中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2009年
6期
510-513
,共4页
宋朝彦%崔建忠%孙东明%王春生
宋朝彥%崔建忠%孫東明%王春生
송조언%최건충%손동명%왕춘생
脑损伤%一氧化氮合酶%大鼠
腦損傷%一氧化氮閤酶%大鼠
뇌손상%일양화담합매%대서
Brain injuries%Nitric oxide synthase%Rats
目的 探讨大鼠创伤性颅脑损伤(traumatic brain injury,TBI)后神经元型一氧化氮合酶(nNOS)及诱生型一氧化氮合酶(iNOS)之间相瓦影响的作用机制.方法 雄性Wistar大鼠250只采用成组设计方法分成假手术组、创伤组、7-硝基吲唑(7-NI)治疗组、氨基胍(AG)治疗组、AG和7-NI联合治疗组共5组,用Marmarou方法造成大鼠TBI,伤后1,3,6,12 h、1,3,7,14 d采用免疫组织化学检测海马CAI区nNOS和iNOS蛋白表达情况.结果 各组nNOS表达在伤后6 h均达高峰,各组高峰值差异无统计学意义(P>0.05),在伤后12 h 7-NI治疗组与创伤组差异无统计学意义(P>0.05),AG治疗组与联合治疗组高于创伤组(P<0.05).各组iNOS表达在伤后3 d达高峰,各治疗组高峰值均低于创伤组(P<0.05).结论 大鼠TBI后nNOS和iNOS之间通过NO的反馈机制相互影响,nNOS活性的增强是iNOS表达的始动因子之一,iNOS活性增强可以下调nNOS的表达.
目的 探討大鼠創傷性顱腦損傷(traumatic brain injury,TBI)後神經元型一氧化氮閤酶(nNOS)及誘生型一氧化氮閤酶(iNOS)之間相瓦影響的作用機製.方法 雄性Wistar大鼠250隻採用成組設計方法分成假手術組、創傷組、7-硝基吲唑(7-NI)治療組、氨基胍(AG)治療組、AG和7-NI聯閤治療組共5組,用Marmarou方法造成大鼠TBI,傷後1,3,6,12 h、1,3,7,14 d採用免疫組織化學檢測海馬CAI區nNOS和iNOS蛋白錶達情況.結果 各組nNOS錶達在傷後6 h均達高峰,各組高峰值差異無統計學意義(P>0.05),在傷後12 h 7-NI治療組與創傷組差異無統計學意義(P>0.05),AG治療組與聯閤治療組高于創傷組(P<0.05).各組iNOS錶達在傷後3 d達高峰,各治療組高峰值均低于創傷組(P<0.05).結論 大鼠TBI後nNOS和iNOS之間通過NO的反饋機製相互影響,nNOS活性的增彊是iNOS錶達的始動因子之一,iNOS活性增彊可以下調nNOS的錶達.
목적 탐토대서창상성로뇌손상(traumatic brain injury,TBI)후신경원형일양화담합매(nNOS)급유생형일양화담합매(iNOS)지간상와영향적작용궤제.방법 웅성Wistar대서250지채용성조설계방법분성가수술조、창상조、7-초기신서(7-NI)치료조、안기고(AG)치료조、AG화7-NI연합치료조공5조,용Marmarou방법조성대서TBI,상후1,3,6,12 h、1,3,7,14 d채용면역조직화학검측해마CAI구nNOS화iNOS단백표체정황.결과 각조nNOS표체재상후6 h균체고봉,각조고봉치차이무통계학의의(P>0.05),재상후12 h 7-NI치료조여창상조차이무통계학의의(P>0.05),AG치료조여연합치료조고우창상조(P<0.05).각조iNOS표체재상후3 d체고봉,각치료조고봉치균저우창상조(P<0.05).결론 대서TBI후nNOS화iNOS지간통과NO적반궤궤제상호영향,nNOS활성적증강시iNOS표체적시동인자지일,iNOS활성증강가이하조nNOS적표체.
Objective To study the mechanism of interaction between neuronal nitric oxide syn-thase (nNOS) and inducible nitric oxide synthase (iNOS) following traumatic brain injury (TBI) in rats. Methods A total of 250 male Wistar rats were randomly divided into five groups, ie, sham oper-ation group, trauma group, 7-nitroindazole (7-NI) treatment group, aminoguanidine (AG) treatment group and combined AG and 7-NI treatment group. Severe closed TBI was made by using Marmarou meth-od. Protein expressions of nNOS and iNOS in hippocampus CAI were detected by means of immunohisto-chemical staining at 1,3, 6, 12 hours and at days 1,3, 7 and 14 after TBI. Results The expression of nNOS reached a peak at 6 hour after injury in all groups, with no statistical difference between groups (P > 0. 05), when there was no statistical difference between 7-NI treatment group and trauma group (P > 0. 05) but statistical difference in AG treatment group and combined AG and 7-NI treatment group compared with trauma group at 12 hours after TBI (P <0.05). The expression of iNOS reached maximal level at day 3 after TBI, with lower level in 7-NI group, AG treatment group and combined AG and 7-NI treatment group compared with trauma group (P < 0.05). Conclusions After TBI, nNOS interacts with iNOS by means of the feedback of nitric oxide. The enhanced expression of nNOS is initial factor for increase of iNOS expression, which can down regulate the expression of iNOS.
