Application of lipopolysaccharide on inflammatory reaction of traumatic brain injury
-
摘要:
目的 评价分析脂多糖在创伤性颅脑损伤（TBI）炎症反应中的应用价值。 方法 选择2014年6月~2016年12月期间佛山市南海区第三人民医院脑科和南方医科大学珠江医院神经外科收治的TBI患者86例，并按照格拉斯哥昏迷评分分为3组：轻度组33例、中度组24例、重度组29例；并且选取同期来本院进行体检的健康者28例作为对照组。通过ELISA方法检测研究对象血清中TNF-α、IL-6、IL-1β，GREISS法检测一氧化氮含量。 结果 轻度组、中度组及重度组患者入院时的血清TNF-α浓度均有升高，其中第3天为最高，第5、7天已逐渐降低，但仍高于对照组。轻度组、中度组及重度组患者入院时的血清IL-6浓度均升高，其中第5天为最高，第7天已开始降低，仍高于对照组；TBI严重分级与血清IL-6浓度（r=0.925，P<0.05）。轻度组、中度组及重度组患者入院时的血清IL-1β浓度均升高，第1、3、5天缓慢增加，第7天增加更加显著，重度组升高幅度明显高于对照组、轻度组和中度组（P<0.05）。TBI严重分级与血清IL-1β浓度（r=1.267，P<0.05）。轻度组、中度组及重度组患者入院时的血清一氧化氮浓度有升高，其中第3天为升高较明显，第5、7天已逐渐降低，仍高于对照组；TBI严重分级与血清一氧化氮浓度（r=0.847，P<0.05）。 结论 脂多糖在TBI患者体内存在不同程度的炎症反应；血清中TNF-α、IL-6、IL-1β、一氧化氮浓度变化与TBI程度密切相关；如果浓度持续保持较高水平，这就说明脑组织损伤严重，预后效果不佳。 -
关键词:
- 创伤性颅脑损伤 /
- 脂多糖 /
- 血清TNF-α: IL-6 /
- IL-1β /
- 一氧化氮
Abstract:Objective To evaluate the value of lipopolysaccharide (LPS) in invasive brain injury (TBI) inflammatory response (Inflammation). Methods Eighty-six patients with TBI in Third People's Hospital of Nanhai Foshan were enrolled.They were divided into 3 groups according to the Glasgow coma scale (GCS) score, with mild group of 33 cases, moderate group of 24 cases and severe group of 29 cases. Twenty-eight cases with health examination in the same period were selected as a control group.The levels of nitric oxide (NO) in serum were detected by GREISS. The levels of TNF-α, IL-6, IL-1β and were measured by ELISA. Results The levels of serum TNF-α were increased in the mild, moderate and severe groups, and the third day was the highest. The levels of serum TNF-α on the 5th and 7th day were gradually decreased and still higher than the control group. The levels of serum IL-6 in the mild, moderate and severe groups were higher than those in the control group (P<0.05). The level of IL-6 in the mild and moderate group was significantly higher than that in the control group (r=0.925, P<0.05). The levels of serum IL-1β in the mild group, moderate group and severe group were higher than those in the control group, and the increasement was significant on the third , fifth day (P<0.05). The severity of TBI was correlated with serum IL-1β concentration (r=1.267, P<0.05). The levels of serum NO in the mild, moderate and severe groups were significantly higher than those in the control group (P<0.05), and serum NO levels on the third day was higher than that in the control group. NO concentration was correlated with the severity of TBI (r=0.847, P<0.05). Conclusion The changes of TNF-α, IL-6, IL-1β and NO in serum are closely related to the degree of TBI. High NO concentration means a serious brain tissue injury and poor prognosis. -
Key words:
- traumatic brain injury /
- lipopolysaccharide /
- serum TNF-α: IL-6 /
- IL-1β /
- nitric oxide
-
表 1 LPS在TBI患者血清中TNF-α浓度变化的比较（
$\bar x \pm s$ ，pg/mL）组别 n 第1天 第3天 第5天 第7天 对照组 28 137.95±9.36 137.95±9.36 137.95±9.36 137.95±9.36 轻度组 29 210.85±7.23 191.68±7.64 176.88±9.21 158.19±8.05 中度组 24 225.67±6.49 233.89±7.52 222.92±8.63 193.86±8.55 重度组 33 247.98±7.72# 268.37±9.76# 244.75±8.41# 218.35±9.32# #P<0.05 vs 其它3组. 
