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Objective To investigate the Expression of interleukin-18(IL-18)and cyclooxygenase2(COX-2)in endometriosis.Methods Enzyme linked immunosorbent assay and innunohistochemistry were used to detrermine the levels of interleukin-18 in peritoneal fluid and serum,the expression difference of cyclooxygenase2 in ectopic endometrium with endometriosis and the normal control.Results The levels of interleukin-18 in peritoneal fluid and serum were higher than that of normal control,the expression of cyclooxygenase2 in ectopic endometrium with endometriosis were higher than that of normal control,and the degree in stage of Ⅲ、Ⅳ were higher than those in stage of Ⅰ、Ⅱ.Conclusions IL-18 and COX-2 is related to the endometriosis,the further studying of IL-18 and COX-2 may be helpful in the diagnosis and treatment of this disease.
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AIM: To investigate the protective effects of total of flavone C (TFC) on acute cerebral ischemia in mice and focal cerebral ischemia in rats. METHODS: The occlusion of bilateral common carotid arteries with vagus nerves in mice was used for make the acute cerebral ischemia models. The survival time and the death rate were observed. The permanent occlusion of the proximal of the right middle cerebral artery (MCA) was used for make the focal cerebral ischemia models. The extent of neurological deficits was observed, and the infarct area was measured by NBT staining technique. The activity of LDH and the content of MDA and NO in the ischemic cerebral cortex were determined. RESULTS: TFC of 80 and 40 mg?kg -1 prolonged the survival time and decreased the death rate of mice with acute cerebral ischemia injury. TFC of 60, 30, and 15 mg?kg -1 ameliorated neurologic deficits score and the infarct size of rats with MCAO. CONCLUSION: TFC provides significant protective effects against cerebral ischemia injury.
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Aim To study protective effects of Total of flacone C(TFC) against cerebral ischemia-reperfusion injury.Methods Four-vessel occlusion method was used to make acute cerebral ischemia-reperfusion model. Rats were initiated by ischemia for 30 min followed by 40 min of reperfusion.The electroencephalography(EEG) during cerebral ischemia and reperfusion was recorded.The level of intracellular calcium ion concentration([Ca~(2+)]i) in cerebral cells after ischemia was measured by using a Ca~(2+) indicator Fura-2/AM.Superoxide dismutase(SOD),Glutathione peroxidase(GSH-Px),Lactate dehydrogenase(LDH),nitric oxide Synthase(NOS) activeties and Malondialdehyde(MDA),Nitric Oxide(NO)contents in the ischemia cerebral cortex were measured.Results TFC can improved the EEG change,significantly attenuated the decrease of the intracellular calcium ion concentration([Ca~(2+)]_i), remarkly increased GSH-Px,SOD and NOS activities in the cerebrum,inhibit the decrease of LDH activity and NO,MDA contents.Conclusion TFC has protective effects on cerebral ischemia-reperfusion injury,the mechanism may be related to attenuating free radical,[Ca~(2+)]i overload and NO.
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Objective To observe the protective effect of total flavone of Camellia (TFC)against cerebral ischemic injury.Methods Decapitation method and close hypoxia method were used to observe the effect of TFC on anoxic tolerance of mice and step down test was used to observe the effect of TFC on learning and memory; after ischemia, the content of malondialdehyde (MDA)and nitric oxide (NO)and the activity of lactate dehydrogenase (LDH)were detected. Rat models with acute incompletely cerebral ischemia were established by means of ligating right common carotid arteries and effect of TFC on cerebral water volume, permeability of cerebral vessels and cerebral histopathological changes were also observed.Results TFC prolonged the grasping time after decapitation and the survival time after anoxia in mice, and improve the learning and memory during the step down test. TFC decreased MDA and NO contents, counteracted the de creases of LDH activities in the mice cerebral cortex, reduced the water volume and permeability of cerebral vessels in ischemic rats and improve the cerebral hitstopathological changes. Conclusion TFC has protective effects against cerebral ischemic injury and the mechanism may be related to the inhibition of free radicals and NO production.