Today one of the most effective ways to treat the effects of spinal cord injury (SCI) is a method of electrical stimulation, which is able to influence the state of the membranes of neurons and muscle cells. Artificial electrical signal replaces the natural nerve impulse and causes muscle contraction. The functional state of spinal cord neurons changes, regeneration of intact structures increases, reducing the phenomenon of "spinal shock" which helps to improve neurological functions. No less effective way of treating injuries of SC was correction the recovery process of motor activity by using pharmacological drugs that is more traditional approach but with using of original compared to classical drugs. Perhaps in role of such drugs can be Cortexin which has both neurotropic and antioxidant action; and Methylprednisolone as a powerful anti-inflammatory immunosuppressive and antiallergic agent. Despite numerous clinical and experimental studies of the efficacy of these treatment modes of vertebrate spinal cord injuries, the use of electrical stimulation, Methylprednisolone and Cortexin treatment provided either in a long rehabilitation period or in the early stages of posttraumatic syndrome as a general pharmacotherapeutic and physiotherapeutic treatment modes.
Based on the experimental conditions and data of proantioxidative balance in homogenate of spinal cord we mentioned process of optimization metabolic recovery on 21st day after spinal cord injury in animals. Thus, the amount of TBA- products in "electrical" and "cortexin" rats groups was reduced by 33,6% compared with the control value. In contrast, the accumulation of lipid peroxidation products in the "methylprednisolone" group rats was excessive – three times higher than the level of control. At the same time, in rats treated with methylprednisolone almost in three times was reduced catalase activity. The level of superoxide dismutase activity – remained at the control value level. Thus, methylprednisolone by inhibiting catalase activity promotes excessive free radical oxidation process and possibly disruption of the membrane structure of neuro-glial fraction of spinal cord. The most favorable process of maintaining pro-anti-oxidative homeostasis was in the "cortexin" group where superoxide dismutase activity was increased by 41,7 % on the base of reduced radical formation process. Obviously, increasing the enzymatic antioxidant protection restrained lipid peroxidation processes that can be seen as adaptive-compensatory response of the CNS to such stressors as spinal cord injury. When electrostimulation against decrease of lipid peroxidation the antioxidant enzymatic activity was decreased: catalase activity was decreased by 65,4%, and superoxide dismutase – by 78%.
Study of spontaneous horizontal mobility of animals in the "open field" test showed that the recovery of the paretic limb function after spinal cord injury was noted in the group "cortexin" and "electrical". Thus, on 5th day after the formation of experimental SCI, number of crossed horizontal squares in rats receiving cortexin practically restored to its original level, which was determined in intact rats. In contrast, spontaneous locomotor activity in groups of "control", "electrical" and "methylprednisolone" did not differ significantly and depressed by 87–94% compared with animals in the initial state before modeling to SCI.
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