下载: 导出CSV
表 2 LPS在TBI患者血清中IL-6浓度变化的比较（
$\bar x \pm s$ ，pg/mL）组别 n 第1天 第3天 第5天 第7天 对照组 28 6.98±0.71 6.98±0.71 6.98±0.71 6.98±0.71 轻度组 29 12.17±1.75 19.05±3.02 36.10±2.87 29.13±2.82 中度组 24 44.39±2.22 53.57±4.89 78.19±6.07 68.15±6.39 重度组 33 103.15±12.06# 143.41±20.04# 233.15±11.16# 168.41±33.01# #P<0.05 vs 其它3组.
下载: 导出CSV
表 3 LPS在TBI患者血清中IL-1β浓度变化的比较（
$\bar x \pm s$ ，pg/mL）组别 n 第1天 第3天 第5天 第7天 对照组 28 61.56±11.49 61.56±11.49 61.56±11.49 61.56±11.49 轻度组 29 95.92±10.16 122.49±4.92 136.42±2.96 171.23±3.87 中度组 24 148.61±6.25 183.88±5.12 199.79±4.02 377.52±49.49 重度组 33 214.23±6.27# 233.61±8.29# 272.91±18.32# 472.73±13.17# #P<0.05 vs 其它3组.
下载: 导出CSV
表 4 LPS在TBI患者血清中NO浓度变化的比较（
$\bar x \pm s$ ，pg/mL）组别 n 第1天 第3天 第5天 第7天 对照组 28 29.38±5.57 29.38±5.57 29.38±5.57 29.38±5.57 轻度组 29 38.59±5.77 39.98±7.31 34.65±6.51 31.66±5.71 中度组 24 44.68±6.49 46.19±8.38 42.98±8.33 38.78±6.76 重度组 33 48.87±6.65# 51.28±8.87# 46.47±7.29# 41.26±6.98# #P<0.05 vs 其它3组.
下载: 导出CSV
-
[1] 武晓灵, 喻 莉, 龙 鼎. su PAR及D-二聚体对创伤性颅脑损伤患者病情严重程度及预后的判断价值[J]. 实用医学杂志, 2017, 33(2): 234-7. http://www.cnki.com.cn/Article/CJFDTOTAL-SYYZ201702022.htm [2] 赵雅度. 神经系统外伤[M]. 北京: 人民军医医出版社, 2001: 3-5. [3] 李 明, 杨继红, 耿维凤, 等. 鼠神经生长因子联合亚低温对重度创伤性颅脑损伤的神经保护作用及其机制[J]. 中国生化药物杂志, 2017, 37(1): 129-32. http://youxian.cnki.com.cn/yxdetail.aspx?filename=SHYW201701036&dbname=CJFDPREP [4] 朱占胜, 吴明灿, 张家均, 等. 创伤性颅脑损伤后白介素-6、18、27变化及临床意义[J]. 广东医学, 2011, 32(6): 762-3. http://www.cnki.com.cn/Article/CJFDTOTAL-GAYX201106033.htm [5] 杨 玺, 杨孟昌, 温开兰. 星状神经节阻滞对创伤性颅脑损伤患者炎症反应的影响[J]. 四川医学, 2016, 37(11): 1241-4. http://www.cnki.com.cn/Article/CJFDTOTAL-SCYX201611017.htm [6] Segev AN, Trudler D, Frenkel D. Preconditioning to mild oxidative stress mediates astroglial neuroprotection in an IL-10-dependent manner[J]. Brain Behav Immun, 2013, 30(7): 176-85. [7] Patterson ZR, Holahan MR. Understanding the neuroinflammatory response following concussion to develop treatment strategies[J]. Front Cell Neurosci, 2012, 6(11): 58-61. [8] Li H, Liao T, Debowski AW, et al. Lipopolysaccharide structure and biosynthesis in helicobacter pylori[J]. Helicobacter, 2016, 21(6): 445-61. doi: 10.1111/hel.2016.21.issue-6 [9] Bryant CE, Spring DR, Gangloff M, et al. The molecular basis of the host response to lipopolysaccharide[J]. Nat Rev Microbiol, 2010, 8(1): 8-14. [10] Meseguer V, Alpizar YA, Luis E, et al. TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins[J]. Nat Commun, 2014, 5(1): 3125-9. [11] 林 祺, 高 亮, 秦 松. 