国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2014年
3期
210-212,216
,共4页
于齐宏%王君涛%杜奕奇%李兆申
于齊宏%王君濤%杜奕奇%李兆申
우제굉%왕군도%두혁기%리조신
α-硫辛酸%重症急性胰腺炎%脑保护
α-硫辛痠%重癥急性胰腺炎%腦保護
α-류신산%중증급성이선염%뇌보호
Alpha-lipoic acid%Severe acute pancreatitis%Brain protection
目的 观察α-硫辛酸(alpha-lipoic acid,α-LA)对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠脑损伤是否具有保护作用并探讨相关机制. 方法 采用经胰胆管注射5％牛磺胆酸钠(sodium taurocholate hydrate,ST)诱发SAP大鼠脑损伤模型,将36只SD大鼠按随机数字表法分为3组,每组12只:假手术组(Sham组)、SAP组和α-LA治疗组(α-LA组).造模12 h后观察各组大鼠脑组织水含量、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)含量、丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)活性及核转录因子-κB(nuclear transcription factor-kappa B,NF-κB)水平的变化. 结果 Sham组大鼠脑组织水含量、TNF-α含量、MDA含量、SOD活性分别为(74.2±1.4)％、(375±79) ng/L、(0.91±0.07)、(156±43) nmol/ml; NF-κB蛋白表达水平为(3.2±1.1)％.SAP组大鼠脑组织水含量、TNF-α含量、MDA含量、SOD活性分别为(81.9±1.6)％、(891±134) ng/L、(1.42±0.11)、(97±34) nmol/ml,NF-κB蛋白表达水平为(28±4)％;与Sham组比较,差异均有统计学意义(P＜0.05).与SAP组比较,α-LA干预可以显著减轻脑组织氧化损伤水平,α-LA组MDA含量与SOD活性分别为(1.05±0.10)、(118±38) nmol/ml,减少细胞因子TNF-α含量(564±119) ng/L及下NF-κB表达水平(P＜0.05). 结论 α-LA对SAP诱发的大鼠脑损伤具有一定的保护作用.
目的 觀察α-硫辛痠(alpha-lipoic acid,α-LA)對重癥急性胰腺炎(severe acute pancreatitis,SAP)大鼠腦損傷是否具有保護作用併探討相關機製. 方法 採用經胰膽管註射5％牛磺膽痠鈉(sodium taurocholate hydrate,ST)誘髮SAP大鼠腦損傷模型,將36隻SD大鼠按隨機數字錶法分為3組,每組12隻:假手術組(Sham組)、SAP組和α-LA治療組(α-LA組).造模12 h後觀察各組大鼠腦組織水含量、腫瘤壞死因子-α(tumor necrosis factor-α,TNF-α)含量、丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)活性及覈轉錄因子-κB(nuclear transcription factor-kappa B,NF-κB)水平的變化. 結果 Sham組大鼠腦組織水含量、TNF-α含量、MDA含量、SOD活性分彆為(74.2±1.4)％、(375±79) ng/L、(0.91±0.07)、(156±43) nmol/ml; NF-κB蛋白錶達水平為(3.2±1.1)％.SAP組大鼠腦組織水含量、TNF-α含量、MDA含量、SOD活性分彆為(81.9±1.6)％、(891±134) ng/L、(1.42±0.11)、(97±34) nmol/ml,NF-κB蛋白錶達水平為(28±4)％;與Sham組比較,差異均有統計學意義(P＜0.05).與SAP組比較,α-LA榦預可以顯著減輕腦組織氧化損傷水平,α-LA組MDA含量與SOD活性分彆為(1.05±0.10)、(118±38) nmol/ml,減少細胞因子TNF-α含量(564±119) ng/L及下NF-κB錶達水平(P＜0.05). 結論 α-LA對SAP誘髮的大鼠腦損傷具有一定的保護作用.
목적 관찰α-류신산(alpha-lipoic acid,α-LA)대중증급성이선염(severe acute pancreatitis,SAP)대서뇌손상시부구유보호작용병탐토상관궤제. 방법 채용경이담관주사5％우광담산납(sodium taurocholate hydrate,ST)유발SAP대서뇌손상모형,장36지SD대서안수궤수자표법분위3조,매조12지:가수술조(Sham조)、SAP조화α-LA치료조(α-LA조).조모12 h후관찰각조대서뇌조직수함량、종류배사인자-α(tumor necrosis factor-α,TNF-α)함량、병이철(malondialdehyde,MDA)함량、초양화물기화매(superoxide dismutase,SOD)활성급핵전록인자-κB(nuclear transcription factor-kappa B,NF-κB)수평적변화. 결과 Sham조대서뇌조직수함량、TNF-α함량、MDA함량、SOD활성분별위(74.2±1.4)％、(375±79) ng/L、(0.91±0.07)、(156±43) nmol/ml; NF-κB단백표체수평위(3.2±1.1)％.SAP조대서뇌조직수함량、TNF-α함량、MDA함량、SOD활성분별위(81.9±1.6)％、(891±134) ng/L、(1.42±0.11)、(97±34) nmol/ml,NF-κB단백표체수평위(28±4)％;여Sham조비교,차이균유통계학의의(P＜0.05).여SAP조비교,α-LA간예가이현저감경뇌조직양화손상수평,α-LA조MDA함량여SOD활성분별위(1.05±0.10)、(118±38) nmol/ml,감소세포인자TNF-α함량(564±119) ng/L급하NF-κB표체수평(P＜0.05). 결론 α-LA대SAP유발적대서뇌손상구유일정적보호작용.
Objective To investigate the effect of alpha-lipoic acid (α-LA) on brain injury induced by severe acute pancreatitis (SAP) in rats.Methods Severe acute pancreatitis model was induced by retrograde injection of 5％ sodium taurocholate into the pancreatobiliary duct.Thirty-six SD rats were randomly divided into sham operation group (Sham group),severe acute pancreatitis (SAP group) and α-LA treatment group (α-LA group).Each rat brain tissue was taken 12 h later to detect the content of tumor necrosis factor-α (TNF-α) and malondialdehyde (MDA),superoxide dismutase (SOD) activity and nuclear transcription factor kappa B(NF-κB) level changes.Results The content of brain water,TNF-α,MDA,SOD activity were (74.2± 1.4)％,(375±79) ng/L,(0.91±0.07),(156±43) nmol/ml respectively and the expression level of NF-κB protein was (3.2±1.1)％ in brain tissues of sham group.Compared with the sham group,these indicators significant changes in SAP group and the content of brain water,TNF-α,MDA,SOD activity and expression level of NF-κB protein were (81.9± 1.6)％,(891 ± 134) ng/L,(1.42±0.11),(97±34) nmol/ml,(28±4)％ respectively.Compared with SAP group,α-LA significantly reduced the level of oxidative damage[the content of MDA and SOD activity were (1.05±0.10),(118±38) nmol/ml respectively],TNF-α content (564±119) ng/L and lowered NF-κB expression in brain tissue(P＜0.05).Conclusions The results suggest that α-LA can protect against brain injury induced by SAP in rats.
