| Objective:Epilepsy is one of the most common syndromes in neurology, which affects people of all ages. The syndrome can repeated attrack in terms of attacks and can also imperil one’s life if one does not get timely treatment. Over the years, through the untiring efforts of scientists over the world, many kinds of anti-epileptic drugs have been developed. However, those drugs mostly focus on symptom control. The drugs also have long treatment course and plenty of side effects. In addition, the symptom of some people cannot be controlled even if they take the pills according to doctor’s advices. There are so many patients who fail to recover, because they stop taking the drugs without permission during the treatment or change the pills without doctor’s direction. All these bring great pressure on life and psychological stress to patients and their families.Epilepsy is produced by brain disorder resulting from excessive electrical discharges. Some studies indicated that too many attacks would bring irreversible damage to central nervous system, especially hippocampus and limbic system. Various kinds of pathological changes could occur after epilepsy attack. Among them are neuronal apoptosis, neuron lost, gliosis, mossy fiber sprouting, synaptic reorganization. The main form of the neuron lost is apoptosis. Brain damage is huge, which is caused by epilepsy, but drugs of epilepsy cerebral protection is still a blank.In this study we chose PTZ kindling SD rats as chronic epilepsy model and magnolol as intervention. Comparing behavior changes and biochemical criterion among groups, the study aimed at whether magnolol has neuronal protection in hippocampus of chronic epilepsy rats from the aspects of control symptom, imflammitonal inhibition and apoptosis.Methods:75 clean grade adult male SD rats which weight 200±20g were chosen, and the rats were randomly divided into the five groups,normal control group( NS group),epilepsy group( PTZ group), High dose of magnolol group(H group), medium dose of magnolol group(M group) and low dose of magnolol group(L group).All of those rats were stimulated by PTZ intraperitoneal injection once daily to make chronic epilepsy models. The study selected the rate of seizure as behavior indexes. Nissle staining was performed to observe the neuron damage in hippocampus. The expression of apoptosis factor caspase-3 in hippocampus was determined by Western Blot and immunohistochemical. Immune enzyme-linked method was used to detect the expression of TNF-α.Results:1 The observational result of behaviorThe induced rate in 7 days, 14 days, 21 days, 28 days, 35 days and 42 days were chosen as behavior indicators for comparison. The results shown that the induced rate of PTZ group was much higher than any other groups, and with the increase of intervention dose the induced rate indicated a downtrend.2 The results of TNF-α expression in each groupAmong the groups, the expression of TNF-αin PTZ group was increased more obviously compared with other groups(P<0.05), and NS group has the lowest increase. Among the control groups, there were no significant difference(P>0.1) between H group(186.43±21.34), M group(189.44±22.12) and L group.3 The results of Caspase-3 protein expression in each groupThe expression of Caspase-3 protein in PTZ group(3.01±0.56) was considerably higher than other groups(P<0.05). Among the control groups, the expression of L group was significantly higher than other two groups(P<0.05) and the expression of H group(1.44±0.32) was lower than M group(1.98±0.40).NS group was the minimum.4 The results of Caspase-3 expression in each groupIn the immunohistochemical experiments that detect Caspase-3 expression in hippocampus of rats in each group, the number of positive cells in CA1 region of PTZ group was 76.57±5.79. The number of CA3 region is 71.05±5.11, and those expression quantities were much more than the control group(P<0.05).In NS group, the number of positive cells in CA1 region was 31.12±5.01, while CA3 region was 17.55±3.56, the lowest number. There are also differences between control groups. In CA1 region, the number of L group was the most while H group was the lowest, the number of M group was in the middle. However, in CA3 region, L group has the largest number of positive cells(47.98±4.33) and other two groups had no significant difference between them while the number of H group was 33.63±1.13 and M group was 33.78±4.39.5 The morphological changes of cerebral tissueIn the Nissle staining of hippocampus in PTZ group, pyknosis of neuron, condensation of chromatin and karyolsis can be found, and some cells had the characteristics of apoptosis. The neuron in CA1 and CA3 region were in scattered in terms of arrangement. In control group, we could also see some swelling neuron and uneven shades of nuclei. But compared with PTZ group, neurons in control group had less injury and lost, and better arrangement. In NS group, the morphological manifestation was normal and the hippocampus structures were completed. The cones there were violet blue and uniformity.Above all, the results shown that the induced rate of PTZ group was much higher than any other groups, and with the increase of intervention dose the induced rate dropped significantly. The expression of Caspase-3 and TNF-α were increased obviously compared with other groups. In control group, the expression was different as the dose was different. All in all, the effect of H group was the best, M group took the second and L group was the worst. The Nissle staining of hippocampus of PTZ group shown the most serious neuron lost and necrosis.Concelusions:1 Magnolol can significantly inhibit epilepsy induced by PTZ and itseffect related to dose.2 Magnolol can protect brain injury coursed by epilepsy, its effect basedon dose.3 The decline of TNF-α and Caspase-3 may involve the process ofneuron protection that coursed by magnolol. Magnolol may regulate Signaling pathways of TNF-α/Caspase-3/apoptosis to realize the effect. Conclusions:... |
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