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Objective To investigate the dynamic expression of the drug resistance protein P-glycoprotein (P-gp) within 72 hours in the pentylenetetrazol (PTZ)-induced status epilepticus (SE) model, and to identify the optimal detection time to inhibit P-gp. Methods mRNA and protein expressions of P-gp in rats hippocampal tissue were detected by using immunohistochemistry , RT-qPCR and Western blot at different time points after modeling (0, 3, 6, 12, 24, 48, 72 h). Results The mean density of P-gp protein in the hippocampus of status epilepticus model was 0.325 1 ± 0.008 2 at 24 h, and was 0.396 3 ± 0.016 8 at 48 h, which were consistently higher than those of the control group (P < 0.05, P < 0.01, respectively). Results of qRT-PCR showed that MDR1a expression was significantly upregulated at 24 h and at 48 h (P < 0.05, P < 0.01, respectively). Western blot assay revealed that P-gp protein was also significantly increased at 48 h after seizures (P < 0.05). Conclusions The upregulation of P-gp after SE peaked at 48 h, which maybe the optimal detection time to detect drug resistant after SE.
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AIM: To investigate the role of NF-κB in diabetic neuropathy.METHODS: The diabetic rats were induced by intraperitoneal injection of streptozocin ( STZ) .The pain behavior test was used to detect the mechanical and thermal withdraw threshold of the rats’ bilateral hind paws.The protein levels of p-NF-κB and t-NF-κB in the rats’ L4 and L5 dorsal root ganglions ( DRG) were determined by Western blotting.The expression of Nav1.7 in DRG of diabetic neuropathy rats with or without NF-κB inhibitor PDTC was detected by the method of immunohistochemistry.RESULTS:The mechanical and thermal withdraw threshold of bilateral hind paws in the diabetic rats was decreased from 4 weeks to 12 weeks after injection of STZ.The protein levels of p-NF-κB in L4 and L5 DRG were significantly increased in the rats with diabetic neuropathy.Intrathecal administration of NF-κB inhibitor PDTC attenuated the increase in p-NF-κB and Nav1.7 in L4 and L5 DRG.Pain behaviors were also alleviated by PDTC.CONCLUSION:The increase in p-NF-κB is closely rela-ted to the generation of diabetic neuropathy.Inhibition of NF-κB blocks pain behaviors and the over-expression of Nav1.7 in DRG.
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AIM: To investigate the anti-apoptotic effect of nerve growth factor (NGF) on PC12 cells and to observe the mechanism of signal transduction of JNK pathway. METHODS: PC12 cells were treated with 6-hydroxydopamine (6-OHDA) to induce cell apoptosis. NGF and SP600125, the c-Jun N-terminal kinase inhibitors, were added respectively in order to study the relationship between the activity of c-Jun N-terminal kinase and apoptosis of PC12 cells. The cells were divided into control group, 6- OHDA group, NGF group, 6-OHDA plus NGF group, NGF plus SP600125 group. The apoptotic rates of PC12 cells with different treatments were detected by flow cytometry and activities of JNK in PC12 cells were determined by Western blotting. RESULTS: 6-OHDA increased the apoptotic rate and activity of JNK1 in PC12 cells. Incubation with SP600125 or NGF for 15 min before adding 6-OHDA decreased the apoptotic rate of PC12 cells and activity of JNK1 in PC12 cells.CONCLUSION: Activity of JNK is involved in the pro-apoptotic effect of 6-OHDA on PC12 cells. Anti-apoptotic effect of NGF on PC12 cells affected by 6-OHDA is related to the decrease in the activity of JNK1.
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AIM: To probe into the anti-epilepsy action of artificial Calculus Bovis,by observing its effect on the behavioral of the experimental epileptic rats,neuron loss in the hippocampus and hilus,and GAD positive cell alteration in the hippocampus.METHODS: SD rats were divided into three groups: group A(artificial Calculus Bovis treatment group);group B(acute epilepsy group) and group C(control group).A model of acute epilepsy rats was established by PTZ.The rat's behavioral alteration was observed by the Racine' scale.The neurons in the hippocampus and hilus were calculated by Nissl staining.The GAD positive cells were observed by immunohistochemical staining.RESULTS: The latency of the first seizure in group A was longer than that in group B,while the seizure times in group A was less than that in group B.Besides,in group A,both the neuron loss amount in the hippocampus and hilus and the GAD positive cell loss amount in the hippocampus were less than those in group B.CONCLUSION: The artificial Calculus Bovis prolonged the latency of the first seizure time,decreased the frequency of seizure,and prevented the neuron loss and protected the GAD positive cells.
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When the fever was induced by leukocytic pyrogen(LP)on rabbits, we observed the effects of acupuncture on the main point of "Du Channel". At the same time measured the changes of cAMP and cGMP levels in CSF of the animals.It was found that cAMP levels increased (cAMP levels of normal group 18.60?1.56 pmol/ml and experimental group 25.30?1.14pmol/ml,P
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The purpose of this study was to investigate the effects of gypsum on LP-induced fever and the CSF levels of cAMP and cGMP in rabbits. It was found that gypsum could inhibit the rise of body temperature caused by LP injection, (△T of gypsum +LP group is 0.40?0.08℃, TRI_3 2.55; LP group 0.91?0.06℃, TRI_3 4.99 P
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This paper showed that levels of cAMP, PGE_2 in plasma and cAMP in spleen tissue and abdominal cavity macrophages in burned rats are increased (cAMP levels in plasma of the control groups were 24.65?4.59pmol/ml; PGE_2 levels were 309.38?77.64Pg/ml. cAMP levels in plasma of burned groups were 36.58?2.74pmol/ml: PGE_2 levels were 937.50+102.91Pg/ml; P
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In order to determine whether the cAMP is a central madiator and participates in the mechanism of the ET-induced fever, in the following experiments, we have compared the cAMP levels in csf, plasma to the cAMP levels in tissues of hypothalamus, brain-stem and brain-cortex during the ET-induced fever. The results obtained demonstrate: the cAMP Ievels in tissues of hypothalamus and in csf are increased markedly during the fever Compared with the normal control. These changes of the cAMP levels are paralleled and correlated apparently with the body temperature. However, there isn't any obvious change of the cAMP levels in the tissues of brain-stem, brain-cortex and in plasma during the fever. This demonstrats that the cAMP increased in csf may indirectly reflect cAMP level in hypothalamus during the fever in rabbits and the main source of cAMP increased in csf may be synthesized and released by hypothalamus.
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AIM:To observe the effects of Sini decoction against pulmonary injury induced by ex vivo ischemia-reperfusion in rats. METHODS: The model of ischemia-reperfusion was established. Twenty-four Sprague-Dawley rats were randomly divided into Sham, I/R, and SND groups. Wet to dry lung weight ratio (W/D), mean pulmonary artery pressure (MPAP), SOD activity and MDA contents in pulmonary perfusate and tissue, NOS activity and NO contents in pulmonary tissue were detected. The pathologic changes in pulmonary tissue were also observed by light microscope. RESULTS: The morphological changes of pulmonary injury were alleviated in SND group. Wet/dry ratio, MPAP and MDA contents in pulmonary perfusate and tissue were significantly lower in SND group after ischemic/reperfusion. SOD activity in pulmonary perfusate and tissue, and NO contents in pulmonary tissue were significantly higher in SND group than those in I/R group. No significant difference in NOS activity in pulmonary tissue among three groups was observed. CONCLUSION: These results indicate that SND may have a protective effect on ischemia-reperfusion injured lung by its antioxidant activity and by adjusting NO level.