中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
Chinese Journal of Nautical Medicine and Hyperbaric Medicine
2015年
5期
347-351
,共5页
周苏键%谭耀武%刘咏武栎%丁政%卢晓欣%彭慧平
週囌鍵%譚耀武%劉詠武櫟%丁政%盧曉訢%彭慧平
주소건%담요무%류영무력%정정%로효흔%팽혜평
高压氧%创伤性颅脑损伤%神经功能评分%细胞基质衍生因子-1%趋化因子受体4%归巢%大鼠
高壓氧%創傷性顱腦損傷%神經功能評分%細胞基質衍生因子-1%趨化因子受體4%歸巢%大鼠
고압양%창상성로뇌손상%신경공능평분%세포기질연생인자-1%추화인자수체4%귀소%대서
Hyperbaric oxygen%Traumatic brain injury%Neurological function scores%Stromal derived factor-1%SDF-1%CXC chemokine receptor 4%Homing%Rat
目的 观察高压氧(hyperbaric oxygen,HBO)对创伤性颅脑损伤(traumatic brain injury,TBI)大鼠受损脑组织中基质细胞衍生因子-1(stromal derived factor-1,SDF-1)及其趋化因子受体4(CXC chemokine receptor 4,CXCR4)表达的影响,探讨高压氧对创伤性颅脑损伤大鼠神经保护作用的潜在机制.方法 采用改良Feeney自由落体法复制建立颅脑损伤模型,SD雄性大鼠72只,按数字表法随机分为3组,假手术组、模型组、高压氧组,每组各24只,各组根据高压氧干预时间,再分为3d和10d2个亚组.高压氧组大鼠于造模后24 h接受高压氧处理,每日1次.在造模后24 h、处理3d、10 d后,运用神经功能评分(neurological severity scores,NSS)比较各组神经功能恢复情况.同时在3d、10 d时,取伤侧脑组织应用蛋白免疫印迹法(Western blotting)检测受损脑组织SDF-1及其受体CXCR4的表达情况.结果 (1)假手术组大鼠未见神经功能缺损,模型组与高压氧组大鼠造模24 h后神经功能缺损评分差异无统计学意义(P＞0.05),治疗3d、10d,神经功能逐渐恢复,高压氧组神经功能缺损评分(分别为8.7±0.4、4.7±0.6)均明显低于模型组(分别为10.5±0.6、6.4±0.6),差异有统计学意义(P＜0.01).(2)假手术组SDF-1及CXCR4蛋白表达量少,不同时间点表达量差异无统计学意义(P＞0.05);治疗3d,模型组与假手术组相比,SDF-1及CXCR4蛋白表达量均明显增多(P＜0.01);治疗10d,模型组SDF-1表达下降,趋于假手术组水平(P＞0.05),CXCR4表达下降,但仍明显高于假手术组(P＜0.01);治疗3d、10 d,高压氧组和模型组比较,SDF-1及CXCR4表达量均明显增多(P＜0.01).结论 HBO治疗可加快TBI大鼠神经功能恢复,可能通过上调SDF-1/CXCR4轴,从而促进内源性骨髓间充质干细胞归巢至受损脑组织.
目的 觀察高壓氧(hyperbaric oxygen,HBO)對創傷性顱腦損傷(traumatic brain injury,TBI)大鼠受損腦組織中基質細胞衍生因子-1(stromal derived factor-1,SDF-1)及其趨化因子受體4(CXC chemokine receptor 4,CXCR4)錶達的影響,探討高壓氧對創傷性顱腦損傷大鼠神經保護作用的潛在機製.方法 採用改良Feeney自由落體法複製建立顱腦損傷模型,SD雄性大鼠72隻,按數字錶法隨機分為3組,假手術組、模型組、高壓氧組,每組各24隻,各組根據高壓氧榦預時間,再分為3d和10d2箇亞組.高壓氧組大鼠于造模後24 h接受高壓氧處理,每日1次.在造模後24 h、處理3d、10 d後,運用神經功能評分(neurological severity scores,NSS)比較各組神經功能恢複情況.同時在3d、10 d時,取傷側腦組織應用蛋白免疫印跡法(Western blotting)檢測受損腦組織SDF-1及其受體CXCR4的錶達情況.結果 (1)假手術組大鼠未見神經功能缺損,模型組與高壓氧組大鼠造模24 h後神經功能缺損評分差異無統計學意義(P＞0.05),治療3d、10d,神經功能逐漸恢複,高壓氧組神經功能缺損評分(分彆為8.7±0.4、4.7±0.6)均明顯低于模型組(分彆為10.5±0.6、6.4±0.6),差異有統計學意義(P＜0.01).(2)假手術組SDF-1及CXCR4蛋白錶達量少,不同時間點錶達量差異無統計學意義(P＞0.05);治療3d,模型組與假手術組相比,SDF-1及CXCR4蛋白錶達量均明顯增多(P＜0.01);治療10d,模型組SDF-1錶達下降,趨于假手術組水平(P＞0.05),CXCR4錶達下降,但仍明顯高于假手術組(P＜0.01);治療3d、10 d,高壓氧組和模型組比較,SDF-1及CXCR4錶達量均明顯增多(P＜0.01).結論 HBO治療可加快TBI大鼠神經功能恢複,可能通過上調SDF-1/CXCR4軸,從而促進內源性骨髓間充質榦細胞歸巢至受損腦組織.
