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
2012年
5期
292-296
,共5页
高压氧%脑缺血再灌注%过氧化损伤%细胞凋亡%超氧化物歧化酶%丙二醛
高壓氧%腦缺血再灌註%過氧化損傷%細胞凋亡%超氧化物歧化酶%丙二醛
고압양%뇌결혈재관주%과양화손상%세포조망%초양화물기화매%병이철
Hyperbaric oxygen%Cerebral ischemia reperfusion%Peroxidative damage%Apoptosis%Superoxide dismutase%Malondialdehyde
目的 通过观察高压氧(HBO)对局灶性脑缺血再灌注(CI/R)所致脑组织细胞线粒体过氧化损伤及凋亡的影响,探讨HBO对抗CI/R损伤的作用及其机制.方法 将80只SD大鼠按随机数字表法分为4组:假手术对照组(假手术组)8只,CI/R组、CI/R后常压吸氧(CI/R+N)组、CI/R后HBO治疗(CI/R+HBO)组,每组24只.采用大脑中动脉内线栓阻断法(MCAO)制备大鼠局灶性CI/R模型.(假手术组)操作步骤相同,但仅将线栓插入大脑中动脉10 mm后退出.假手术组、CI/R组术后不予任何处理,CI/R+N组术后30 min常压下吸纯氧,CI/R+HBO组术后30 min行常规HBO处理,均为60 min/次,1次/12 h.每组于CI/R术后12、24、48 h各处死8只大鼠,取CI/R损伤灶脑组织,采用比色法检测脑组织内线粒体超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,流式细胞技术检测脑细胞凋亡率.结果 CI/R组术后12、24、48 h SOD活性持续下降,显著低于假手术组[(139.21±11.52与(214.13±13.76)、(127.41±12.36)与(214.13±13.76)、(112.33±11.69)与(214.33±13.76)×10-6U/g)](均P＜0.01);CI/R+N组12、24、48 h SOD活性[(157.16±8.91)、(146.33±9.93)、(133.49±10.21)×10-6 U/g)]明显高于CI/R组(均P＜0.05),CI/R+HBO组12、24、48 h SOD活性[(176.80±12.35)、(169.43±12.41)、(161.56±13.81)×10-6 U/g)]显著高于CI/R组和CI/R+N组(均P＜0.05),显示CI/R后HBO治疗能有效地保护线粒体SOD的活性.CI/R组MDA含量术后持续增高,12、24、48 h显著高于假手术组(均P＜0.01).CI/R+N组MDA含量术后12、24、48 h时均低于CI/R组,但差异均无统计学意义(均P＞0.05);CI/R+HBO组MDA含量术后24、48 h时均显著低于CI/R组(均为P＜0.01)和CI/R+N48 h组(均P＜0.05),显示HBO治疗可有效抑制MDA的产生.CI/R组术后12、24、48 h脑细胞凋亡率持续增高,均显著高于假手术组(均P＜0.01);CI/R+N组术后24、48 h组脑细胞凋亡率均低于CI/R组,但差异无统计学意义(均P＞0.05);CI/R+HBO组术后24、48 h脑细胞凋亡率均显著低于CI/R组(均P＜0.05)和CUR+N 48 h组时(均P＜0.05);显示HBO治疗能有效降低CI/R后脑细胞凋亡率.结论 HBO治疗可明显增强细胞线粒体的稳定性,有效保护CI/R后脑组织线粒体SOD的活性,减轻大鼠CI/R所致线粒体过氧化损伤及脑细胞凋亡,较常压吸氧具有更显著的脑保护作用.
