实用心脑肺血管病杂志
實用心腦肺血管病雜誌
실용심뇌폐혈관병잡지
Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease
2015年
8期
38-42
,共5页
张睿%杨祖悌%张同寅%宋海军%王斌
張睿%楊祖悌%張同寅%宋海軍%王斌
장예%양조제%장동인%송해군%왕빈
脑损伤%异氟烷%大鼠
腦損傷%異氟烷%大鼠
뇌손상%이불완%대서
Brain injuries%Isoflurane%Rats
目的：探讨异氟烷对创伤性脑损伤大鼠的神经保护作用及作用机制。方法选择成年健康雄性SD大鼠80只，采用随机数字表法分为假手术组、脑损伤组、异氟烷预处理组和异氟烷后处理组，每组20只。采用改良Feeney自由落体法制作大鼠创伤性脑损伤模型，假手术组大鼠仅做开窗手术处理，异氟烷预处理组大鼠在造模前给予异氟烷持续麻醉，脑损伤组和异氟烷后处理组大鼠造模成功后立即进行复苏，且异氟烷后处理组大鼠于复苏后给予异氟烷持续麻醉。采用神经功能缺损评分表（ NSS）评定各组大鼠创伤性脑损伤后12 h、24 h神经功能缺损情况，免疫印迹法检测各组大鼠创伤性脑损伤后24 h损伤灶周围脑组织磷酸化Akt（ P-Akt）、磷酸化糖原合酶激酶-3β（ P-GSK3β）、Bcl-2、cleaved-caspase-3蛋白表达量，TUNEL法检测各组大鼠创伤性脑损伤后24 h损伤灶周围脑组织凋亡神经元数量。结果脑损伤组大鼠创伤性脑损伤后12 h、24 h NSS评分高于假手术组、异氟烷预处理组及异氟烷后处理组，异氟烷预处理组和异氟烷后处理组大鼠创伤性脑损伤后12 h、24 h NSS评分高于假手术组（ P<0.05）。脑损伤组、异氟烷预处理组及异氟烷后处理组大鼠创伤性脑损伤后24 h损伤灶周围脑组织P-Akt蛋白和P-GSK3β蛋白表达量高于假手术组，异氟烷预处理组和异氟烷后处理组大鼠创伤性脑损伤后24 h损伤灶周围脑组织P-AktA蛋白和P-GSK3β蛋白表达量高于脑损伤组（P<0.05）。脑损伤组大鼠创伤性脑损伤后24 h损伤灶周围脑组织Bcl-2蛋白表达量低于假手术组、异氟烷预处理组及异氟烷后处理组，cleaved-caspase-3蛋白表达量及凋亡神经元数量高于假手术组、异氟烷预处理组及异氟烷后处理组，异氟烷预处理组和异氟烷后处理组大鼠创伤性脑损伤后24 h损伤灶周围脑组织cleaved-caspase-3蛋白表达量、凋亡神经元数量高于假手术组（ P<0.05）。结论异氟烷对创伤性脑损伤大鼠具有神经保护作用，其可能通过激活Akt/GSK3β信号通路而发挥神经保护作用。
目的：探討異氟烷對創傷性腦損傷大鼠的神經保護作用及作用機製。方法選擇成年健康雄性SD大鼠80隻，採用隨機數字錶法分為假手術組、腦損傷組、異氟烷預處理組和異氟烷後處理組，每組20隻。採用改良Feeney自由落體法製作大鼠創傷性腦損傷模型，假手術組大鼠僅做開窗手術處理，異氟烷預處理組大鼠在造模前給予異氟烷持續痳醉，腦損傷組和異氟烷後處理組大鼠造模成功後立即進行複囌，且異氟烷後處理組大鼠于複囌後給予異氟烷持續痳醉。採用神經功能缺損評分錶（ NSS）評定各組大鼠創傷性腦損傷後12 h、24 h神經功能缺損情況，免疫印跡法檢測各組大鼠創傷性腦損傷後24 h損傷竈週圍腦組織燐痠化Akt（ P-Akt）、燐痠化糖原閤酶激酶-3β（ P-GSK3β）、Bcl-2、cleaved-caspase-3蛋白錶達量，TUNEL法檢測各組大鼠創傷性腦損傷後24 h損傷竈週圍腦組織凋亡神經元數量。結果腦損傷組大鼠創傷性腦損傷後12 h、24 h NSS評分高于假手術組、異氟烷預處理組及異氟烷後處理組，異氟烷預處理組和異氟烷後處理組大鼠創傷性腦損傷後12 h、24 h NSS評分高于假手術組（ P<0.05）。腦損傷組、異氟烷預處理組及異氟烷後處理組大鼠創傷性腦損傷後24 h損傷竈週圍腦組織P-Akt蛋白和P-GSK3β蛋白錶達量高于假手術組，異氟烷預處理組和異氟烷後處理組大鼠創傷性腦損傷後24 h損傷竈週圍腦組織P-AktA蛋白和P-GSK3β蛋白錶達量高于腦損傷組（P<0.05）。腦損傷組大鼠創傷性腦損傷後24 h損傷竈週圍腦組織Bcl-2蛋白錶達量低于假手術組、異氟烷預處理組及異氟烷後處理組，cleaved-caspase-3蛋白錶達量及凋亡神經元數量高于假手術組、異氟烷預處理組及異氟烷後處理組，異氟烷預處理組和異氟烷後處理組大鼠創傷性腦損傷後24 h損傷竈週圍腦組織cleaved-caspase-3蛋白錶達量、凋亡神經元數量高于假手術組（ P<0.05）。結論異氟烷對創傷性腦損傷大鼠具有神經保護作用，其可能通過激活Akt/GSK3β信號通路而髮揮神經保護作用。
목적：탐토이불완대창상성뇌손상대서적신경보호작용급작용궤제。방법선택성년건강웅성SD대서80지，채용수궤수자표법분위가수술조、뇌손상조、이불완예처리조화이불완후처리조，매조20지。채용개량Feeney자유락체법제작대서창상성뇌손상모형，가수술조대서부주개창수술처리，이불완예처리조대서재조모전급여이불완지속마취，뇌손상조화이불완후처리조대서조모성공후립즉진행복소，차이불완후처리조대서우복소후급여이불완지속마취。채용신경공능결손평분표（ NSS）평정각조대서창상성뇌손상후12 h、24 h신경공능결손정황，면역인적법검측각조대서창상성뇌손상후24 h손상조주위뇌조직린산화Akt（ P-Akt）、린산화당원합매격매-3β（ P-GSK3β）、Bcl-2、cleaved-caspase-3단백표체량，TUNEL법검측각조대서창상성뇌손상후24 h손상조주위뇌조직조망신경원수량。결과뇌손상조대서창상성뇌손상후12 h、24 h NSS평분고우가수술조、이불완예처리조급이불완후처리조，이불완예처리조화이불완후처리조대서창상성뇌손상후12 h、24 h NSS평분고우가수술조（ P<0.05）。뇌손상조、이불완예처리조급이불완후처리조대서창상성뇌손상후24 h손상조주위뇌조직P-Akt단백화P-GSK3β단백표체량고우가수술조，이불완예처리조화이불완후처리조대서창상성뇌손상후24 h손상조주위뇌조직P-AktA단백화P-GSK3β단백표체량고우뇌손상조（P<0.05）。뇌손상조대서창상성뇌손상후24 h손상조주위뇌조직Bcl-2단백표체량저우가수술조、이불완예처리조급이불완후처리조，cleaved-caspase-3단백표체량급조망신경원수량고우가수술조、이불완예처리조급이불완후처리조，이불완예처리조화이불완후처리조대서창상성뇌손상후24 h손상조주위뇌조직cleaved-caspase-3단백표체량、조망신경원수량고우가수술조（ P<0.05）。결론이불완대창상성뇌손상대서구유신경보호작용，기가능통과격활Akt/GSK3β신호통로이발휘신경보호작용。
