ABSTRACT
Objective To investigate effects of magnetic stimulation on apoptosis of nerve cells and the production of inducible nitric oxidate synthase (iNOS) after spinal cord injury (SCI). Methods Thirty-two SpragueDawley male rats were randomly divided into a magnetic stimulation group (n = 16) and a control group (n = 16).SCI models were established by spinal cord transection in both groups. Rats were sacrificed at the 6th, 12th, 24th and 72nd hour post-injury, but the rats in the stimulation group received magnetic stimulation before being sacrificed.Apoptosis index (AI) and iNOS-positive cells rate were recorded at each time point. Results Apoptotic cells could be observed by the 6th hour post-injury, and were elevated from the 24th to the 72th hour. iNOS-positive cells were few at the first two time points, but had increased significantly at the 24th and 72nd hour post-injury. Compared with the control group, the apoptosis index of the stimulation group decreased a little at the 6th and 12th hour, but not significantly. The difference was quite significant at the 24th and 72nd hour, however, and the AI in the stimulation group decreased much more than that in the control group. There was little difference in the rate of iNOS-positive cells between the control and stimulation groups at any time point. Conclusions Magnetic stimulation could inhibit neural apoptosis and protect neurons from secondary SCI, but it has little effect on iNOS production.
ABSTRACT
Insulin resistance(IR) is a independent risk factor of ichemic angiopathy .The abnormal state of thrombosis and fibrinolysis is a critical pathology component of IR,and play a vital role in initiating and developing cardiovasculer disease. Under IR state, the,inhancement of plasminogen-activator inhibitior-1(PAI-1)synthesis by adipose tissue and the reduced generation of nitric oxide with endothelial dysfunction contribute to the hypo-fibrinolytic/pro-thrombotic state and promote atherosclerotic. Accompanied with IR developing, when B cell function can't keep normal glycemia, the advanced glycosylation end products(AGEs) are increased as a result of hyperglycemia. AGEs can aggravate endothelial injury and accelerate the course of atherosclerotic. Fully comprehending the pathogenesis of thrombosis and fibrinolysis in IR and taking therapy for the pathology have clinical significance.