星形胶质细胞激活与创伤性颅脑损伤研究进展[J]. 中国临床神经科学, 2017, 25(1): 81-7. http://www.cnki.com.cn/Article/CJFDTOTAL-LCSK201701016.htm [12] 刘兴华, 陈春有, 郑 璘, 等. 神经生长因子对急性颅脑损伤患者血清S100β与IL-6的影响[J]. 中国生化药物杂志, 2016, 36(4): 167-9. http://www.cnki.com.cn/Article/CJFDTOTAL-SHYW201604055.htm [13] 乔智慧. 唐兰芬抵抗素与炎症相关性疾病研究进展[J]. 医学综述, 2010, 16(11): 1632-4. doi: 10.3969/j.issn.1006-2084.2010.11.011 [14] Juengst SB, Kumar RG, Failla MD, et al. Acute inflammatory biomarker profiles predict depression risk following moderate to severe traumatic brain injury[J]. J Head Trauma Rehabil, 2015, 30(3): 207-18. doi: 10.1097/HTR.0000000000000031 [15] Tompkins P, Tesiram Y, Lerner M, et al. Brain injury: neuro-inflammation, cognitive deficit, and magnetic resonance imaging in a model of blast induced traumatic brain injury[J]. J Neurotrauma, 2013, 30(22): 1888-97. doi: 10.1089/neu.2012.2674 [16] Hu YC, Sun Q, Li W, et al. Biphasic activation of nuclear factor kappa B and expression of p65 and c-Rel after traumatic brain injury in rats[J]. Inflamm Res, 2014, 63(2): 109-15. doi: 10.1007/s00011-013-0677-1 [17] Putker F, Bos MP, Tommassen J. Transport of lipopolysaccharide to the Gram-negative bacterial cell surface[J]. FEMS Microbiol Rev, 2015, 39(6): 985-1002. doi: 10.1093/femsre/fuv026 [18] Burda JE, Bernstein AM, Sofroniew MV. Astrocyte roles in traumatic brain injury[J]. Exp Neurol, 2016, 275(3, SI): 305-15. [19] 李 莹, 杜旭飞, 杜久林. 小胶质细胞的生理特性和功能[J]. 生理学报, 2013, 65(5): 471-82. http://www.cnki.com.cn/Article/CJFDTOTAL-SLXU201305001.htm [20] 黄红伟, 沈 伟. 脂多糖对BV-2细胞的形态及肿瘤坏死因子-α表达的影响[J]. 临床神经病学杂志, 2011, 24(5): 365-7. http://www.cnki.com.cn/Article/CJFDTOTAL-LCSJ201105021.htm [21] He Y, Appel S, Le W. Minocycline inhibits microglial activation and protects nigral cells after 6-hydroxydopamine injection into mouse striatum[J]. Brain Res, 2001, 909(1/2): 187-93. [22] 吴晓平, 张大明, 陈伟良. 口服普萘洛尔治疗婴幼儿头颈部血管瘤的临床效果观察[J]. 口腔疾病防治, 2016, 24(3): 158-61. -
点击查看大图
表(4)
计量
- 文章访问数: 517
- HTML全文浏览量: 191
- PDF下载量: 0
- 被引次数: 0
