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目的观察氧化苦参碱对大鼠脑外伤后神经细胞凋亡、氧化损伤和炎症反应的影响,探讨氧化苦参碱抗神经细胞凋亡的机制。方法选用健康Wistar大鼠140只,♂,随机分成假手术组、脑外伤组、氧化苦参碱60 mg.kg?1组和氧化苦参碱120 mg.kg?1组,每组35只,利用改进的Feeney自由落体损伤装置制作脑外伤动物模型,分别于脑外伤模型形成后给予1 mL 0.9%氯化钠注射液及不同剂量氧化苦参碱(60和120 mg.kg?1)腹腔注射,每日1次,共5 d,在脑外伤后2,6,12 h,1,2,3和5 d断头取血和获取脑组织,利用黄嘌呤氧化酶法检测血清超氧化物歧化酶活性,利用硫代巴比妥酸法测定血清丙二醛浓度,利用酶联免疫吸附试验测定血清白介素-1β、肿瘤坏死因子-?和白介素-6浓度,利用原位末端转移酶标记技术检测脑组织中凋亡神经细胞,同时进行统计分析。结果脑外伤后2,6,12 h,1,2,3和5 d,氧化苦参碱60 mg.kg?1组大鼠凋亡神经细胞数量、血清超氧化物歧化酶活性及丙二醛、白介素-1β、肿瘤坏死因子-?和白介素-6浓度与脑外伤组比较差异没有统计学意义(P>0.05);脑外伤后12 h,1,2,3和5 d,氧化苦参碱120 mg.kg?1组大鼠凋亡神经细胞数量、血清超氧化物歧化酶活性及丙二醛、白介素-1β、肿瘤坏死因子-?和白介素-6浓度较脑外伤组显著减少(P<0.05),脑外伤后2 h和6 h,氧化苦参碱120 mg.kg?1组大鼠凋亡神经细胞数量、血清超氧化物歧化酶活性及丙二醛、白介素-1β、肿瘤坏死因子-?和白介素-6浓度与脑外伤组比较差异没有统计学意义(P>0.05)。结论氧化苦参碱可能通过降低体内自由基和炎症反应,从而抑制脑外伤后神经细胞凋亡,达到神经保护作用。
Objective To observe the effects of oxymatrine on the apoptosis, oxidative damage and inflammatory reaction in rat brain after traumatic brain injury and to explore the mechanism of oxymatrine in preventing neuronal apoptosis. Methods Forty healthy Wistar rats were randomly divided into sham operation group, traumatic brain injury group, oxymatrine 60 mg · kg -1 group and oxymatrine 120 mg · kg -1 group (35 rats in each group) An animal model of traumatic brain injury was established by using an improved Feeney free-fall injury device. After the traumatic brain injury models were formed, 1 mL of 0.9% sodium chloride injection and different doses of oxymatrine (60 and 120 mg.kg? 1) were injected intraperitoneally , Once a day for 5 days. Blood was taken from the heads of the rats at 2, 6, 12, 1, 2, 3 and 5 days after traumatic brain injury and the brain tissues were harvested. The serum superoxide dismutase Serum malondialdehyde concentration was measured by thiobarbituric acid method. Serum levels of interleukin-1β, tumor necrosis factor-α and interleukin-6 were measured by enzyme-linked immunosorbent assay (ELISA) and detected by in situ end-transferase labeling Apoptotic nerve cells in brain tissue, at the same time for statistical analysis. Results At 2, 6, 12, 1, 2, 3 and 5 days after traumatic brain injury, the number of apoptotic nerve cells, the activity of serum superoxide dismutase and malondialdehyde in 60 mg · kg -1 oxymatrine group , Interleukin-1β, tumor necrosis factor-α and interleukin-6 levels were not significantly different from those in traumatic brain injury group (P> 0.05). At 12 h, 1, 2, 3 and 5 d after traumatic brain injury, The number of apoptotic nerve cells, serum superoxide dismutase (SOD) and the concentrations of malondialdehyde, interleukin-1β, tumor necrosis factor-α and interleukin-6 in 120 mg · kg -1 group were significantly decreased compared with those in traumatic brain injury group (P < 0.05), 2 h and 6 h after traumatic brain injury, the number of apoptotic nerve cells, the activity of serum superoxide dismutase and the levels of malondialdehyde, interleukin-1β, tumor necrosis factor -? And interleukin -6 concentrations compared with traumatic brain injury group showed no significant difference (P> 0.05). Conclusion Oxymatrine may inhibit neuronal apoptosis after traumatic brain injury by reducing free radical and inflammatory reaction in vivo and achieve neuroprotective effect.