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AIM: To investigate the effects of auricularia auricular polysaccharide (AAP) on chronic cerebral ischemia injury in rats. METHODS: The chronic cerebral ischemia mode1 was made by permanent middle cerebral artery occlusion (MCAO) on the right side. AAP at different doses (50 mg/kg and 100 mg/kg) was intragastrically administered at the onset of ischemia and in the following days after operation, once a day for 4 weeks. After 4 weeks of MCAO, Morris water maze test was introduced to examine the learning and memory functions. Nissl staining was performed to detect the survival neurons in hippocampal slices. Level of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in brain tissue were measured. RESULTS: Rats treated with AAP showed a shorter escaping latency in spacial navigation test because the AAP treated rats spent less time to find the platform in spatial probe test. More survival neurons in hippocampal slices were observed from AAP treated rats. Also, the MDA level in brain tissue was reduced and SOD activity in brain tissue was increased in the AAP treated rats with MCAO. CONCLUSION: AAP protects rats from chronic brain ischemic injury, in which its anti-oxidative effect might be involved.
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AIM: To investigate the protective effect of auricularia auricular polysaccharide (AAP) on the myocardial injury induced by ischemia and its underlying mechanism. METHODS:AAP was orally administrated to rats at the does of 50, 100 or 200 mg·kg~(-1)·d~(-1) for 20 d. Myocardial injury was induced in anesthetized Sprague - Dawley rats by left anterior descending coronary artery ligation. Myocardial infarct size, the level of lactate dehydrogenase (LDH), the activity of superoxide dismutase (SOD) , the production of lipid peroxidation malondialdehyde (MDA) and protein level of myocardial collagen of the heart were measured. RESULTS: The average myocardial infarct size in AAP groups was significantly smaller than that in ischemia group. The level of serum LDH induced by regional myocardial ischemia was significantly decreased in AAP group compared to ischemia group ( P < 0.01). AAP inhibited the production of MDA and increased the activity of SOD. Furthermore, AAP reduced the protein level of myocardial collagen after ischemia (P < 0.01).CONCLUSION: AAP prevents myocardium from ischemia injury as an antioxidant.
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AIM: We examined the effect of interleukin- 2 (IL-2) on calcium handlin g of rat cardiomyocytes. METHODS: The effects of steady state an d transient chan ges in stimulus frequency on the intracellular calcium transient were investigat ed in the isolated ventricular myocytes with spectrofluorometry technique. RESULTS: Under the steady state (0.2 Hz), IL-2 at 2?10 5 U/L decr eased the peak [Ca 2+ ] i and amplitude of the [Ca 2+ ] i transient, increas ed the diastolic calcium level, and prolonged the decay of the calcium transient . At 1.25 mmol/L of extracellular [Ca 2+ ], when increasing the stimulus frequency from 0.2 to 1.0 Hz, diastolic calcium level and peak [Ca 2+ ] i as well as the amplitude of the transient were inc reased. The positive frequency relationship was blunted in the IL-2-treated myoc ytes and this was not normalized by increasing extracellular [Ca 2+ ] t o 2.5 mmol/L . The caffeine induced Ca 2+ release was increased with increase in stimu lus freq uency. IL-2 inhibited the frequency relationship of caffeine induced Ca 2+ releas e. The restitution was not different between control and IL-2 groups at the 1.25 mmol/L of extracellular [Ca 2+ ], which was slowed in IL-2-treated myo cytes when t he extracellular [Ca 2+ ] was increased to 2.5 mmol/L. CONCLUSIO NS: It is concluded that the blunted frequency response of IL-2-treated myocytes was resulted from the decrease in SR Ca 2+ release, which was related to depression of SR funct ion. Despite the evidence of depressed SR Ca 2+ uptake, the restitution o f ca lcium transient at 1.25 mmol/L of extracellular [Ca 2+ ] remains uncha nged, which maybe due to the increase in the Na +/Ca 2+ exchanger activi ty.
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AIM: To investigate the effect of interleukin-2 (IL-2) on the intracellular calcium in electrically stimulated adult rat ventricular myocytes during anoxia and reoxygenation. METHODS: The isolated cardiac ventricular myocytes were exposed to 5 min anoxia followed by 10 min reoxygenation. Chemical anoxia was introduced by Krebs-Henseleit (K-H) solution containing 10 -3 mol/L sodium dithionite. The spectrofluorometric method was used to verify intracellular calcium transient with fura-2/AM as calcium fluorescence probe. RESULTS: It was shown that during anoxia, the amplitude of Ca 2+ transient was decreased, diastolic [Ca 2+ ] i, time to peak and time to relaxation of Ca 2+ transient were increased. All the parameters were got back but did not returned to the pre-anoxia level during reoxygenation. IL-2 at 2?10 5 U/L administrated during anoxia aggravated the effect of rexoxygenation on [Ca 2+ ] i transient. Pretreatment with a specific ? opioid antagonist, nor-BNI (10 -8 mol/L), abolished the effect induced by IL-2 during anoxia on the [Ca 2+ ] i transients, whereas specific ? opioid antagonist, naltrindole (10 -6 mol/L), did not cancel the effect. CONCLUSION: It is concluded that administration of IL-2 during anoxia aggravated the effect of reoxygenation on the [Ca 2+ ] i transients of isolated ventricular myocytes, which was mediated by cardiac ? opioid receptor pathway.
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AIM: To investigate the effect of Dendranthema morifolium (Ramat) Tzvel (DM) on isolated rat heart and ventricular myocytes during ischemia/anoxia and reperfusion/reoxygenation.METHODS: The Langendorff perfused rat hearts were used to measure intraventricular pressure and coronary flow. The cell contraction and intracellular calcium transient in enzymatically isolated ventricular myocytes were determined. RESULTS: (1) DM (0.5 g/L) significantly attenuated the inhibitory effects induced by ischemia/reperfusion on left ventricular developed pressure (LVDP), ?dp/dt max, coronary flow and LVDP?HR, meanwhile increased the content of SOD and decreased the content of MDA in the myocardium; (2) DM (0.5 g/L) attenuated the inhibitory effects of anoxia and reoxygenation on [Ca 2+]i transient and cell contraction in isolated ventricular myocytes. CONCLUSION: DM attenuated the effects on contractility and intracellular calcium induced by ischemia/anoxia and reperfusion/reoxygenation in the isolated rat heart and the ventricular myocytes. The mechanism might be related to increase in SOD activity and maintaining [Ca 2+]i homeostasis.
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AIM: To study the effect of salvia miltiorrhiza (SM) on cell contraction and intracellular calcium of enzymatically isolated rat ventricular myocytes during normoxia and anoxia/reoxygenation. METHODS: Contraction and intracellular calcium were determined with video tracking system and spectrofluorometric method, and the chemical anoxic method was employed. RESULTS: The ?d L /d t max , dL of cell contraction and the amplitude of [Ca 2+ ] i in the cardiomyocytes following SM treatment were decreased in a dose-dependent manner. During anoxia, the ?d L /d t max , dL and amplitude of [Ca 2+ ] i were decreased, while the diastolic Ca 2+ level was elevated compared with control group. All the contractile parameters and the diastolic Ca 2+ level were back toward pretreatment values during reoxygenation, but could not return to control level. After the treatment with SM (3 g/L), ?d L /d t max and dL of cell contraction and the amplitude of [Ca 2+ ] i were higher and the diastolic Ca 2+ level was lower than those in anoxia/reoxygenation group. CONCLUSION: SM antagonized effects of anoxia and reoxygenation on cell contraction and intracellular calcium in isolated ventricular myocytes.