牡丹江医学院学报
牡丹江醫學院學報
모단강의학원학보
JOURNAL OF MUDANJIANG MEDICAL COLLEGE
2015年
2期
8-11
,共4页
灵芝酸A%海马神经元%癫痫
靈芝痠A%海馬神經元%癲癇
령지산A%해마신경원%전간
Ganoderma acid A%hippocampal neurons%epilepsy
目的:旨在验证灵芝酸A对海马神经元异常放电的影响。方法分离24h新生Wistar大鼠原代海马神经元。正常对照组:将培养9d的海马神经元全液换成正常细胞外液处理3h,然后恢复正常培养24h;无Mg2+诱导组、灵芝酸A组、紫杉醇组、γ-氨基丁酸组、丙戊酸钠组分别将培养9d的海马神经元全液换成无镁细胞外液或添加相应的50μg/mL的灵芝酸A、50μmol/L的紫杉醇、100μmol/L的γ-氨基丁酸、100mg/L的丙戊酸钠混悬液处理3h,然后恢复正常培养,MTT法检测细胞存活率;分光光度计检测超氧化物歧化酶活性;流式细胞仪检测细胞线粒体膜电位的变化。结果50μg/mL灵芝酸A可提高海马神经元细胞存活率;能升高癫痫样海马神经元细胞SOD活性、升高线粒体膜电位。结论灵芝酸A可通过抑制细胞氧化损伤、抑制凋亡而保护异常放电的海马神经元。
目的:旨在驗證靈芝痠A對海馬神經元異常放電的影響。方法分離24h新生Wistar大鼠原代海馬神經元。正常對照組:將培養9d的海馬神經元全液換成正常細胞外液處理3h,然後恢複正常培養24h;無Mg2+誘導組、靈芝痠A組、紫杉醇組、γ-氨基丁痠組、丙戊痠鈉組分彆將培養9d的海馬神經元全液換成無鎂細胞外液或添加相應的50μg/mL的靈芝痠A、50μmol/L的紫杉醇、100μmol/L的γ-氨基丁痠、100mg/L的丙戊痠鈉混懸液處理3h,然後恢複正常培養,MTT法檢測細胞存活率;分光光度計檢測超氧化物歧化酶活性;流式細胞儀檢測細胞線粒體膜電位的變化。結果50μg/mL靈芝痠A可提高海馬神經元細胞存活率;能升高癲癇樣海馬神經元細胞SOD活性、升高線粒體膜電位。結論靈芝痠A可通過抑製細胞氧化損傷、抑製凋亡而保護異常放電的海馬神經元。
목적:지재험증령지산A대해마신경원이상방전적영향。방법분리24h신생Wistar대서원대해마신경원。정상대조조:장배양9d적해마신경원전액환성정상세포외액처리3h,연후회복정상배양24h;무Mg2+유도조、령지산A조、자삼순조、γ-안기정산조、병무산납조분별장배양9d적해마신경원전액환성무미세포외액혹첨가상응적50μg/mL적령지산A、50μmol/L적자삼순、100μmol/L적γ-안기정산、100mg/L적병무산납혼현액처리3h,연후회복정상배양,MTT법검측세포존활솔;분광광도계검측초양화물기화매활성;류식세포의검측세포선립체막전위적변화。결과50μg/mL령지산A가제고해마신경원세포존활솔;능승고전간양해마신경원세포SOD활성、승고선립체막전위。결론령지산A가통과억제세포양화손상、억제조망이보호이상방전적해마신경원。
Objective To isolate rat primary hippocampal neurons , detect the impact of Ganoderma acid A on the epileptic cell mitochondrial membrane potential and superoxide dismutase in ouder to investigate the antiepileptic mechanism of Ganoderma acid A , provide clinical antiepileptic drugs theory basis.Methods 24h newborn Wistar rat primary hippocampal neurons rere isolated , and then the experimental groups were divided into normal control group: the 9th days cultured hippocampal neurons in complete medium were treated with normal extracellular fluid for 3 hours, and recovered complete medium for 24h;no Mg2+induction group , Ganoderma acid group A , paclitaxel ,γ-aminobutyric acid group , sodium valproate group were treated with Mg 2+-free extracellular fluid or ad-ditional added 50μg /mL Ganoderma acid A, 50μmol /L paclitaxel, 100μmol /L γ-aminobutyric acid, 100mg /L sodium val-proate suspensions for 3h, and recovered complete medium for 24h;We detect the changes of the mitochondrial membrane potential by flow cytometry, superoxide dismutase activity by spectrophotometer , to explore the pathogenesis of epilepsy and the antiepileptic mecha-nism of Ganoderma acid A.Results We successfully isolated rat primary hippocampal neurons;Ganoderma acid A at 50μg /mL con-centration were nontoxic to hippocampal neurons;Ganoderma acid A increased the activity of SOD in hippocampal neurons , Ganoderma acid A elevated the epileptic mitochondrial membrane potential.Conclusion Ganoderma acid A has anti -epileptic effect by antioxi-dant and inhibiting apoptosis.