Clinical Observation of L-carnitine in Patients with Acute Cerebral Infarction
|Keywords||Levocarnitine Nitric oxide Malondialdehyde Superoxide dismutase S100B protein Neuron-specific enolase Acute cerebral infarction Neuroprotective|
Objective: To study patients with cerebral infarction NO, MDA, SOD, S100B and NSE changes observed levocarnitine protective effect on the brain of patients with acute cerebral infarction, verify its clinical efficacy. Methods: 60 cases of the incidence within 72h of acute cerebral infarction patients, were randomly divided into conventional group and levocarnitine group, which conventional group, 25 males and 5 females; levocarnitine group of 21 males and 9 females. Conventional group levocarnitine the same group was given conventional treatment, including anti-platelet aggregation, improve cerebral circulation and treatment. Levocarnitine group on the basis of conventional treatment plus the levocarnitine 2-3g / d, shared 10 days. NIHSS score recorded before and after the admission of the two groups of patients of the conventional group and levocarnitine group to evaluate the clinical efficacy; all patients before treatment, after treatment with nitrate reductase method for the determination of serum NO content, colorimetric determination of serum MDA content and SOD activity, measured by ELISA in serum S100B, NSE content. The results were statistically analyzed using SPSS17.0 package P lt; 0.05 difference was statistically significant. Results: (1) treatment of nerve function levocarnitine group and the conventional group defected NIHSS score difference was not statistically significant (P gt; 0.05) after treatment on day 11 NIHSS score of the two groups were significantly decreased (P lt; 0.01 ), which levocarnitine group decreased value (△ NIHSS) greater than the conventional group difference was statistically significant (P lt; 0.01). (2) pre-treatment levocarnitine group with conventional serum NO, MDA, S100B and NSE content differences without statistical significance (P gt; 0.05), 11 days after treatment, serum NO, MDA, S100B NSE levels were significantly decreased (P lt; 0.01), levocarnitine group of serum NO, MDA, S100B, NSE levels lower than the conventional group, the difference was statistically significant (P lt; 0.05). (3) before treatment left the carnitine group with conventional serum SOD activity difference was not statistically significant (P gt; 0.05), and 11 days after treatment, the SOD activity in serum were significantly higher (P lt; 0.01) levocarnitine serum SOD activity than the conventional group, the difference was statistically significant (P lt; 0.05). Conclusion: levocarnitine can significantly improve the neurological deficit scores of patients with acute cerebral infarction, lowering of serum NO, MDA, S100B, NSE content and increase SOD activity, play a protective effect of ischemic brain tissue . Its mechanism may be related to reduced oxygen free radicals, inhibition of lipid peroxidation, reducing the damage of free radical-mediated toxicity. Levocarnitine clinical treatment of acute cerebral infarction as a safe and effective neuroprotective strategy.