Buyang Huanwu Decoction fraction protects against cerebral ischemia/reperfusion injury by attenuating the inflammatory response and cellular apoptosis

Buyang Huanwu Decoction fraction extracted from Buyang Huanwu Decoction contains saponins of Astragalus, total paeony glycoside and safflower flavones. The aim of this study was to demonstrate the neuroprotective effect and mechanism of Buyang Huanwu Decoction fraction on ischemic injury both in vivo and in vitro. In vivo experiments showed that 50-200 mg/kg Buyang Huanwu Decoction fraction reduced infarct volume and pathological injury in ischemia/reperfusion rats, markedly inhibited expression of nuclear factor-KB and tumor necrosis factor-a and promoted nestin protein expression in brain tissue. Buyang Huanwu Decoction fraction （200 mg/kg） exhibited significant effects, which were similar to those of 100 mg/kg Ginkgo biloba extract. In vitro experimental results demonstrated that 10-100 mg/L Buyang Huanwu Decoction fraction significantly improved cell viability, decreased the release of lactate dehydrogenase and malondialdehyde levels, and inhibited the rate of apoptosis in HT22 cells following oxygen-glucose deprivation. Buyang Huanwu Decoction fraction （100 mg/L） exhibited significant effects, which were similar to those of 100 mg/L Ginkgo biloba extract. These findings suggest that Buyang Huanwu Decoction fraction may represent a novel, protective strategy against cerebral ischemia/reperfusion injury in rats and oxygen-glucose deprivation-induced damage in HT22 cells in vitro by attenuating the inflammatory response and cellular apoptosis.

铅对海马神经细胞Brn-3a表达的影响与致凋亡作用

目的 探讨体外条件下铅对神经细胞内转录因子Brn 3a的表达和致凋亡作用。方法 采用海马神经细胞体外培养建立细胞模型 ,醋酸铅的染毒浓度分别为 0 1、1、10、10 0、10 0 0 μmol L ,对照组给予等量培养液。染毒后 2 4h及 4 8h时MTT法测定各组细胞的存活率 ;免疫组织化学法测定Brn 3a的表达以及TUNEL法检测神经细胞凋亡。结果 引起海马神经细胞存活率明显下降的醋酸铅的最低浓度是 10 μmol L ,醋酸铅浓度越高 ,细胞存活率越低。1μmol L醋酸铅可引起Brn 3a阳性细胞积分光密度显著下降 (P <0 0 5 ) ,10 μmol L醋酸铅可引起Brn 3a阳性面积比的显著下降 (P <0 0 1)。 1μmol L是醋酸铅引起培养海马神经细胞凋亡的最低浓度 ,各组细胞凋亡程度呈现明显的浓度依赖效应。结论 铅对发育期海马组织的损害至少部分是与铅所致神经细胞凋亡相关联的 ,并且铅导致培养海马神经细胞Brn

糖皮质激素对成体海马神经祖细胞的影响

背景:体内研究显示,高浓度糖皮质激素可抑制大鼠内源性神经前体细胞增殖。而神经胶质抗原2蛋白聚糖阳性神经祖细胞(NG2细胞)是成熟中枢神经系统中最大的增殖细胞群体,具有多分化潜能。目的:观察糖皮质激素对体外培养的成熟大鼠海马由来的NG2细胞生存和增殖的影响。方法:原代及传代培养成年大鼠海马NG2细胞,以0,0.1,1,10,100μmol浓度糖皮质激素类药物地塞米松干预48h后,采用乳酸脱氢酶分析法测定细胞活性,原位缺口末端标记技术(即TUNEL法)观察细胞凋亡情况,5’-溴脱氧尿嘧啶核苷掺入法鉴定细胞增殖状况。结果与结论:1,10,100μmol浓度地塞米松干预明显减少NG2细胞数,并显著增加TUNEL阳性细胞率,明显减少BrdU阳性细胞率。结果可见高浓度糖皮质激素能抑制NG2细胞分裂增殖,并诱导细胞凋亡,从而明显减少NG2细胞数。

加味圣愈汤对大鼠脑外伤后神经细胞凋亡的影响

目的:研究加味圣愈汤对脑外伤大鼠海马结构神经细胞凋亡的影响,探讨其抑制创伤性脑损伤后继发性脑损伤的作用机制。方法:采用改良的Feeney法建立脑外伤模型,将动物随机分为假手术组、脑外伤组、加味圣愈汤治疗组。72h处死后行尼氏染色,光镜下观察损伤侧海马细胞形态并计数,分别用凋亡细胞原位末端标记(TUNEL)法和免疫组织化学法观察海马神经细胞凋亡及凋亡相关基因caspase-3的蛋白表达情况。结果:加味圣愈汤治疗组与脑外伤组比较,损伤侧海马神经细胞损害减轻,细胞数明显增加,神经细胞凋亡减少,caspase-3表达减少(P<0.01)。结论:加味圣愈汤治疗可减轻脑外伤后的继发性损伤,其机制可能与抑制caspase-3的表达,减少TBI后神经细胞的凋亡有关。

补肾益智方含药血清对培养海马神经元过度凋亡的抑制作用

目的：探讨天然促智药复方──补肾益智方含药血清对培养海马神经元过度凋亡的抑制作用。方法：取补肾益智方治疗组及各对照组大鼠的血清进行海马神经元培养，荧光标记，计量分析。结果：各组血清培养的海马神经元凋亡率，中药组明显低于模型组、石杉碱甲（ＨｕｐＡ）组明显高于青年组，与老年正常组没有明显差异。结论：补肾益智方含药血清可减少培养海马神经元的过度调亡。