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目的研究丁苯酞氯化钠联合依达拉奉治疗急性脑梗死患者对血清丙二醛(MDA)水平和超氧化物歧化酶(SOD)活力的影响。方法急性期脑梗死患者160例随机分对照组、丁苯酞组、依达拉奉组和联合组,每组40例。对照组应用阿司匹林、胞二磷胆碱和奥扎格雷钠注射液治疗。丁苯酞组在对照组治疗的基础上加用丁苯酞氯化钠治疗。依达拉奉组在对照组治疗的基础上加用依达拉奉治疗。联合组在对照组治疗基础上加用丁苯酞氯化钠和依达拉奉治疗。采用比色法检测4组患者血清MDA水平和SOD活力。结果 4组患者入院1 d时MDA水平、SOD活性比较,差异无统计学意义(P>0.05)。入院7、14 d时丁苯酞组、依达拉奉组和联合组MDA水平、MOD活性与对照组比较,差异有统计学意义(P<0.05)。联合组入院7、14 d MDA水平、MOD活性与丁苯酞组和依达拉奉组比较,差异有统计学意义(P<0.05),而丁苯酞组与依达拉奉组比较,差异无统计学意义(P>0.05)。对照组入院14 d时MDA水平与入院1 d比较,差异有统计学意义(P<0.05)。丁苯酞组、依达拉奉组和联合组治疗7、14 d时MDA水平明显低于入院1 d,入院14 d时明显低于入院7 d(P<0.05)。对照组入院7 d时MOD水平与入院1 d时比较显著降低(P<0.05),而入院14 d时恢复到入院1 d时的水平。丁苯酞组、依达拉奉组入院7 d时SOD活性与入院1 d相当(P>0.05),而联合组呈升高趋势(P<0.05)。入院14 d时丁苯酞组、依达拉奉组、联合组SOD水平显著高于入院1、7 d(P<0.05)。结论丁苯酞氯化钠联合依达拉奉治疗急性脑梗死,可以显著降低血清MDA水平,提高SOD活性,对减少脑细胞损伤,维持脑细胞活性和正常功能,清除氧化自由基和有害物质有重要作用。
Objective To investigate the effects of butylphthalide and sodium chloride combined with edaravone on serum malondialdehyde (MDA) and superoxide dismutase (SOD) activity in patients with acute cerebral infarction. Methods 160 patients with acute cerebral infarction were randomly divided into control group, butylphthalide group, edaravone group and combined group, 40 cases in each group. The control group was treated with aspirin, citicoline and ozagrel sodium. Butylphthalide group in the control group based on the addition of butylphthalide sodium chloride treatment. Edaravone group in the control group based on the treatment with edaravone treatment. The combination group was treated with butylphthalide sodium chloride and edaravone on the basis of the control group. Colorimetry was used to detect serum MDA level and SOD activity in 4 groups. Results There was no significant difference in MDA level and SOD activity between the 4 groups on the first day after admission (P> 0.05). On the 7th, 14th day after admission, the MDA level, the activity of MOD in the butylphthalide group, the edaravone group and the combined group were significantly different from those in the control group (P <0.05). There were significant differences in MDA level and MOD activity between the combination group and the butylphthalide group and the edaravone group on the 7th, 14th day after admission (P <0.05), but there was no significant difference between the butylphthalide group and the edaravone group No statistical significance (P> 0.05). The level of MDA in the control group on the 14th day after admission was significantly higher than that on the 1st day after admission (P <0.05). Butylphthalide group, edaravone group and combined group 7 and 14 d after treatment, the MDA level was significantly lower than that of admission 1 d, and significantly lower than that of admission 7 d after admission (P <0.05). At 7 days after admission, the MOD level in the control group decreased significantly (P <0.05) on the 1st day and returned to the level on the 1st day after admission on the 14th day. Butylphthalide group and edaravone group had similar SOD activity on the 7th day after admission (P> 0.05), while the combined group showed an increasing trend (P <0.05). On the 14th day after admission, the levels of SOD in the butylphthalide group and the edaravone group were significantly higher than those on the admission day (P <0.05). Conclusion Sodium butyrate phthalate combined with edaravone in the treatment of acute cerebral infarction can significantly reduce serum MDA levels and improve the activity of SOD, reduce the damage of brain cells, maintain the activity of brain cells and normal function, remove oxidized free radicals and harmful substances Important role.