Objective To investigate the neuroprotective effect of isoflurane in rats with traumatic brain injury and its mechanism. Methods A total of 80 healthy male adult S-D rats were selected and divided into groups A,B,C,D,each of 20 rats. Modified Feeney freely falling body method was used to prepare rat model of traumatic brain injury,rats of A group were given open-window operation,rats of B group were given continue anesthesia of isoflurane before prepartion,rats of C group and D group were given CPR after preparation,and rats of D group were given extra continue anesthesia of isoflurane after CPR. NSS was used to evaluate the neurologic deficits after 12 hours and 24 hours of traumatic brain injury,immunoblotting was used to detect the protein expression of P-Akt,P-GSK3β,Bcl-2 and cleaved-caspase-3 in brain tissues around nidus after 24 hours of traumatic brain injury,and TUNEL was used to detect the apoptotic nerve cell amount in brain tissues around nidus after 24 hours of traumatic brain injury. Results NSS score after 12 hours and 24 hours of traumatic brain injury of C group was statistically significantly higher than that of A group,B group and D group,respectively,and that of B group and D group was statistically significantly higher than that of A group ( P<0. 05 ). Protein expression of P-Akt and P-GSK3β in brain tissues around nidus after 24 hours of traumatic brain injury of B group,C group and D group were statistically significantly higher than those of A group,those of B group and D group were statistically significantly higher than those of C group( P<0. 05). Protein expression of Bcl -2 in brain tissues around nidus after 24 hours of traumatic brain injury of C group was statistically significantly lower than that of A group,B group and D group,respectively,while protein expression of cleaved-caspase-3 and apoptotic nerve cell amount of C group were statistically significantly higher than those of A group,B group and D group,protein expression of cleaved-caspase -3 and apoptotic nerve cell amount of B group and D group were statistically significantly higher than those of A group ( P <0. 05 ). Conclusion Isoflurane has certain neuroprotective effect in rats with traumatic brain injury,it may play a role of neuroprotection by activating the Akt/GSK3β signal pathway.
