中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
Chinese Journal of Clinical Nutrition
2015年
4期
224-228
,共5页
陈英杰%谢良杰%庄耀东%郭森仁
陳英傑%謝良傑%莊耀東%郭森仁
진영걸%사량걸%장요동%곽삼인
重型颅脑损伤%ω-3多不饱和脂肪酸%炎症反应%神经保护
重型顱腦損傷%ω-3多不飽和脂肪痠%炎癥反應%神經保護
중형로뇌손상%ω-3다불포화지방산%염증반응%신경보호
Severe traumatic brain injury%Omega-3 polyunsaturated fatty acids%Inflammatory response%Neuroprotection
目的 探讨ω-3多不饱和脂肪酸对重型颅脑损伤患者炎症反应、神经损害及预后的影响.方法 2013年1月至2014年9月福建中医药大学附属晋江中医院收治的重型颅脑损伤患者120例,随机数字表法随机分为试验组(添加ω-3脂肪酸脑损伤组60例)和对照组(未添加ω-3脂肪酸脑损伤组60例).另选择60份健康体检血液标本作为健康人群组.利用酶联免疫吸附测定法检测血清肿瘤坏死因子(TNF)-α、白细胞介素(IL)-I、IL-6、S100B蛋白和神经元特异性烯醇化酶(NSE)浓度,比较两组患者格拉斯哥昏迷指数评分(GCS评分)、急性生理学及慢性健康状况(APACHEⅡ)评分和预后.结果 重型颅脑损伤患者伤后各时点血清TNF-α、IL-1、IL-6和神经损伤标志物S100B和NSE蛋白表达明显高于健康人群组(均P＜0.05).试验组患者在干预3d后TNF-α、IL-1、IL-6表达明显低于对照组患者[(213.81 ±29.33)μg/L比(267.76 ±31.35) μg/L, (121.81±10.63) μg/L比(152.60±11.45)μg/L, (81.89 ±8.34) μg/L比(106.62±10.35)μg/L,均P＜0.05],S100B和NSE蛋白表达在干预7d后表达低于对照组[(1.32±0.09) μg/L比(1.67±0.12) μg/L,(12.57±1.53) μg/L比(17.57±2.30) μg/L,均P＜0.05];在干预第14天时,试验组GCS评分高于对照组[(9.32±1.64)分比(7.14±1.30)分,P=0.02],APACHEⅡ评分低于对照组[(14.37±2.27)分比(17.00±1.85)分,P=0.04].随访1个月时,试验组病死率低于对照组[11.7％ (7/60)比15.0％ (9/60)],但差异无统计学意义(P=0.49).结论 对重型颅脑损伤患者,ω-3不饱和脂肪酸可通过减轻伤后炎症反应,减少神经胶质和神经元细胞损害,起到神经保护作用,值得临床推广应用.
目的 探討ω-3多不飽和脂肪痠對重型顱腦損傷患者炎癥反應、神經損害及預後的影響.方法 2013年1月至2014年9月福建中醫藥大學附屬晉江中醫院收治的重型顱腦損傷患者120例,隨機數字錶法隨機分為試驗組(添加ω-3脂肪痠腦損傷組60例)和對照組(未添加ω-3脂肪痠腦損傷組60例).另選擇60份健康體檢血液標本作為健康人群組.利用酶聯免疫吸附測定法檢測血清腫瘤壞死因子(TNF)-α、白細胞介素(IL)-I、IL-6、S100B蛋白和神經元特異性烯醇化酶(NSE)濃度,比較兩組患者格拉斯哥昏迷指數評分(GCS評分)、急性生理學及慢性健康狀況(APACHEⅡ)評分和預後.結果 重型顱腦損傷患者傷後各時點血清TNF-α、IL-1、IL-6和神經損傷標誌物S100B和NSE蛋白錶達明顯高于健康人群組(均P＜0.05).試驗組患者在榦預3d後TNF-α、IL-1、IL-6錶達明顯低于對照組患者[(213.81 ±29.33)μg/L比(267.76 ±31.35) μg/L, (121.81±10.63) μg/L比(152.60±11.45)μg/L, (81.89 ±8.34) μg/L比(106.62±10.35)μg/L,均P＜0.05],S100B和NSE蛋白錶達在榦預7d後錶達低于對照組[(1.32±0.09) μg/L比(1.67±0.12) μg/L,(12.57±1.53) μg/L比(17.57±2.30) μg/L,均P＜0.05];在榦預第14天時,試驗組GCS評分高于對照組[(9.32±1.64)分比(7.14±1.30)分,P=0.02],APACHEⅡ評分低于對照組[(14.37±2.27)分比(17.00±1.85)分,P=0.04].隨訪1箇月時,試驗組病死率低于對照組[11.7％ (7/60)比15.0％ (9/60)],但差異無統計學意義(P=0.49).結論 對重型顱腦損傷患者,ω-3不飽和脂肪痠可通過減輕傷後炎癥反應,減少神經膠質和神經元細胞損害,起到神經保護作用,值得臨床推廣應用.
