国际中医中药杂志
國際中醫中藥雜誌
국제중의중약잡지
INTERNATIONAL JOURNAL OF TRIDITIONAL CHINESE MEDICINE
2015年
3期
243-246
,共4页
肝疾病%缺血再灌注%刺五加注射液%氧化性应激%大鼠
肝疾病%缺血再灌註%刺五加註射液%氧化性應激%大鼠
간질병%결혈재관주%자오가주사액%양화성응격%대서
Liver diseases%Reperfusion injury%Ci Wu Jia Zhu She Ye%Oxidative stress%Rats
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。
目的:探討刺五加註射液(acanthopanax senticosus injection, ASI)對肝髒缺血再灌註大鼠肝組織氧化應激和細胞凋亡的影響。方法100隻大鼠按隨機數字錶法分為假手術組,模型組,刺五加註射液高、中、低劑量組,每組20隻。造模前7 d,ASI高、中、低劑量組分彆腹腔註射ASI 40、80和120 mg/kg,假手術組和模型組腹腔註射等體積生理鹽水。採用無創動脈夾夾閉法製備大鼠肝髒跼部缺血再灌註模型。再灌註2 h後,檢測肝組織超氧化物歧化酶(SOD)、穀胱甘肽過氧化物酶(GSH-Px)、穀胱甘肽硫轉移酶(GST)、丙二醛(MDA)水平以及血清丙氨痠轉氨酶(ALT)和天鼕氨痠轉氨酶(AST)水平;HE染色法觀察肝組織病理學改變;TUNEL染色法檢測肝組織細胞凋亡。結果與模型組比較,ASI中、高劑量組肝組織 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]水平顯著增高, 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]水平顯著下降,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]水平顯著降低;ASI高、中、低劑量組肝組織病理學改變和細胞凋亡均減輕。結論 ASI可減輕肝組織氧化應激,改善肝組織病理損傷,抑製肝細胞凋亡,保護肝髒缺血再灌註大鼠。
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.