목적 관찰고압양(hyperbaric oxygen,HBO)대창상성로뇌손상(traumatic brain injury,TBI)대서수손뇌조직중기질세포연생인자-1(stromal derived factor-1,SDF-1)급기추화인자수체4(CXC chemokine receptor 4,CXCR4)표체적영향,탐토고압양대창상성로뇌손상대서신경보호작용적잠재궤제.방법 채용개량Feeney자유락체법복제건립로뇌손상모형,SD웅성대서72지,안수자표법수궤분위3조,가수술조、모형조、고압양조,매조각24지,각조근거고압양간예시간,재분위3d화10d2개아조.고압양조대서우조모후24 h접수고압양처리,매일1차.재조모후24 h、처리3d、10 d후,운용신경공능평분(neurological severity scores,NSS)비교각조신경공능회복정황.동시재3d、10 d시,취상측뇌조직응용단백면역인적법(Western blotting)검측수손뇌조직SDF-1급기수체CXCR4적표체정황.결과 (1)가수술조대서미견신경공능결손,모형조여고압양조대서조모24 h후신경공능결손평분차이무통계학의의(P＞0.05),치료3d、10d,신경공능축점회복,고압양조신경공능결손평분(분별위8.7±0.4、4.7±0.6)균명현저우모형조(분별위10.5±0.6、6.4±0.6),차이유통계학의의(P＜0.01).(2)가수술조SDF-1급CXCR4단백표체량소,불동시간점표체량차이무통계학의의(P＞0.05);치료3d,모형조여가수술조상비,SDF-1급CXCR4단백표체량균명현증다(P＜0.01);치료10d,모형조SDF-1표체하강,추우가수술조수평(P＞0.05),CXCR4표체하강,단잉명현고우가수술조(P＜0.01);치료3d、10 d,고압양조화모형조비교,SDF-1급CXCR4표체량균명현증다(P＜0.01).결론 HBO치료가가쾌TBI대서신경공능회복,가능통과상조SDF-1/CXCR4축,종이촉진내원성골수간충질간세포귀소지수손뇌조직.
Objective To observe the effects of hyperbaric oxygen (HBO) on the expressions of stromal derived factor-1 (SDF-1) and CXC chemokine receptor 4(CXCR4) in rats with traumatic brain injury and also to discuss potential mechanism of HBO in the protection of the nerve system of the rats with TBI.Methods The experimental models of traumatic brain injury were developed by modified Feeney free-falling method.Seventy-two SD male rats were randomly divided into 3 groups: the sham surgery group, the model group and the HBO group, each consisting of 24 rats.Then, in accordance with HBO intervention time, the HBO group was subdivided into the 3-day and 10-day subgroups.The rats in the HBO group received HBO therapy 24 hours after development of the model, one session a day.Recovery of the nerve system, 24 hours after development of the model, 3 and 10 days after therapy, was assessed by using Neurological Severity Scores (NSS), and neurological function recovery was compared between the groups.At the same time, samples of damaged brain tissues were taken for the detection of expression levels of SDF-1 and CXCR4 by using Western blotting.Results (1)Neurological function deficiency was not noted in the sham surgery group.There were no significant differences in neurological function deficiency scores detected 24 hours after the development of the model, when comparisons were made between the model group and the HBO group(P ＞0.05).Three and 10 days after therapy, neural function recovered gradually, with the neural function deficiency scores of the HBO group being(8.7 ± 0.4)and(4.7 ±0.6)respectively, which were obviously lower than those of the model group(10.5 ±0.6 and 6.40.6 respectively)(P ＜0.01).(2)The expressions of SDF-1 and CXCR4 in the sham surgery group were low, and there was no statistical significance in the expression levels at different time points(P ＞0.05).Three days after therapy, the expression levels of SDF-1 and CXCR4 for the model group were all significantly increased, as compared with those of the sham surgery group(P ＞ 0.05).Ten days after therapy, the expression level of SDF-1 for the model group was decreased, which tended to be the identical level of the sham surgery group(P ＞0.05).Though the expression level of CXCR4 was also decreased, it was obviously higher than that of the sham surgery group (P ＞ 0.01).Three and 10 days after therapy, the expression levels of SDF-1 and CXCR4 for the HBO group were significantly increased, as compared with those of the model group(P ＞ 0.01).Conclusions HBO therapy could accelerate neurological function recovery of the rats with TBI and promote homing of endogenous mesenchymal stem cells to the injured brain tissues by upregulating SDF-1/CXCR4 axis.
