中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2015年
8期
748-752
,共5页
张礼均%胡荣%李飞%孟辉%林江凯%朱刚%冯华
張禮均%鬍榮%李飛%孟輝%林江凱%硃剛%馮華
장례균%호영%리비%맹휘%림강개%주강%풍화
脑损伤%自噬%去铁胺
腦損傷%自噬%去鐵胺
뇌손상%자서%거철알
Brain injuries%Autophagy%Deferoxamine
目的 探讨去铁胺对大鼠脑冲击伤后脑组织自噬损伤的影响. 方法 选择健康成年雄性SD大鼠39只,按随机数字表法分为假手术组、致伤组和去铁胺治疗组,每组13只大鼠.参照Feeney法建立大鼠脑冲击伤模型,致伤后2h分别予以等量等渗盐水及去铁胺(100 mg/kg)腹腔注射,间隔12h给药,持续28 d.并于伤后1,3,7,14,28 d检测大鼠血红蛋白、肛温、血糖和死亡率.动物处死前完成Morris水迷宫实验,后取大鼠大脑标本计算大脑缺损体积.取致伤灶周围脑组织,采用免疫组化和Western blot方法检测Beclin 1的表达. 结果 各组大鼠同一时相点血红蛋白、肛温、血糖差异均无统计学意义(P>0.05),致伤组和去铁胺治疗组死亡率差异无统计学意义;去铁胺治疗组大脑缺损体积为(115.35±13.70) mm3,较致伤组的(209.99±16.70)mm明显减小(P <0.05);Morris水迷宫试验显示,去铁胺治疗组动物平台搜索策略(3.13±0.35)和搜索时间[(36.15±26.63)s]均较致伤组[分别为2.13±0.64和(110±47.34)s]显著改善(P<0.05);免疫组化显示,致伤后Beclin 1表达显著上调,予去铁胺治疗后,Beclin 1显著下调;进一步Western blot定量检测显示,伤后Beclin 1表达显著增强(P<0.05),去铁胺治疗后,其表达显著下调(P<0.01). 结论 大鼠大脑冲击伤后Beclin 1表达上调,提示脑冲击伤后自噬损伤增强,去铁胺的治疗效果可能是通过减轻自噬损伤来实现的.
目的 探討去鐵胺對大鼠腦遲擊傷後腦組織自噬損傷的影響. 方法 選擇健康成年雄性SD大鼠39隻,按隨機數字錶法分為假手術組、緻傷組和去鐵胺治療組,每組13隻大鼠.參照Feeney法建立大鼠腦遲擊傷模型,緻傷後2h分彆予以等量等滲鹽水及去鐵胺(100 mg/kg)腹腔註射,間隔12h給藥,持續28 d.併于傷後1,3,7,14,28 d檢測大鼠血紅蛋白、肛溫、血糖和死亡率.動物處死前完成Morris水迷宮實驗,後取大鼠大腦標本計算大腦缺損體積.取緻傷竈週圍腦組織,採用免疫組化和Western blot方法檢測Beclin 1的錶達. 結果 各組大鼠同一時相點血紅蛋白、肛溫、血糖差異均無統計學意義(P>0.05),緻傷組和去鐵胺治療組死亡率差異無統計學意義;去鐵胺治療組大腦缺損體積為(115.35±13.70) mm3,較緻傷組的(209.99±16.70)mm明顯減小(P <0.05);Morris水迷宮試驗顯示,去鐵胺治療組動物平檯搜索策略(3.13±0.35)和搜索時間[(36.15±26.63)s]均較緻傷組[分彆為2.13±0.64和(110±47.34)s]顯著改善(P<0.05);免疫組化顯示,緻傷後Beclin 1錶達顯著上調,予去鐵胺治療後,Beclin 1顯著下調;進一步Western blot定量檢測顯示,傷後Beclin 1錶達顯著增彊(P<0.05),去鐵胺治療後,其錶達顯著下調(P<0.01). 結論 大鼠大腦遲擊傷後Beclin 1錶達上調,提示腦遲擊傷後自噬損傷增彊,去鐵胺的治療效果可能是通過減輕自噬損傷來實現的.
목적 탐토거철알대대서뇌충격상후뇌조직자서손상적영향. 방법 선택건강성년웅성SD대서39지,안수궤수자표법분위가수술조、치상조화거철알치료조,매조13지대서.삼조Feeney법건립대서뇌충격상모형,치상후2h분별여이등량등삼염수급거철알(100 mg/kg)복강주사,간격12h급약,지속28 d.병우상후1,3,7,14,28 d검측대서혈홍단백、항온、혈당화사망솔.동물처사전완성Morris수미궁실험,후취대서대뇌표본계산대뇌결손체적.취치상조주위뇌조직,채용면역조화화Western blot방법검측Beclin 1적표체. 결과 각조대서동일시상점혈홍단백、항온、혈당차이균무통계학의의(P>0.05),치상조화거철알치료조사망솔차이무통계학의의;거철알치료조대뇌결손체적위(115.35±13.70) mm3,교치상조적(209.99±16.70)mm명현감소(P <0.05);Morris수미궁시험현시,거철알치료조동물평태수색책략(3.13±0.35)화수색시간[(36.15±26.63)s]균교치상조[분별위2.13±0.64화(110±47.34)s]현저개선(P<0.05);면역조화현시,치상후Beclin 1표체현저상조,여거철알치료후,Beclin 1현저하조;진일보Western blot정량검측현시,상후Beclin 1표체현저증강(P<0.05),거철알치료후,기표체현저하조(P<0.01). 결론 대서대뇌충격상후Beclin 1표체상조,제시뇌충격상후자서손상증강,거철알적치료효과가능시통과감경자서손상래실현적.
Objective To determine the effect of deferoxamine administration on autophagy in a rat model of blast-induced brain injury.Methods Thirty-nine male SD rats were allotted to shamoperated group,injury group and deferoxamine group with 13 rats in each,according to the random number table.Feeney's method was applied to establish the model.Deferoxamine group received deferoxamine of 100 mg/kg intraperitoneally.Sham-operated and injury group were injected with saline intraperitoneally.All treatments were started two hours postinjury at 12 hour interval for up to 28 days.Hemoglobin,rectal temperature,blood glucose and mortality were detected at 1,3,7,14 and 28 days.Morris water maze was conducted.Rats were killed later for detecting the brain defect volume and level of Beclin 1 at the site of injury.Results There were no significant differences among the three groups with respect to hemoglobin,rectal temperature and blood glucose (P > 0.05).Mortality in injury versus deferoxamine groups did not differ significantly (P > 0.05).Volume of defected brain in deferoxamine group was (115.35 ± 13.70) mm3,smaller than (209.99 ± 16.70) mm3 in injury group (P < 0.05).In Morris water maze test,the time spent in the searching the platform and latency to reach the platform were improved in deferoxamine group compared to those in injury group [(3.13 ± 0.35) vs (2.13 ± 0.64);(36.15 ± 26.63) s vs (110 ± 47.34) s respectively] (P < 0.05).Both immunohistochemisty and western blot showed dramatically increased level of Beclin 1 after injury,but treatment with deferoxamine significantly reduced the Beclin 1 expression.Conclusion Level of Beclin 1 is significantly upregulated after blast-induced brain injury in rats,resulting in elevated autophagy postinjury,but the treatment with deferoxamine is neuroprotective possible by lessening autophagy damage.