antidepressant effects of bioactivecompounds from entomogenous fungi(BCEF) in mice models of depression. METHODS The antidepressant effects of Bioactive compounds from entomogenous fungi were examined in the learned helplessness model( forced swimming mice, tail suspension mice) and chronic unpredictable stress mice models. Spectrofluorometer and UV spectrophotometer were used to detect the activity of MAO, central monoamine neurotransmitter in mice brain mitochondria. RESULTS BCEF0083 25,50,100 mg?kg -1 could obviously shorten the immobility time in forced swimming mice, tail suspension mice and showed some extent of dose-effect relationship. BCEF0083 25,50,100 mg?kg -1 could obviously inhibite the activity of MAO-A,B on brain remitochondria in chronic unpredictable stress mice models and could rise the content of NE,5-HT,5-HIAA,DA in defferent degree. CONCLUSION The results suggested that BCEF0083 had antidepressant effects in mice depression models. The mechanisms of BCEF0083 antidepressant effects may be related with the inhibition of MAO-A,B activity and the increased content of central monoamine neurotransmitter.
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AIM To study the inhibitory effect of nimodipine on apoptosis induced by cerebral ischemia. METHODS Incomplete cerebral ischemia was made by ligating bilateral common carotid arteries(CCA) in rats. The apoptosis was determined by terminal deoxy-nucleotidyl transforase-mediated dUTP-digoxigenin nick end-labeling(Tunel) method. The DNA fragmentation analysis was measured with the diphenylamine reagent method. RESULTS Ligting of bilateral CCA markedly produced apoptotic cell in cerebral cortex. Nim 2 mg?kg -1 significantly decreased the numbers of apoptotic cells in cortex; Nim 1 mg?kg -1 , 2 mg?kg -1 also inhibited the increase of DNA fragmentation induced by cerebral ischemia. CONCLUSION Nim has inhibitory effect on ischemia-induced apoptosis of cerebral cortex.