| Objective:By analyzing the difference between Interlekin(IL)-33 in Acute ischemic stroke(AIS)group and control group explore the possible effect of IL-33 on AIS.By analyzing the differences of IL-33 in different TOAST classifications,different carotid plaque stability,and different vascular stenosis degree in head and neck arteries,this paper explores whether IL-33 can promote or inhibit atherosclerosis.Methods:157 cases of AIS patients admitted to our department from February 2018 to February 2019 were selected as the case group,and 30 cases of non-AIS patients with matching general data were selected as the control group.General information,laboratory biochemical tests(IL-33,LDL,Uric acid,etc.),color doppler ultrasound of head and neck arteries and imaging findings were collected from all subjects.The case groups were grouped again according to TOAST classification,carotid plaque stability and degree of head and neck artery stenosis.Statistical software was used to analyze the differences of IL-33,LDL and UA levels in different groups and draw conclusions.Results:1.The serum IL-33(pg/ml)level in the AIS group was1970.02(1761.09,2193.68)and lower than that in the control group 2302.13(2112.65,2416.51),By rank-sum test,the difference was statistically significant(P<0.001).The level of LDL(mmol/L)in the AIS group 2.87±0.65 was higher than that in the control group 2.57±0.28.By T test,the difference was statistically significant(P<0.001).2.The level of IL-33(pg/ml)in the large-volume AIS group was 1579.68(1361.55,1740.41),which was lower than that in the small-volume AIS groupV1970.02(1761.09,2193.68)and the control group 2302.13(2112.65,2416.51).The difference was statistically significant(P < 0.001).The small-volume AIS group1970.02(1761.09,2193.68)was lower than that in the control group 2302.13(2112.65,2416.51).The difference was statistically significant(P < 0.05).The level of LDL(mmol/L)in the large-volume AIS group was 3.02(2.73,3.47),which was higher than that in the small-volume AIS group 2.77(2.29,3.04)and the control group 2.53(2.35,2.75).The differences were statistically significant(P <0.05).Small-volume AIS group 2.77(2.29,3.04)was higher than the control group2.53(2.35,2.75),but the difference was not statistically significant(P>0.05).3.The level of IL-33(pg/ml)in LAA group was 1630.92(1468.84,1875.43),which was lower than that in SAA group 1986.75(1835.59,2212.23)and control group 2302.13(2112.65,2416.51).The differences were statistically significant(P <0.001).SAA group 1986.75(1835.59,2212.23)was lower than the control group2302.13(2112.65,2416.51),but the difference was not statistically significant(P >0.05).The level of LDL(mmol/L)in LAA group was 2.94(2.62,3.33),which was higher than that in SAA group 2.65(2.27,3.04)and control group 2.53(2.35,2.75),the differences were statistically significant(P<0.05).SAA group 2.65(2.27,3.04)higher than the control group2.53(2.35,2.75),but the difference was not statistically significant(P>0.05).4.The level of IL-33(pg/ml)in the vulnerable plaque group was 1740.41(1499.32,1968.54),which was lower than 1864.90(1665.32,2108.53)in the stable plaque group and 2302.13(2112.65,2416.51)in the control group,the differences were statistically significant(P<0.05).In the stable plaque group 1864.90(1665.32,2108.53)was lower than that in the control group 2302.13(2112.65,2416.51).The difference was statistically significant(P<0.001).The level of LDL 2.92(2.56,3.45)in the vulnerable plaque group was higher than the control group 2.53(2.35,2.75),stable plaques 2.91(2.53,3.19)higher than the control group 2.53(2.35,2.75),the differences were statistically significant(P <0.05).The vulnerable plaque group 2.92(2.56,3.45)was higher than the stableplaques 2.91(2.53,3.19),but the difference was not statistically significant(P >0.05).5.Serum IL-33(pg/ml)level in the severe stenosis group was 1579.68(1377.47,1714.48),which was lower than that in the mild and moderate stenosis group2003.67(1786.29,2214.78)and control group 2302.13(2112.65,2416.51),the differences were statistically significant(P < 0.05).In the mild and moderate stenosis group,2003.67(1786.29,2214.78)was lower than that in the control group 2302.13(2112.65,2416.51),but the difference was not statistically significant(P > 0.05).The level of LDL(mmol/L)2.96(2.51,3.49)in the severe stenosis group was higher than 2.78(2.30,3.04)in the mild and moderate stenosis group and2.53(2.35,2.75)in the control group,the differences were statistically significant(P< 0.05).In the mild and moderate stenosis group 2.78(2.30,3.04)was higher than that in the control group 2.53(2.35,2.75),but the difference was not statistically significant(P>0.05).6.Spearman correlation analysis found that IL-33 was negatively correlated with LDL,the stability of carotid plaque,the degree of vascular stenosis of head and carotid artery.Conclusions:1.In patients with acute cerebral infarction,the level of IL-33 in peripheral blood decreased with the aggravation of cerebral infarction within 72 hours,suggesting that IL-33 has a protective effect on brain tissue after ischemia.2.The level of IL-33 in peripheral blood was lower in both the atherosclerotic vulnerable plaque group and the severe carotid stenosis group,suggesting that IL-33 is related to the degree of atherosclerosis in the head and neck arteries,and may have an inhibitory effect on atherosclerosis.3.The level of LDL is closely related to the degree of cerebral infarction and the progression of carotid atherosclerosis.4.Serum UA levels were not associated with susceptibility to AIS. |
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