急性脑梗死患者细胞因子信号转导抑制因子3水平的变化及意义

目的探讨急性脑梗死(ACI)患者细胞因子信号转导抑制因子3(SOCS-3)及TNF-α和白细胞介素6(IL-6)水平变化的临床意义。方法选择发病72 h的ACI患者65例作为脑梗死组,同期选择年龄匹配的健康体检者20例作为对照组。脑梗死组按不同梗死体积、不同神经功能缺损进行分析,对照组体检时,脑梗死组入院第1、3、7天用ELISA检测血清SOCS-3水平,用化学发光法检测入院第1、7天血清IL-6与TNF-α水平,并进行相关分析。结果与对照组比较,脑梗死组第1、3、7天SOCS-3、IL-6和TNF-α明显上升(P0.01),大梗死体积患者IL-6和TNF-α表达较中、小梗死体积患者明显上升(P0.05)。入院第21天Barthel指数与SOCS-3水平呈正相关(r=0.810,P0.05),与IL-6、TNF-α水平呈负相关(r=-0.672,-0.822,P0.05)。结论 SOCS-3可能参与ACI炎性反应发生、发展的病理过程,观察SOCS-3的变化,对ACI病情评价及预后分析有益。

Significance and dynamic variation of inhibitive factor of cytokine signaling-3 in ACI patients

Objective To observe the expression of inhibitive factor of cytokine signaling-3 (SOCS-3),TNF-α and IL-6 in acute cerebral infarction(ACI) patients and to investigate its significance and dynamic variation.Methods 65 ACI patients admitted within 72 hours were enrolled into ACI group and 20 healthy people with the age and sex matched were selected as the control group.The expression of SOCS-3 was detected by enzyme-linked immuno sorbent assay on day 1, day 3 and day 7 after admission and the expression of IL-6 and TNF-α was detected by chemiluminescence on day 1 and day 7 after admission.The ACI group was analyzed from the aspects of different cerebral infarction volumes (CIV) and different levels of neurologic impairment.Results Compared with control group,the expression of SOCS-3,TNF-α and IL-6 in ACI group significantly increased (P < 0.01).Compared with patients with middle and small infarct volumes,the expression of TNF-α and IL-6 in patients with large infarct volume markedly increased (P < 0.05).Barthel index in ACI group correlated positively with SOCS-3 (r = 0.810,P < 0.05) and correlated negatively with the expression of IL-6 and TNF-α (r = - 0.672,P-<0.05,r = - 0.822, P < 0.05) on day 21 after admission.Conclusions SOCS-3 may be involved in the pathological process of inflammatory reaction after ACI.Understanding and assessment of dynamic variation of SOCS-3 may benefit the evaluation of the illness condition and prognosis of ACI patients.