四川医学
四川醫學
사천의학
Sichuan Medical Journal
2015年
8期
1099-1102
,共4页
高压氧%新生鼠%缺氧缺血%脑损伤%凋亡%NF-κB
高壓氧%新生鼠%缺氧缺血%腦損傷%凋亡%NF-κB
고압양%신생서%결양결혈%뇌손상%조망%NF-κB
hyperbaric oxygenation%neonatal rat%hypoxic-ischemic%brain damage%NF-κB%apoptosis
目的 研究高压氧( HBO)对新生大鼠缺氧缺血性脑损伤( HIBD)海马区神经细胞凋亡及NF-κB表达的影响,探讨HBO对缺氧缺血性脑损伤的神经保护作用机制. 方法 新生7 日龄SD大鼠72 只,随机分为,假手术组( 24只)、缺氧缺血(HIBD)组(24 只)、高压氧(HBO)组(24 只). 各组处理后分别于6h、24h、48h、72h 各处死6 只,采用TUNEL方法检测神经细胞凋亡,免疫组化法(SABC)检测NF-κB p65在海马区的表达. 采用Image Pro Plus5. 0专业图像分析软件,测量NF-κB p65表达阳性细胞数及凋亡阳性细胞数. 结果 假手术组新生大鼠脑海马区有少量凋亡细胞,各时间点之间无显著差异(P>0. 05);HIBD组凋亡细胞数随时间变化明显减少(P<0. 05),与假手术组相比差异有统计学意义(P<0. 05);HBO组凋亡细胞数减少明显,与HIBD组差异有统计学意义(P<0. 05). 假手术组NF-κB P65在海马区有少量表达,各时间点无明显变化(P>0. 05);HIBD组NF-κB P65表达增高(P<0. 05),与假手术组相比差异有统计学意义(P<0. 05);HBO组NF-κB P65表达增加更加明显,在各时间点与HIBD组和假手术组差异均有统计学意义(P<0. 05). 结论 高压氧(HBO)可减少新生大鼠缺氧缺血性脑损伤(HIBD)的神经细胞凋亡,对神经系统具有保护作用;高压氧的神经保护机制可能与其促进NF-κB的持续活化、抗神经细胞凋亡有关.
目的 研究高壓氧( HBO)對新生大鼠缺氧缺血性腦損傷( HIBD)海馬區神經細胞凋亡及NF-κB錶達的影響,探討HBO對缺氧缺血性腦損傷的神經保護作用機製. 方法 新生7 日齡SD大鼠72 隻,隨機分為,假手術組( 24隻)、缺氧缺血(HIBD)組(24 隻)、高壓氧(HBO)組(24 隻). 各組處理後分彆于6h、24h、48h、72h 各處死6 隻,採用TUNEL方法檢測神經細胞凋亡,免疫組化法(SABC)檢測NF-κB p65在海馬區的錶達. 採用Image Pro Plus5. 0專業圖像分析軟件,測量NF-κB p65錶達暘性細胞數及凋亡暘性細胞數. 結果 假手術組新生大鼠腦海馬區有少量凋亡細胞,各時間點之間無顯著差異(P>0. 05);HIBD組凋亡細胞數隨時間變化明顯減少(P<0. 05),與假手術組相比差異有統計學意義(P<0. 05);HBO組凋亡細胞數減少明顯,與HIBD組差異有統計學意義(P<0. 05). 假手術組NF-κB P65在海馬區有少量錶達,各時間點無明顯變化(P>0. 05);HIBD組NF-κB P65錶達增高(P<0. 05),與假手術組相比差異有統計學意義(P<0. 05);HBO組NF-κB P65錶達增加更加明顯,在各時間點與HIBD組和假手術組差異均有統計學意義(P<0. 05). 結論 高壓氧(HBO)可減少新生大鼠缺氧缺血性腦損傷(HIBD)的神經細胞凋亡,對神經繫統具有保護作用;高壓氧的神經保護機製可能與其促進NF-κB的持續活化、抗神經細胞凋亡有關.
목적 연구고압양( HBO)대신생대서결양결혈성뇌손상( HIBD)해마구신경세포조망급NF-κB표체적영향,탐토HBO대결양결혈성뇌손상적신경보호작용궤제. 방법 신생7 일령SD대서72 지,수궤분위,가수술조( 24지)、결양결혈(HIBD)조(24 지)、고압양(HBO)조(24 지). 각조처리후분별우6h、24h、48h、72h 각처사6 지,채용TUNEL방법검측신경세포조망,면역조화법(SABC)검측NF-κB p65재해마구적표체. 채용Image Pro Plus5. 0전업도상분석연건,측량NF-κB p65표체양성세포수급조망양성세포수. 결과 가수술조신생대서뇌해마구유소량조망세포,각시간점지간무현저차이(P>0. 05);HIBD조조망세포수수시간변화명현감소(P<0. 05),여가수술조상비차이유통계학의의(P<0. 05);HBO조조망세포수감소명현,여HIBD조차이유통계학의의(P<0. 05). 가수술조NF-κB P65재해마구유소량표체,각시간점무명현변화(P>0. 05);HIBD조NF-κB P65표체증고(P<0. 05),여가수술조상비차이유통계학의의(P<0. 05);HBO조NF-κB P65표체증가경가명현,재각시간점여HIBD조화가수술조차이균유통계학의의(P<0. 05). 결론 고압양(HBO)가감소신생대서결양결혈성뇌손상(HIBD)적신경세포조망,대신경계통구유보호작용;고압양적신경보호궤제가능여기촉진NF-κB적지속활화、항신경세포조망유관.
Objective To observe the effect of hyperbaric oxygenation( HBO) on apoptosis and NF-κBexpression of neo-natal rat hippocampus after hypoxia-ischemic brain damage( HIBD) and study the neuronal protective mechanism of HBO. Meth-ods Seventy-two 7-day postnatal Sprague-Dawley(SD) rats were randomly divided into 3 groups:control group (n =24),hy-poxic-ischemic brain damage group (n=24),HBO-treated group (n=24). In the HBO-treated group, rats received hyperbaric oxygenation at 6h, 24h, 48h and 72h after HIBD. The control group was not administrated. The expression of NF-κB in the hipp-ocampal was measured by Immunohistochemical method. The apoptosis of the hippocampal cell was detected by terminal deoxynu-cleotidyltransferase-mediated 2-deoxyuridine 5-triphosphate-biotin nick end labeling ( TUNEL) straining. The quantities of NF-κB and apoptosis cells were counted by Image plus-pro system. All data were analyses by SPSS 11. 0 software. Results Very few TUNEL-positive cells were found by TUNEL staining in the control group, comparing with markedly increasing cells in the HIBD group(P <0. 05);In the HBO-treated group, the number of TUNEL-positive cells was significantly reduced comparing with the HIBD group(P<0. 05)at 24h, 48h and 72h. However no significant difference was observed at 72h comparing with the control group.⒉ The expression of the NF-κB in the hippocampal cell was increased at 24h after HIBD by immunohistochemical techni-cal, and lasted to 72h when compared with the control group(P<0. 05). In the HBO-treated group, the expression of the NF-κB was significantly increased compared with HIBD group(P<0. 05). Conclusion Hyperbaric oxygenation(HBO) have neuronal protective effect on the neonatal rats after HIBD. The protective mechanism of HBO may be through the promotion of NF-κB activa-tion which may inhibitate of neuronal apoptosis on neonatal rats after HIBD.
