CAJ | 학술논문

目的观察外源性H2S对缺氧性脑损伤小鼠空间学习记忆障碍的影响,并探究其作用机制.方法连续4dsc给予NaNO2 120 mg·kg-1·d-1制备缺氧模型；氢硫化钠(NaHS)治疗组在制备模型的同时ip给予NaHS 1 mg· kg-·d-1.每天给药前进行Morris水迷宫实验,测定逃避潜伏期、原平台象限停留时间和穿越平台次数.比色法检测小鼠脑组织中超氧化物歧化酶( SOD)活性及丙二醛(MDA)含量.HE染色观察海马组织切片CA1区神经元形态学改变.结果水迷宫实验第3天和第4天,模型组小鼠逃避潜伏期分别为(26.0 ±7.3)s和(23.3 ±8.7)s,明显长于正常对照组的(16.1±9.6)s(P ＜0.05)和(11.1±6.2)s(P＜0.01).第5天,模型组小鼠穿越平台次数为4.1±1.9,在原平台象限停留时间为(20±8)s,与正常对照组穿越平台次数(7.2±1.6)次和在原平台象限停留时间(28±8)s比较明显减少(P＜0.01).与正常对照组相比,模型组小鼠脑组织中SOD活性降低12.6% (P ＜0.01),MDA含量升高43.9% (P ＜0.01).在模型组小鼠海马CA1区,锥体细胞出现明显的核固缩、胞浆深染和排列紊乱等变性改变.与模型组比较,NaHS组小鼠在水迷宫实验的第3天和第4天逃避潜伏期明显缩短(P＜0.05),分别为(17.9±7.0)s和(15.8±8.5)s；在平台所在象限停留时间和穿越平台次数明显增加(P＜0.01),分别为(30±9)s和(6.7±2.5)次；SOD活性升高了8.9%(P＜0.05),MDA含量显著下降了29.6% (P ＜0.01)；海马CA1区神经元变性改变较模型组得到显著缓解.结论 NaHS减轻了脑缺氧损伤诱发的小鼠学习记忆的损害,其作用机制可能与H2S衰减海马区神经元损伤和抗氧化作用有关.
목적 관찰외원성H2S대결양성뇌손상소서공간학습기억장애적영향,병탐구기작용궤제.방법 련속4dsc급여NaNO2 120 mg·kg-1·d-1제비결양모형；경류화납(NaHS)치료조재제비모형적동시ip급여NaHS 1 mg· kg-·d-1.매천급약전진행Morris수미궁실험,측정도피잠복기、원평태상한정류시간화천월평태차수.비색법검측소서뇌조직중초양화물기화매( SOD)활성급병이철(MDA)함량.HE염색관찰해마조직절편CA1구신경원형태학개변.결과 수미궁실험제3천화제4천,모형조소서도피잠복기분별위(26.0 ±7.3)s화(23.3 ±8.7)s,명현장우정상대조조적(16.1±9.6)s(P ＜0.05)화(11.1±6.2)s(P＜0.01).제5천,모형조소서천월평태차수위4.1±1.9,재원평태상한정류시간위(20±8)s,여정상대조조천월평태차수(7.2±1.6)차화재원평태상한정류시간(28±8)s비교명현감소(P＜0.01).여정상대조조상비,모형조소서뇌조직중SOD활성강저12.6% (P ＜0.01),MDA함량승고43.9% (P ＜0.01).재모형조소서해마CA1구,추체세포출현명현적핵고축、포장심염화배렬문란등변성개변.여모형조비교,NaHS조소서재수미궁실험적제3천화제4천도피잠복기명현축단(P＜0.05),분별위(17.9±7.0)s화(15.8±8.5)s；재평태소재상한정류시간화천월평태차수명현증가(P＜0.01),분별위(30±9)s화(6.7±2.5)차；SOD활성승고료8.9%(P＜0.05),MDA함량현저하강료29.6% (P ＜0.01)；해마CA1구신경원변성개변교모형조득도현저완해.결론 NaHS감경료뇌결양손상유발적소서학습기억적손해,기작용궤제가능여H2S쇠감해마구신경원손상화항양화작용유관.
OBJECTIVE To investigate effects of exogenous hydrogen sulfide ( H2 S) on the spatial memory disorder induced by cerebral anoxia in mice and explore related mechanism.METHODS Sodium nitrite (NaNO2) 120 mg·kg-1 was sc given to mice for4 d in model group.Sodium hydrosulfide (NaHS) 1 mg·kg-1 was ip given and NaNO2 120 mg·kg-1 simultaneously was sc given to mice for4 d in NaHS group.All drugs were given to mice immediately after Morris water maze experiment every day and escape latency.The number of crossings over the target area (NCTA) and search time in target quadrant (STTQ) were recorded.The activity of superoxide dismutase (SOD) and malondialdehyde (MDA) level in the brain was determined with colorimetry.The morphological alterations in hippocampus slices were assessed by microscope.RESULTS On the third and fourth days in Morris water maze experiment,compared with ( 16.1 ±9.6)s and ( 11.1 ±6.2)s in normal control group,the escape latency in model group was longer,(26.0 ±7.3)s(P＜0.05) and (23.3 ±8.7)s(P＜0.01).On the fifth day,compared with 7.2 ± 1.6 and (28 ± 8) s in normal control group NCTA and STTQ in model group were 4.1 ± 1.9 and (20 ± 8 ) s ( P ＜ 0.05 ),and they were obviously less.Compared with normal control group,SOD activity and M DA content of mice in model group were reduced by 12.6％ (P ＜ 0.01 ) and increased by 43.9％ (P ＜ 0.01 ),respectively.The neuron degenerative changes including karyopyknosis,dark cytoplasm and irregular pyramidal layer were observed in model group.On the third and fourth day,compared with model group,the escape latency in NaHS group was shorter,(17.9 ±7.0)s and (15.8 ±8.5)s (P＜0.05).Compared with model group,NCTA and STTQ in NaHS group increased to 6.7 ± 2.5 and ( 30 ± 9) s ( P ＜ 0.01 ).SOD activity and MDA content in NaHS group were increased by 8.9％ ( P ＜ 0.05 ) and reduced by 29.6％ ( P ＜ 0.01 ),respectively.Neuron degeneration was significantly attenuated in NaHS group (P ＜ 0.01 ).CONCLUSION NaHS can attenuate the spatial memory disorder induced by cerebral anoxia and the mechanism may be related to the antioxidation effect and alleviation of neuron damage of H2S.