中华外科杂志
中華外科雜誌
중화외과잡지
CHINESE JOURNAL OF SURGERY
2014年
3期
193-197
,共5页
黄汉飞%侯美玲%许坚吉%庞天龙%段键%李珍%曾仲%王昆华
黃漢飛%侯美玲%許堅吉%龐天龍%段鍵%李珍%曾仲%王昆華
황한비%후미령%허견길%방천룡%단건%리진%증중%왕곤화
胆管疾病%再灌注损伤%血红素加氧酶-1%新生血管化,生理性
膽管疾病%再灌註損傷%血紅素加氧酶-1%新生血管化,生理性
담관질병%재관주손상%혈홍소가양매-1%신생혈관화,생이성
Bile duct diseases%Reperfusion injury%Heme oxygenase-1%Neovascularization,physiologic
目的 探讨血红素氧合酶-1(HO-1)在大鼠胆道缺血再灌注损伤中对胆道周围血管丛(PVP)的影响.方法 将128只雄性SD大鼠随机分为盐水组(Saline)、空病毒组(Adv)、诱导组(Adv-HO-1)和抑制组(HO-1 siRNA),每组各32只.分别于术前24 h经阴茎背静脉注射生理盐水、空白腺病毒、H0-1腺病毒和siRNA腺病毒0.5 ml,腺病毒注射剂量为2×109 TU/只.再灌注1h及1、7、14 d检测肝功能,Western blot分析HO-1、血管内皮生长因子(VEGF)、基质细胞衍生因子-1α(SDF-1α)和缺氧诱导因子-1α(HIF-1α)蛋白含量,流式细胞仪检测肝脏和外周血内皮祖细胞(EPCs)比例,进行α-平滑肌肌动蛋白(α-SMA)和血管性血友病因子(vWF)免疫荧光双标染色观察胆管周围的微小血管.结果 手术后诱导组肝功能损伤减轻,诱导HIF-1α、SDF-1α和VEGF的高表达(q =5.68 ～7.52,P＜0.01),诱导组术后7d外周血及肝脏中EPCs的比例分别为盐水组的6、9倍(q=12.14、15.26),而抑制组EPCs的比例明显减少(q=4.83、5.07),差异有统计学意义(P＜0.01).诱导组术后14 d胆管周围微小血管密度明显高于抑制组.结论 HO-1能诱导HIF-1α、SDF-1α和VEGF的表达,动员EPCs从骨髓向外周血释放,并向肝脏内迁移促进肝内、外PVP损伤的修复和再生.
目的 探討血紅素氧閤酶-1(HO-1)在大鼠膽道缺血再灌註損傷中對膽道週圍血管叢(PVP)的影響.方法 將128隻雄性SD大鼠隨機分為鹽水組(Saline)、空病毒組(Adv)、誘導組(Adv-HO-1)和抑製組(HO-1 siRNA),每組各32隻.分彆于術前24 h經陰莖揹靜脈註射生理鹽水、空白腺病毒、H0-1腺病毒和siRNA腺病毒0.5 ml,腺病毒註射劑量為2×109 TU/隻.再灌註1h及1、7、14 d檢測肝功能,Western blot分析HO-1、血管內皮生長因子(VEGF)、基質細胞衍生因子-1α(SDF-1α)和缺氧誘導因子-1α(HIF-1α)蛋白含量,流式細胞儀檢測肝髒和外週血內皮祖細胞(EPCs)比例,進行α-平滑肌肌動蛋白(α-SMA)和血管性血友病因子(vWF)免疫熒光雙標染色觀察膽管週圍的微小血管.結果 手術後誘導組肝功能損傷減輕,誘導HIF-1α、SDF-1α和VEGF的高錶達(q =5.68 ～7.52,P＜0.01),誘導組術後7d外週血及肝髒中EPCs的比例分彆為鹽水組的6、9倍(q=12.14、15.26),而抑製組EPCs的比例明顯減少(q=4.83、5.07),差異有統計學意義(P＜0.01).誘導組術後14 d膽管週圍微小血管密度明顯高于抑製組.結論 HO-1能誘導HIF-1α、SDF-1α和VEGF的錶達,動員EPCs從骨髓嚮外週血釋放,併嚮肝髒內遷移促進肝內、外PVP損傷的脩複和再生.
목적 탐토혈홍소양합매-1(HO-1)재대서담도결혈재관주손상중대담도주위혈관총(PVP)적영향.방법 장128지웅성SD대서수궤분위염수조(Saline)、공병독조(Adv)、유도조(Adv-HO-1)화억제조(HO-1 siRNA),매조각32지.분별우술전24 h경음경배정맥주사생리염수、공백선병독、H0-1선병독화siRNA선병독0.5 ml,선병독주사제량위2×109 TU/지.재관주1h급1、7、14 d검측간공능,Western blot분석HO-1、혈관내피생장인자(VEGF)、기질세포연생인자-1α(SDF-1α)화결양유도인자-1α(HIF-1α)단백함량,류식세포의검측간장화외주혈내피조세포(EPCs)비례,진행α-평활기기동단백(α-SMA)화혈관성혈우병인자(vWF)면역형광쌍표염색관찰담관주위적미소혈관.결과 수술후유도조간공능손상감경,유도HIF-1α、SDF-1α화VEGF적고표체(q =5.68 ～7.52,P＜0.01),유도조술후7d외주혈급간장중EPCs적비례분별위염수조적6、9배(q=12.14、15.26),이억제조EPCs적비례명현감소(q=4.83、5.07),차이유통계학의의(P＜0.01).유도조술후14 d담관주위미소혈관밀도명현고우억제조.결론 HO-1능유도HIF-1α、SDF-1α화VEGF적표체,동원EPCs종골수향외주혈석방,병향간장내천이촉진간내、외PVP손상적수복화재생.
Objective To study the effect of heme oxygenase-1 (HO-1) on peribiliary vascular plexus (PVP) in rat bile duct ischemia/reperfusion injury.Methods Total 128 male SD rats were randomly divided into saline group (Saline),empty virus group (Adv),induced group (Adv-HO-1) and suppressed group (HO-1 siRNA),and there were 32 rats in each group.Rats were injected using 0.5 ml of saline,empty adenovirus,HO-1 adenovirus and siRNA adenovirus (2 × 109 TU/rat) via the dorsal penile vein 24 hours before surgery.Liver function was analyzed at 1 hour and 1,7,14 days after reperfusion.HO-1,hypoxiainducible factor-lαt (HIF-1α),stromal cell derived factor-1α (SDF-1α) and vascular endothelial growth factor (VEGF) protein content was analyzed by Western blot.The endothelial progenitor cells (EPCs) ratio in the liver and peripheral blood was detected by flow cytometry.Small vascular around the bile duct was observed by α-smooth muscle actin and yon Willebrand factor double immunofluorescence staining.Results Reduced liver injury and higher expression of HIF-1α,SDF-1α and VEGF in the induced group after surgery (q =5.68-7.52,P ＜0.01).EPCs ratio in the liver and peripheral blood was significantly higher in the induced group than saline group (q =12.14 and 15.26,P ＜ 0.01),and the suppressed group at 7 days after surgery were less than saline group significantly (q =4.83 and 5.07,P ＜ 0.01).In comparison to the suppressed group,higher density of small vascular around the bile duct was seen in the liver tissue of induced group.Conclusions HO-1 can induce the expression of HIF-1α,SDF-1α and VEGF,and mobilize the release of EPCs to the peripheral from the bone marrow.EPCs migrate to the liver and promote damaged PVP repair and regeneration.