目的 通過觀察高壓氧(HBO)對跼竈性腦缺血再灌註(CI/R)所緻腦組織細胞線粒體過氧化損傷及凋亡的影響,探討HBO對抗CI/R損傷的作用及其機製.方法 將80隻SD大鼠按隨機數字錶法分為4組:假手術對照組(假手術組)8隻,CI/R組、CI/R後常壓吸氧(CI/R+N)組、CI/R後HBO治療(CI/R+HBO)組,每組24隻.採用大腦中動脈內線栓阻斷法(MCAO)製備大鼠跼竈性CI/R模型.(假手術組)操作步驟相同,但僅將線栓插入大腦中動脈10 mm後退齣.假手術組、CI/R組術後不予任何處理,CI/R+N組術後30 min常壓下吸純氧,CI/R+HBO組術後30 min行常規HBO處理,均為60 min/次,1次/12 h.每組于CI/R術後12、24、48 h各處死8隻大鼠,取CI/R損傷竈腦組織,採用比色法檢測腦組織內線粒體超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,流式細胞技術檢測腦細胞凋亡率.結果 CI/R組術後12、24、48 h SOD活性持續下降,顯著低于假手術組[(139.21±11.52與(214.13±13.76)、(127.41±12.36)與(214.13±13.76)、(112.33±11.69)與(214.33±13.76)×10-6U/g)](均P＜0.01);CI/R+N組12、24、48 h SOD活性[(157.16±8.91)、(146.33±9.93)、(133.49±10.21)×10-6 U/g)]明顯高于CI/R組(均P＜0.05),CI/R+HBO組12、24、48 h SOD活性[(176.80±12.35)、(169.43±12.41)、(161.56±13.81)×10-6 U/g)]顯著高于CI/R組和CI/R+N組(均P＜0.05),顯示CI/R後HBO治療能有效地保護線粒體SOD的活性.CI/R組MDA含量術後持續增高,12、24、48 h顯著高于假手術組(均P＜0.01).CI/R+N組MDA含量術後12、24、48 h時均低于CI/R組,但差異均無統計學意義(均P＞0.05);CI/R+HBO組MDA含量術後24、48 h時均顯著低于CI/R組(均為P＜0.01)和CI/R+N48 h組(均P＜0.05),顯示HBO治療可有效抑製MDA的產生.CI/R組術後12、24、48 h腦細胞凋亡率持續增高,均顯著高于假手術組(均P＜0.01);CI/R+N組術後24、48 h組腦細胞凋亡率均低于CI/R組,但差異無統計學意義(均P＞0.05);CI/R+HBO組術後24、48 h腦細胞凋亡率均顯著低于CI/R組(均P＜0.05)和CUR+N 48 h組時(均P＜0.05);顯示HBO治療能有效降低CI/R後腦細胞凋亡率.結論 HBO治療可明顯增彊細胞線粒體的穩定性,有效保護CI/R後腦組織線粒體SOD的活性,減輕大鼠CI/R所緻線粒體過氧化損傷及腦細胞凋亡,較常壓吸氧具有更顯著的腦保護作用.
목적 통과관찰고압양(HBO)대국조성뇌결혈재관주(CI/R)소치뇌조직세포선립체과양화손상급조망적영향,탐토HBO대항CI/R손상적작용급기궤제.방법 장80지SD대서안수궤수자표법분위4조:가수술대조조(가수술조)8지,CI/R조、CI/R후상압흡양(CI/R+N)조、CI/R후HBO치료(CI/R+HBO)조,매조24지.채용대뇌중동맥내선전조단법(MCAO)제비대서국조성CI/R모형.(가수술조)조작보취상동,단부장선전삽입대뇌중동맥10 mm후퇴출.가수술조、CI/R조술후불여임하처리,CI/R+N조술후30 min상압하흡순양,CI/R+HBO조술후30 min행상규HBO처리,균위60 min/차,1차/12 h.매조우CI/R술후12、24、48 h각처사8지대서,취CI/R손상조뇌조직,채용비색법검측뇌조직내선립체초양화물기화매(SOD)활성、병이철(MDA)함량,류식세포기술검측뇌세포조망솔.결과 CI/R조술후12、24、48 h SOD활성지속하강,현저저우가수술조[(139.21±11.52여(214.13±13.76)、(127.41±12.36)여(214.13±13.76)、(112.33±11.69)여(214.33±13.76)×10-6U/g)](균P＜0.01);CI/R+N조12、24、48 h SOD활성[(157.16±8.91)、(146.33±9.93)、(133.49±10.21)×10-6 U/g)]명현고우CI/R조(균P＜0.05),CI/R+HBO조12、24、48 h SOD활성[(176.80±12.35)、(169.43±12.41)、(161.56±13.81)×10-6 U/g)]현저고우CI/R조화CI/R+N조(균P＜0.05),현시CI/R후HBO치료능유효지보호선립체SOD적활성.CI/R조MDA함량술후지속증고,12、24、48 h현저고우가수술조(균P＜0.01).CI/R+N조MDA함량술후12、24、48 h시균저우CI/R조,단차이균무통계학의의(균P＞0.05);CI/R+HBO조MDA함량술후24、48 h시균현저저우CI/R조(균위P＜0.01)화CI/R+N48 h조(균P＜0.05),현시HBO치료가유효억제MDA적산생.CI/R조술후12、24、48 h뇌세포조망솔지속증고,균현저고우가수술조(균P＜0.01);CI/R+N조술후24、48 h조뇌세포조망솔균저우CI/R조,단차이무통계학의의(균P＞0.05);CI/R+HBO조술후24、48 h뇌세포조망솔균현저저우CI/R조(균P＜0.05)화CUR+N 48 h조시(균P＜0.05);현시HBO치료능유효강저CI/R후뇌세포조망솔.결론 HBO치료가명현증강세포선립체적은정성,유효보호CI/R후뇌조직선립체SOD적활성,감경대서CI/R소치선립체과양화손상급뇌세포조망,교상압흡양구유경현저적뇌보호작용.
