中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2015年
3期
436-440
,共5页
高广荣%张成%吕晨光%张宝磊%张雪峰
高廣榮%張成%呂晨光%張寶磊%張雪峰
고엄영%장성%려신광%장보뢰%장설봉
休克,出血性%PPARγ%热休克蛋白质70%肿瘤坏死因子α%低温复苏
休剋,齣血性%PPARγ%熱休剋蛋白質70%腫瘤壞死因子α%低溫複囌
휴극,출혈성%PPARγ%열휴극단백질70%종류배사인자α%저온복소
Shock,hemorrhagic%PPAR gamma%Heat-shock proteins 70%Tumor necrosis factor-alpha%Hypothermia resuscitation
目的：探讨低温复苏对大鼠失血性休克肝损伤的保护作用及其机制。方法24只成年雄性Wistar大鼠随机平均分为3组，对照组（S）、常温复苏组（N）（37～38℃）和低温复苏组（H）（33～34℃）。S组只进行外科插管操作，不建立失血性休克模型及复苏，N组和H组在建立失血性休克模型后分别在预定温度下进行复苏。Real-time PCR法检测复苏240 min肝组织PPAR-γ、HSP70和TNF-α mRNA表达变化。ELISA法检测血清TNF-α浓度变化。生化法检测血清ALT和AST浓度变化。结果（1）休克复苏240 min大鼠血清TNF-α浓度为S组（8.53±1.90）ng/ml，N组（74.08±8.81）ng/ml，H组（32.13±5.82）ng/ml，两个实验组差异具有统计学意义（P＜0.05）；（2）休克复苏240 min大鼠血清ALT和AST浓度分别为是S组（61±11）U/L、（47±9）U/L，N组（187±20） U/L、（139±15）U/L，H组（141±11）U/L、（97±11）U/L，两个实验组差异有统计学意义（P＜0.05）；（3）与S组比较，休克复苏240 min N组肝组织PPAR-γ mRNA表达量为0.50±0.11，H组PPAR-γmRNA表达量为2.01±0.48（P＜0.05）；（4）与S组比较，休克复苏240 min N组肝组织HSP70 mRNA表达量为4.12±1.36，H组HSP70 mRNA表达量为11.69±3.88（P＜0.05）；（5）与S组比较，休克复苏后240 min N组肝组织TNF-α mRNA表达量为15.10±4.99，H组TNF-α mRNA表达量为10.10±2.95（P＜0.05）。结论失血性休克后的低温复苏能够上调大鼠肝组织内PPAR-γ和HSP70基因的表达，同时抑制TNF-α基因表达，降低血清中TNF-α、ALT和AST的浓度，减轻肝脏损伤，利于休克的复苏。
目的：探討低溫複囌對大鼠失血性休剋肝損傷的保護作用及其機製。方法24隻成年雄性Wistar大鼠隨機平均分為3組，對照組（S）、常溫複囌組（N）（37～38℃）和低溫複囌組（H）（33～34℃）。S組隻進行外科插管操作，不建立失血性休剋模型及複囌，N組和H組在建立失血性休剋模型後分彆在預定溫度下進行複囌。Real-time PCR法檢測複囌240 min肝組織PPAR-γ、HSP70和TNF-α mRNA錶達變化。ELISA法檢測血清TNF-α濃度變化。生化法檢測血清ALT和AST濃度變化。結果（1）休剋複囌240 min大鼠血清TNF-α濃度為S組（8.53±1.90）ng/ml，N組（74.08±8.81）ng/ml，H組（32.13±5.82）ng/ml，兩箇實驗組差異具有統計學意義（P＜0.05）；（2）休剋複囌240 min大鼠血清ALT和AST濃度分彆為是S組（61±11）U/L、（47±9）U/L，N組（187±20） U/L、（139±15）U/L，H組（141±11）U/L、（97±11）U/L，兩箇實驗組差異有統計學意義（P＜0.05）；（3）與S組比較，休剋複囌240 min N組肝組織PPAR-γ mRNA錶達量為0.50±0.11，H組PPAR-γmRNA錶達量為2.01±0.48（P＜0.05）；（4）與S組比較，休剋複囌240 min N組肝組織HSP70 mRNA錶達量為4.12±1.36，H組HSP70 mRNA錶達量為11.69±3.88（P＜0.05）；（5）與S組比較，休剋複囌後240 min N組肝組織TNF-α mRNA錶達量為15.10±4.99，H組TNF-α mRNA錶達量為10.10±2.95（P＜0.05）。結論失血性休剋後的低溫複囌能夠上調大鼠肝組織內PPAR-γ和HSP70基因的錶達，同時抑製TNF-α基因錶達，降低血清中TNF-α、ALT和AST的濃度，減輕肝髒損傷，利于休剋的複囌。
목적：탐토저온복소대대서실혈성휴극간손상적보호작용급기궤제。방법24지성년웅성Wistar대서수궤평균분위3조，대조조（S）、상온복소조（N）（37～38℃）화저온복소조（H）（33～34℃）。S조지진행외과삽관조작，불건립실혈성휴극모형급복소，N조화H조재건립실혈성휴극모형후분별재예정온도하진행복소。Real-time PCR법검측복소240 min간조직PPAR-γ、HSP70화TNF-α mRNA표체변화。ELISA법검측혈청TNF-α농도변화。생화법검측혈청ALT화AST농도변화。결과（1）휴극복소240 min대서혈청TNF-α농도위S조（8.53±1.90）ng/ml，N조（74.08±8.81）ng/ml，H조（32.13±5.82）ng/ml，량개실험조차이구유통계학의의（P＜0.05）；（2）휴극복소240 min대서혈청ALT화AST농도분별위시S조（61±11）U/L、（47±9）U/L，N조（187±20） U/L、（139±15）U/L，H조（141±11）U/L、（97±11）U/L，량개실험조차이유통계학의의（P＜0.05）；（3）여S조비교，휴극복소240 min N조간조직PPAR-γ mRNA표체량위0.50±0.11，H조PPAR-γmRNA표체량위2.01±0.48（P＜0.05）；（4）여S조비교，휴극복소240 min N조간조직HSP70 mRNA표체량위4.12±1.36，H조HSP70 mRNA표체량위11.69±3.88（P＜0.05）；（5）여S조비교，휴극복소후240 min N조간조직TNF-α mRNA표체량위15.10±4.99，H조TNF-α mRNA표체량위10.10±2.95（P＜0.05）。결론실혈성휴극후적저온복소능구상조대서간조직내PPAR-γ화HSP70기인적표체，동시억제TNF-α기인표체，강저혈청중TNF-α、ALT화AST적농도，감경간장손상，리우휴극적복소。
