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作 者:刘云涛[1] 潘敬芳[1] 简磊[1] 吴娇[1] LIU Yun-tao PAN J ing- fang J IAN Lei et al.(Department of Endocrinology, Renhe Hospital of China Three Gorges University , Yichang 443000, Chin)
出 处:《中国糖尿病杂志》2017年第2期112-115,共4页Chinese Journal of Diabetes
摘 要:目的探讨血清脂氧素A4(LXA4)与糖尿病周围神经病变(DPN)的相关性。方法选择新诊断的单纯T2DM患者41例(T2DM组),DPN患者42例(DPN组),另选体检者42名(NGT组)。采用ELISA测定血清LXA4水平。结果与NGT组比较,T2DM组和DPN组血清LXA4水平降低[(540.23±55.87)vs(511.49±51.23)vs(476.53±47.23)pg/ml,P<0.05或P<0.01];相关分析显示,血清LXA4水平与FPG、HbA_1 c、TNF-α、半胱氨酸天冬氨酸酶3(Caspase-3)、病程呈负相关(r=-0.501、0.541、-0.627、-0.638,-0.591,P<0.05或P<0.01);与血红素加氧酶-1(HO-1)、超氧化物歧化酶(SOD)、正中神经运动神经传导速度(MMCV)、腓总神经运动神经传导速度(PMCV)、正中神经感觉神经传导速度(MSCV)、腓总神经感觉神经传导速度(PSCV)呈正相关(r=0.578、0.510、0.628、0.611、0.549、0.625,P<0.05或P<0.01);Logistic回归分析显示,LXA4、TNF-α是DPN的独立影响因素。结论DPN患者血清LXA4水平下降,在DPN的发生中发挥重要作用。Objective To explore the association between serum lipoxin A4(LXA4) and type 2diabetic peripheral neuropathy(DPN).Methods A total of 125 subjects were enrolled in this study and divided into three groups:patients with newly diagnosed type 2 diabetes(T2DM group,n = 41),patients with diabetic peripheral neuropathyCDPN group,w=42),and healthy people with normal glucose tolerance(NGT group,n=42).Serum LXA4 was measured by ELISA.Results The serum LXA4 were lower in T2 DM and DPN group than in NGT group[(511.49 ± 51.23) vs(476.53 ± 47.23) vs(540.23±55.87)pg/ml;P〈0.05 or P0.OlJ.Correlation analysis showed that LXA4 levels were negatively correlated with FPG,HbA1C,TNF-α,Caspase-3 and duration of diabetes(r=-0.501,-0.541,-0.627,-0.638,-0.591,P〈0.05 or P〈0.01),and positively correlated with haem oxygenase(HOI),SOD,median nerve motor nerve conduction velocity(MMCV),peroneal nerve motor nerve conduction velocity(PMCV),median nerve sensory nerve conduction velocity(MSCV),and peroneal nerve sensory nerve conduction velocity(PSCV)(r = 0.578,0.510,0.628,0.611,0.549,0.625;P〈0.05 or P〈0.01].Logistic regression analysis showed that LXA4 and TNF-α were the independent influencing factors for DPN.Conclusion Serum LXA4 decreases in patients with DPN,and plays an important role in the pathogenesis of DPN.
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