CAJ | 학술논문

目的：探讨刺五加注射液（acanthopanax senticosus injection, ASI）对肝脏缺血再灌注大鼠肝组织氧化应激和细胞凋亡的影响。方法100只大鼠按随机数字表法分为假手术组，模型组，刺五加注射液高、中、低剂量组，每组20只。造模前7 d，ASI高、中、低剂量组分别腹腔注射ASI 40、80和120 mg/kg，假手术组和模型组腹腔注射等体积生理盐水。采用无创动脉夹夹闭法制备大鼠肝脏局部缺血再灌注模型。再灌注2 h后，检测肝组织超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、谷胱甘肽硫转移酶（GST）、丙二醛（MDA）水平以及血清丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）水平；HE染色法观察肝组织病理学改变；TUNEL染色法检测肝组织细胞凋亡。结果与模型组比较，ASI中、高剂量组肝组织 SOD[(11.16±2.31)U/mg、(10.63±1.92)U/mg 比(7.34±1.78)U/mg；P＜0.01或 P＜0.05]、GSH-Px[(15.48±2..91)U/mg、(13.23±1.87)U/mg比(10.35±2.04)U/mg；P＜0.01或P＜0.05]、GST[(1.76±0.25)U/mg、(1.55±0.22)U/mg 比(0.94±0.18)U/mg；P＜0.01或 P＜0.05]水平显著增高， MDA[(4.67±1.24)nmol/mg、(4.93±1.53)nmol/mg比（10.29±2.41)nmol/mg；P＜0.01或P＜0.05]水平显著下降，血清ALT[(671.82±338.37)U/L、(803.91±441.63)U/L比(1416.22±538.94)U/L；P＜0.01或P＜0.05]、AST[(329.02±161.88)U/L、(417.26±182.37)U/L比(751.93±262.75)U/L；P＜0.01或P＜0.05]水平显著降低；ASI高、中、低剂量组肝组织病理学改变和细胞凋亡均减轻。结论 ASI可减轻肝组织氧化应激，改善肝组织病理损伤，抑制肝细胞凋亡，保护肝脏缺血再灌注大鼠。
목적：탐토자오가주사액（acanthopanax senticosus injection, ASI）대간장결혈재관주대서간조직양화응격화세포조망적영향。방법100지대서안수궤수자표법분위가수술조，모형조，자오가주사액고、중、저제량조，매조20지。조모전7 d，ASI고、중、저제량조분별복강주사ASI 40、80화120 mg/kg，가수술조화모형조복강주사등체적생리염수。채용무창동맥협협폐법제비대서간장국부결혈재관주모형。재관주2 h후，검측간조직초양화물기화매（SOD）、곡광감태과양화물매（GSH-Px）、곡광감태류전이매（GST）、병이철（MDA）수평이급혈청병안산전안매（ALT）화천동안산전안매（AST）수평；HE염색법관찰간조직병이학개변；TUNEL염색법검측간조직세포조망。결과여모형조비교，ASI중、고제량조간조직 SOD[(11.16±2.31)U/mg、(10.63±1.92)U/mg 비(7.34±1.78)U/mg；P＜0.01혹 P＜0.05]、GSH-Px[(15.48±2..91)U/mg、(13.23±1.87)U/mg비(10.35±2.04)U/mg；P＜0.01혹P＜0.05]、GST[(1.76±0.25)U/mg、(1.55±0.22)U/mg 비(0.94±0.18)U/mg；P＜0.01혹 P＜0.05]수평현저증고， MDA[(4.67±1.24)nmol/mg、(4.93±1.53)nmol/mg비（10.29±2.41)nmol/mg；P＜0.01혹P＜0.05]수평현저하강，혈청ALT[(671.82±338.37)U/L、(803.91±441.63)U/L비(1416.22±538.94)U/L；P＜0.01혹P＜0.05]、AST[(329.02±161.88)U/L、(417.26±182.37)U/L비(751.93±262.75)U/L；P＜0.01혹P＜0.05]수평현저강저；ASI고、중、저제량조간조직병이학개변화세포조망균감경。결론 ASI가감경간조직양화응격，개선간조직병리손상，억제간세포조망，보호간장결혈재관주대서。
Objective To investigate the effects of Acanthopanax Senticosus Injection (ASI) on free radical metabolism and apoptosis in the hepatic tissue after hepatic ischemia-reperfusion in rats.Methods A total of 100 rats were randomly divided into 5 groups: a sham operation group, a model group, and groups of high-, medium- and low-dose ASI, 20 rats in each group. Seven days before modeling, the drugs had been given by intraperitoneal injection. The rats in the high-, medium- and low-dose groups were given ASI 40, 80 and 120 mg/kg, respectively, and the rats in the sham operation and model groups were given equivalent volume of normal saline. A rat model of hepatic ischemia reperfusion was induced by partial hepatic pedicle clamping followed by reperfusion. 2 h after reperfusion, the activities of SOD, GSH-Px, GST and the MDA level in the hepatic tissue were determined; the activities of ALT and AST in serum were also determined; the histopathological changes and hepatocyte apoptosis were observed using the HE staining and the TUNEL staining, respectively.Results In comparison with the model group, the activities of SOD (11.16 ± 2.31 U/mg, 10.63 ± 1.92 U/mgvs.7.34 ± 1.78 U/mg;P<0.01 orP<0.05), GSH-Px (15.48 ± 2..91 U/mg, 13.23 ± 1.87 U/mgvs. 10.35 ± 2.04 U/mg;P<0.01 orP<0.05), GST(1.76 ± 0.25 U/mg, 1.55 ± 0.22 U/mgvs.0.94 ± 0.18 U/mg;P<0.01 orP<0.05) in the hepatic tissue in the ASI high- and medium-dose groups were significantly increased; and the MDA level in the hepatic tissue significantly decreased (4.67 ± 1.24 nmol/mg, 4.93 ± 1.53 nmol/mgvs.10.29 ± 2.41 nmol/mg); the serum levels of ALT(671.82 ± 338.37 U/L, 803.91 ± 441.63 U/Lvs.1 416.22 ± 538.94 U/L;P<0.01 orP<0.05), AST(329.02 ± 161.88 U/L, 417.26 ± 182.37 U/Lvs.751.93 ± 262.75 U/L;P<0.01 or P<0.05) were significantly decreased; the histopathological changes and hepatocyte apoptosis in the ASI high-, medium - and low-dose groups were significantly reduced.Conclusions ASI could effectively attenuate oxidative stress in the, improve the histopathological changes, inhibit hepatocyte apoptosis, and protect against hepatic ischemia reperfusion injury in rats.