| Objective: The study was to investigate the effects of reduced glutathione(GSH) on the content of malondialdehyde(MDA) and the activity of glutathione peroxidase (GSH-PX) and superoxide dismutase(SOD) after focal cerebral ischemia-reperfusion in rats, as well as to observe the volume of brain infarction, neurobehavioral function and brain morphosis. The purpose of the study was to explore the potential mechanism of neuron-protective effects of GSH on focal cerebral ischemia-reperfusion.Methods: Rats were divided into three groups randomly: (1) Ischemia-reperfusion model group (IM): 0.9% sodium chloride injection(10ml/kg) was peritoneal injection after the rat models of middle cerebral artery occlusion were established. (2) Sham-operated group (SO): thread was inserted into rat common carotid artery only 10 mm deep;(3) Ischemia-reperfusion model+GSH treatment group (IM+GSH): GSH(1200mg/kg) was peritoneal injection after the ischemia model was performed. Followed 2-hour ischemia and 6-hour reperfusion, the neurology deficit score and the infarct volume were evaluated, and the brain morphosis in ischemic areas with hematoxylin-eosin staining were observed under light microscope, moreover the content of Malondialdehyde (MDA), the activity of superoxide dismetase (SOD)and glutathione peroxidase (GSH-PX) were measured, respectively.Results: (1) Compared with SO group, the neurology deficit score of IM+GSH group (1.80±0.96) and IM group (2.75+0.44) increased significantly (P <0.05), besides IM+GSH group improved neurological dysfunctions as compared with IM group (P <0.05). (2) SO group had no focal infarction. The difference of infarct volume between IM (26.83±6.50) group and IM+GSH group (17.55±5.07) was significant (P <0.05). (3) Under light microscope, the brain morphosis in SO group was normal. In IM group, there were marked infarction and a lot of dead neuron in cortex and striatum, and the cerebral cortex edema located the ischemia region of right brain was obvious, besides the interstitial space of neural cell was enlarged and the perivascular space became larger. There were also infarction in IM+GSH group, but the region of infarction was smaller than that of IM group. The stratum of cerebral neuron in IM+GSH group was still clear, moreover the edema of cortex and interstitium were alleviated in comparison with IM group. (4) The MDA content of IM group increased(18.48±5.73) than that of SO group and IM+GSH group, while the activity of SOD (118.24+40.73) and GSH-PX (9.41+3.56) decreased significantly (F <0.05). In IM+GSH group, the activity of SOD(394.37±51.45) and the MDA content (12.64±4.21) increased markedly in comparison with SO group, whereas the activity of GSH-PX (15.09+3.52) decreased (P <0.05).Conclusion: (1) Reactive oxygen species (ROS) is an important contributor to cerebral cell death after ischemia reperfusion. (2) GSH can ameliorate neurological deficit score, reduce infarct volume induced by middle cerebral artery occlusion in the rat (MCAO), and alleviate the death and edema of neural cell significantly. (3) GSH could enhance the capability of eliminating free radical oxygen by reducing content of MDA, improving the activity of SODand GSH-PX, and play a neuroprotective effect after focal cerebral ischemia reperfusion.
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