中国药物与临床
中國藥物與臨床
중국약물여림상
CHINESE REMEDIES & CLINICS
2014年
11期
1488-1490
,共3页
神经元%缺氧%阿司匹林
神經元%缺氧%阿司匹林
신경원%결양%아사필림
Neurons%Anoxia%Aspirin
目的:观察神经细胞缺氧/缺糖损伤后线粒体膜电位(MMP)和凋亡的变化情况及阿司匹林的保护作用。方法用体外培养7 d的Wistar大鼠皮质神经细胞,随机分为正常对照组、缺氧/缺糖模型组、缺氧/缺糖加100μmol/L浓度阿司匹林组。缺氧/缺糖2 h处理后,四甲基偶氮唑盐(MTT)比色分析法检测神经元线粒体活性;流式细胞术检测神经元线粒体膜电位、双染法检测不同组神经元的凋亡情况。结果缺氧/缺糖损伤2h后,模型组的线粒体活性和MMP 水平较对照组显著降低(P<0.01)。细胞凋亡百分率均较对照组显著升高(P<0.01)。而阿司匹林组能显著提高神经元线粒体活性、膜电位,降低细胞凋亡的百分率。结论阿司匹林可抑制缺氧/缺糖损伤所致的神经元线粒体活性和膜电位的降低、稳定线粒体膜电位,抑制神经元凋亡,起到神经元保护作用。
目的:觀察神經細胞缺氧/缺糖損傷後線粒體膜電位(MMP)和凋亡的變化情況及阿司匹林的保護作用。方法用體外培養7 d的Wistar大鼠皮質神經細胞,隨機分為正常對照組、缺氧/缺糖模型組、缺氧/缺糖加100μmol/L濃度阿司匹林組。缺氧/缺糖2 h處理後,四甲基偶氮唑鹽(MTT)比色分析法檢測神經元線粒體活性;流式細胞術檢測神經元線粒體膜電位、雙染法檢測不同組神經元的凋亡情況。結果缺氧/缺糖損傷2h後,模型組的線粒體活性和MMP 水平較對照組顯著降低(P<0.01)。細胞凋亡百分率均較對照組顯著升高(P<0.01)。而阿司匹林組能顯著提高神經元線粒體活性、膜電位,降低細胞凋亡的百分率。結論阿司匹林可抑製缺氧/缺糖損傷所緻的神經元線粒體活性和膜電位的降低、穩定線粒體膜電位,抑製神經元凋亡,起到神經元保護作用。
목적:관찰신경세포결양/결당손상후선립체막전위(MMP)화조망적변화정황급아사필림적보호작용。방법용체외배양7 d적Wistar대서피질신경세포,수궤분위정상대조조、결양/결당모형조、결양/결당가100μmol/L농도아사필림조。결양/결당2 h처리후,사갑기우담서염(MTT)비색분석법검측신경원선립체활성;류식세포술검측신경원선립체막전위、쌍염법검측불동조신경원적조망정황。결과결양/결당손상2h후,모형조적선립체활성화MMP 수평교대조조현저강저(P<0.01)。세포조망백분솔균교대조조현저승고(P<0.01)。이아사필림조능현저제고신경원선립체활성、막전위,강저세포조망적백분솔。결론아사필림가억제결양/결당손상소치적신경원선립체활성화막전위적강저、은정선립체막전위,억제신경원조망,기도신경원보호작용。
Objective To investigate the neuroprotective effects of aspirin on mitochondrial membrane potential (MMP) and apoptosis following oxygen/glucose deprivation (OGD)-induced injury in neurons. Methods Cultured cor-tex neurons harvested from Wistar rats at day 7 were randomly assigned to normal control group, OGD group, and OGD plus aspirin treatment (100 μmol/L) group, respectively. Following OGD for 2 hours, mitochondrion activity was measured based on the methyl thiazolyl tetrazolium (MTT) test. The MMP was measured by flow cytometry. Neuronal necrosis were assayed with annexin-FITC and PI double immunofluorescence microscopy. Results Following OGD for 2 hours, the MMP and mitochondrion activity were consistently reduced and the percentage of neuronal apoptosis increased (all P<0.01). Aspirin significantly restored mitochondrion activity, decreased the percentage of neuron apop-tosis, and increased the MMP. Conclusion Aspirin significantly abrogates the decline of MMP, restores mitochondri-on activity, stabilizes the MMP and inhibits neuronal apoptosis following OGD induced injury, which represents the neuroprotective effects.