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CD28基因在爆震致肠道损伤中作用及机制

The role and mechanism of CD28 gene in intestinal injury induced by detonation
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摘要 目的探讨CD28基因在爆震致肠道损伤中的作用及机制。方法将16只健康雄性C577BL/6小鼠随机分入正常对照组(n=8)和爆震伤模型组(n=8),将16只健康雄性CD28基因敲除小鼠随机分入CD28基因缺失组(n=8)和PI3K抑制剂组(n=8)。通过自主研发的爆震伤模型装置建立爆震致肠道损伤模型。每日观察小鼠情况,测量体质量变化;HE染色观察各组肠道损伤情况;TUNEL检测组织细胞凋亡损伤;Western-blot检测肠道组织氧化应激相关蛋白丙二醛(MDA)、超氧化物歧化酶(SOD)-1、SOD-2及PI3K、AKT、Nrf2通路蛋白表达情况。结果爆震伤模型组小鼠活动度降低,体质量明显减轻(P<0.05)。爆震48 h后,爆震伤模型组小鼠HE染色可见肠道组织形态结构紊乱、坏死严重,TUNEL染色可见肠道组织细胞发生凋亡损伤。与正常对照组小鼠比较,爆震伤模型组肠道组织中MDA蛋白表达升高,SOD-1和SOD-2蛋白表达降低(P<0.05);与爆震伤模型组小鼠比较,CD28基因缺失组MDA蛋白表达降低,SOD-1和SOD-2蛋白表达升高(P<0.05);PI3K抑制剂组MDA、SOD-1、SOD-2蛋白表达趋近于爆震伤模型组(P>0.05)。与正常对照组小鼠比较,爆震伤模型组肠道组织中PI3K、AKT、Nrf2通路蛋白表达升高(P<0.05);与爆震伤模型组小鼠比较,CD28基因缺失组PI3K、AKT、Nrf2通路蛋白表达升高(P<0.05);PI3K抑制剂组小鼠PI3K、AKT、Nrf2通路蛋白表达低于CD28基因缺失组(P<0.05),趋近于爆震伤模型组(P>0.05)。结论CD28基因在爆震致肠道损伤中发挥重要作用,其机制可能与PI3K/AKT/Nrf2通路有关。 Objective To investigate the role and mechanism of CD28 gene in intestinal injury induced by detonation.Methods Sixteen healthy male C577 BL/6 mice were randomly divided into normal control group(n=8)and blast injury model group(n=8),while 16 healthy male CD28 knockout mice were randomly divided into CD28 deletion group(n=8)and PI3 K inhibitor group(n=8).The model of intestinal injury induced by detonation was established by the detonation injury model device independently developed.The mice were observed daily and the changes of body weight were measured.HE staining was used to observe intestinal injury in each group.TUNEL was used to detect apoptosis of tissue cells.The expression of oxidative stress related proteins malonaldehyde(MDA),superoxide dismutase(SOD)-1,SOD-2 and PI3 K,AKT,Nrf2 pathways in intestinal tissues were detected by Western-blot.Results The activity and body weight of blast injury model group were decreased significantly(P<0.05).48 h after detonation,HE staining showed intestinal tissue disorder and severe necrosis,and TUNEL staining showed intestinal tissue apoptosis damage.Compared with normal control group,MDA protein expression in intestinal tissue of blast injury model group was increased,while SOD-1 and SOD-2 protein expression were decreased(P<0.05).Compared with blast injury model group,the expression of MDA protein in CD28 deletion group was decreased,and the expression of SOD-1 and SOD-2 protein was increased(P<0.05).The protein expressions of MDA,SOD-1 and SOD-2 in PI3 K inhibitor group were similar to those in blast injury model group(P>0.05).Compared with normal control group,the expression of PI3 K,AKT and Nrf2 pathway proteins in intestinal tissue of blast injury model group was increased(P<0.05).Compared with blast injury model group,the expression of PI3 K,AKT and Nrf2 pathway proteins in CD28 deletion group was increased(P<0.05).The protein expressions of PI3 K,AKT and Nrf2 pathways in PI3 K inhibitor group were lower than those in CD28 deletion group(P<0.05),and close to th
作者 刘颖 丛培芳 史秀云 马瑞珩 金红旭 LIU Ying;CONG Pei-fang;SHI Xiu-yun;MA Rui-heng;JIN Hong-xu(Department of Emergency Medicine,General Hospital of Northern Theater Command,Shenyang 110016,China)
出处 《临床军医杂志》 CAS 2022年第3期224-228,共5页 Clinical Journal of Medical Officers
基金 全军面上项目(CLB20C036) 辽宁省重点研发计划(2019010205,2021JH2/10300024)
关键词 CD28基因 爆震 肠道损伤 PI3K/AKT/Nrf2 CD28 gene Blast Intestinal injury PI3K/AKT/Nrf2
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