목적 탐토ω-3다불포화지방산대중형로뇌손상환자염증반응、신경손해급예후적영향.방법 2013년1월지2014년9월복건중의약대학부속진강중의원수치적중형로뇌손상환자120례,수궤수자표법수궤분위시험조(첨가ω-3지방산뇌손상조60례)화대조조(미첨가ω-3지방산뇌손상조60례).령선택60빈건강체검혈액표본작위건강인군조.이용매련면역흡부측정법검측혈청종류배사인자(TNF)-α、백세포개소(IL)-I、IL-6、S100B단백화신경원특이성희순화매(NSE)농도,비교량조환자격랍사가혼미지수평분(GCS평분)、급성생이학급만성건강상황(APACHEⅡ)평분화예후.결과 중형로뇌손상환자상후각시점혈청TNF-α、IL-1、IL-6화신경손상표지물S100B화NSE단백표체명현고우건강인군조(균P＜0.05).시험조환자재간예3d후TNF-α、IL-1、IL-6표체명현저우대조조환자[(213.81 ±29.33)μg/L비(267.76 ±31.35) μg/L, (121.81±10.63) μg/L비(152.60±11.45)μg/L, (81.89 ±8.34) μg/L비(106.62±10.35)μg/L,균P＜0.05],S100B화NSE단백표체재간예7d후표체저우대조조[(1.32±0.09) μg/L비(1.67±0.12) μg/L,(12.57±1.53) μg/L비(17.57±2.30) μg/L,균P＜0.05];재간예제14천시,시험조GCS평분고우대조조[(9.32±1.64)분비(7.14±1.30)분,P=0.02],APACHEⅡ평분저우대조조[(14.37±2.27)분비(17.00±1.85)분,P=0.04].수방1개월시,시험조병사솔저우대조조[11.7％ (7/60)비15.0％ (9/60)],단차이무통계학의의(P=0.49).결론 대중형로뇌손상환자,ω-3불포화지방산가통과감경상후염증반응,감소신경효질화신경원세포손해,기도신경보호작용,치득림상추엄응용.
Objective To investigate the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFA) on inflammatory response,nerve damage,and outcomes in patients with severe traumatic brain injury (sTBI).Methods Altogether 120 sTBI patients were selected from January 2013 to September 2014 in Jinjiang Hospital of Traditional Chinese Medicine and divided with a random number table into experimental group (with ω-3 PUFA supplementation,n =60) and control group (without ω-3 PUFA supplementation,n =60).Sixty blood samples from healthy people visiting the physical examination clinic were collected as normal controls.The serum levels of tumor necrosis factor-α (TNF-α),interleukin (IL)-1,IL-6,S100B and neuron-specific enolase (NSE) were detected with enzyme-linked immunosorbent assay (ELISA).Glasgow Coma Scale (GCS) score,Acute Physiology and Chronic Health Evaluation (APACHE) Ⅱ score and outcomes of the two groups were compared.Results The serum levels ofTNF-α,IL-1,IL-6,S100B,and NSE protein significantly increased in patients with sTBI compared with the normal controls (all P ＜ 0.05).Compared with the control group,the serum levels of inflammatory related factors (TNF-α,IL-1,IL-6) in the experimental group were significantly decreased on the 3rd day [(213.81 ±29.33) μg/L vs.(267.76 ±31.35) μg/L,(121.81 ± 10.63) μg/L vs.(152.60 ± 11.45) μg/L,(81.89 ± 8.34) μg/L vs.(106.62 ± 10.35) μg/L,all P ＜ 0.05],S100B and NSE protein expressions were significantly decreased on the 7th day [(1.32 ± 0.09) μg/L vs.(1.67 ± 0.12) μg/L,(12.57 ± 1.53) μg/L vs.(17.57 ±2.30) μg/L,both P ＜0.05].Compresd with the control group,the experimental group showed significantly higher GCS scores (9.32 ± 1.64 vs.7.14 ± 1.30,P =0.02) and significantly lower APACHE Ⅱ scores (14.37 ± 2.27 vs.17.00 ± 1.85,P =0.04) on the 14th day.Compresd with the control group,the experimental group showed lower mortality during the follow-up [11.7％ (7/60) vs.15.0％ (9/60)],but with no significant differences (P =0.49).Conclusion Supplementation of ω-3 PUFA could exert neuroprotective effect by effectively regulating inflammatory response and reducing the damages to glia and neurons in patients with sTBI,which is a promising agent for clinical application.