Objective To observe the effects of hyperbaric oxygen(HBO)on peroxidative damage and apoptosis induced by focal cerebral ischemia and reperfusion(CI/R)in rats,and to further investigate the effects of HBO on CI/R-induced damage and the mechanism involved.Methods Eighty SD rats were randomly divided into 4 groups:the sham control group(n=8),the cerebral ischemia/reperfusion group(or the CI/R group,n=24),and the cerebral ischemia/reperfusion plus normal oxygen breathing group(or the CI/R+N group,n=24),the cerebral ischemia/reperfusion plus HBO group(or the CI/R+HBO group,n=24).The focal cerebral ischemia and reperfusion rat model was developed by using the middle cerebral artery occlusion method(MCAO).The animals in the control and the CI/R groups were left there without any treatment after surgery.The animals in the CI/R+N group breathed oxygen under normal pressure,30 min after surgery,while the animals in the CI/R+HBO group received routine HBO treatment 30 min after surgery,with 60 min a session for a duration of 12 h.Eight animals of each group were killed at hour 12,24 and 48,following surgery,for collection of CI/R-damaged focal cerebral tissue.Colorimetric method was used to monitor the activity of mitochondrial superoxide dismutase(SOD)in the brain tissue and the content of malondialdehyde(MDA),and cell flowmetry was applied to detect apoptosis of brain cells.Results The activity of SOD in the CI/R group decreased continuously at hour 12,24 and 48,and was significantly lower than that of the control group(P＜0.01).The activity of SOD in the CI/R+N group at hour 12,24 and 48 was obviously higher than that of the CI/R group(P＜0.05),and the activity of SOD in the CI/R+HBO group at hour 12,24 and 48 was significantly higher than those of the CI/R group and the CI/R+N group(P＜0.05),indicating that HBO could most effectively protect the activity of SOD in mitochondria,following cerebral ischemia induced by reperfusion.After surgery,the content of MDA for the CI/R group increased continuously at hour 12,24 and 48,and was significantly higher than that of the control group(P＜0.01).The contents of MDA for the CI/R+N group at hour 12,24 and 48 were lower than those of the CI/R group,but without statistical significance(P＜0.05).The contents of MDA for the CI/R+HBO group at hour 12,24 and 48 were all significantly lower than those of the CL/R group(P＜0.01),indicating that HBO could effectively inhibit the production of MDA.After surgery,apoptosis of brain cells at hour 12,24 and 48 for the CI/R group increased continuously,and was significantly higher than that of the control group(P＜0.01).Apoptosis of brain cells at hour 12,24 and 48 for the CI/R+N group was lower than that of the CI/R group(P＞0.05),but without statistical significance(P＜0.05).Apoptosis of brain cells at hour 24 and 48 for the CI/R+HBO group was significantly lower than that of the CI/R group and the CI/R+N group at hour 48(P＜0.05),indicating that HBO could effectively alleviate apoptosis of brain cells following cerebral ischemia induced by reperfusion.Conclusions HBO could obviously increase the stability of mitochondria,effectively protect the activity of SOD of mitochondria in the brain tissue following cerebral ischemia induced by reperfusion,alleviate peroxidative mitochondrial damage induced by ischemia reperfusion.All this indicated that HBO was obviously more effective than normal oxygen breathing in the protection of the injured brain.
