Objective:Observed the changes of serum Nitric oxide (NO), Malondialdehyde(MDA), S-100B protein (S100B), Neuron specific enolase (NSE) content and Superoxide dismutase(SOD) activity in patients with acute cerebral infarction, to further explore the cerebral protection and clinical efficacy of levocarnitine.Methods:60 patients with acute cerebral infarction within 72h were randomly divided into routine treatment group(male 25 cases,female 5 cases)and L-carnitine group(male 21cases, female 9 cases).Tow groups received the same routine treatment,including anti-platelet aggregation, improving cerebral circulation etc, Patients in the L-carnitine treatment group received L-carnitine 2-3g/d for 10 days on the routine treatment. The scores of NIHSS were recorded before and after admission in patients with ACI,in both routine group and L-carnitine group, to evaluate the clinical efficacy.Before and after treatment, the serum levels of NO was measured through nitrate reductase method, the serum levels of MDA content and SOD activity was measured through colorimetric determination, the serum levels of S100B and NSE was measured through enzyme immunoassay. SPSS 17.0 version was used for statistical analysis and P<0.05 was regared as statistical significance.Results:(1)There was no significant difference between routine treatment group and L-carnitine group in the NIHSS scores of neurological deficits before treatment(P> 0.05); the scores of the two groups significantly decreased on the 11th day after treatment(P<0.01), but the decreased value(â–³NIHSS) of L-carnitine group was greater than the routine treatment group(P <0.01).(2)There was no significant difference between routine treatment group and L-carnitine group in the serum levels of NO,MDA,S100B and NSE content before treatment(P> 0.05); the levels of serum NO,MDA,S100B and NSE content significantly decreased on the 11th day after treatment in two groups(P<0.01),however,the levels of serum NO,MDA,S100B and NSE were significantly lower in L-carnitine group than in routine treatment group(P<0.05).(3)There was no significant difference between routine treatment group and L-carnitine group in the serum levels of SOD before treatment(P> 0.05); the levels of serum SOD significantly increased on the 11th day after treatment in two groups(P<0.01),however,the levels of serum SOD was significantly higher in L-carnitine group than in routine treatment group(P<0.05).Conclusions:L-carnitine can improve the neurological deficit,reduce the serum levels of NO,MDA,S100B and NSE content, and increase SOD activity in patients with acute cerebral infarction,protect ischemic brain tissue. The protective neural function mechanisms may be derived from clearing oxygen free radicals,inhibiting lipid peroxidation,reducing the damage of free radical-induced.L-carnitine may be used as a possible,safe and effective neuroprotective strategy in patients with acute cerebral infarction. |