Objective The aim was to investigate the protective effect and mechanism of hypothermia resuscitation on hepatic injury of hemorrhagic shock in rats.Methods 24 adult male Wistar rats were randomly assigned to three groups: control group(S), normalthermia group(N) and hypothermia group(H). Rats in the control group underwent the surgical procedure but were not bled. Rats in the normal thermia group and hypothermia group were received normal thermia (37-38℃) resuscitation or hypothermia (33-34℃) resuscitation respectively during resuscitation and hourly thereafter. Real-time PCR method detected the PPAR-γ, HSP70 and TNF-α mRNA expression in the rat hepatic tissues after resuscitation 240 minutes of hemorrhagic shock. The serum contents of TNF-α was assayed with ELISA. The serum contents of ALT and AST were assayed with biochemical methods.Results (1) The serum contents of TNF-α after 240 min of resuscitation was S group(8.53±1.90)ng/ml, N group (74.08±8.81)ng/ml, H group (32.13±5.82)ng/ml, the H group was lower than the N group (P<0.05); (2) The serum contents of ALT and AST after 240 min of resuscitation were S group (61±11)U/L, (47±9)U/L, N group (187±20)U/L, (139±15)U/L, H group (141±11)U/L, (97±11)U/L, the H group was lower than the N group (P<0.05); (3)compared with the control group, PPAR-γ mRNA expression in the N group and H group were 0.50±0.11 and 2.01±0.48 (P<0.05) after resuscitation 240 minutes of hemorrhagic shock; (4) compared with the control group, HSP70 mRNA expression in the N group and H group were 4.12±1.36 and 11.69±3.88 (P<0.05) after resuscitation 240 minutes of hemorrhagic shock; (5)compared with the control group, TNF-α mRNA expression in the NR group and HR group were 15.10±4.99 and 10.10±2.95 (P<0.05) after resuscitation 240 minutes of hemorrhagic shock (P<0.05).ConclusionHypothermia resuscitation after hemorrhagic shock can raise the PPAR-γ and HSP70 gene expression and inhibit TNF-α gene expression in the rat hepatic tissues. Hypothermia resuscitation also can inhibit the serum contents of TNF-α, ALT and AST. Hypothermia resuscitation can protect the hepatic function and was salutary effects for hemorrhagic shock.
