作者机构：
[何清湖; 朱闽] School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;[朱闽; 戴芳; 徐楠] Department of Andrology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, China;[赵自垒; 荀建宁] Graduate School, Guangxi University of Chinese Medicine, Nanning, Guangxi 530001, China;[荀建宁] Department of Andrology, Yucheng People's Hospital, Yucheng, Henan 476300, China
关键词：
total Astragalus extract;total Panax notoginseng saponins;combination;cerebral ischemiareperfusion;energy metabolism;C-Jun N-terminal kinase signal transduction;mitochondrial apoptosis pathway;Chinese medicine
摘要：
Objective: To explore the effects and molecular mechanisms of the combination between total Astragalus extract (TAE) and total Panax notoginseng saponins (TPNS) against cerebral ischemiareperfusion injury. Methods: C57BL/6 mice were randomly divided into sham-operated group, model group, TAE (110 mg/kg) group, TPNS (115 mg/kg) group, TAE-TPNS combination group and Edaravone (4 mg/kg) group, treated for 4 days, then, cerebral ischemia-reperfusion injury was established by bilateral common carotid artery (CCA) ligation for 20 min followed by reperfusion for 1 and 24 h. Results: TPNS could increase adenosine triphosphate (ATP) level, TAE and TAE-TPNS combination increased ATP, adenosine diphosphate (ADP) contents and Na~+-K~+-ATPase activity, and the effects of TAE-TPNS combination were stronger than those of TAE or TPNS alone after reperfusion for 1 h. After reperfusion for 24 h, TAE, TPNS and TAE-TPNS combination significantly increased neurocyte survival rate and decreased the apoptosis rate as well as down-regulated the expression of phosphorylated c-June N-terminal kinase1/2 (p-JNK1/2), cytochrome C (Cyt C), cysteine aspartic acid-specific protease (Caspase)-9 and Caspase-3. Furthermore, the effects in TAE-TPNS combination were better than those in TAE or TPNS alone. Conclusion: The combination of TAE 110 mg/kg and TPNS 115 mg/kg could strengthen protective effects on cerebral ischemia injury, the mechanism underlying might be related to improving jointly the early energy metabolism, and relieving the delayed apoptosis via inhibiting the mitochondrial apoptosis pathway of JNK signal transduction.
摘要：
Danggui Buxue Tang (DBT), a combination of Astragalus and Angelica at a 5 : 1 ratio, mainly promotes hematopoiesis. However, in the clinic, the combination ratio of Astragalus and Angelica to treat low hematopoietic function is not an absolute 5 : 1 ratio, suggesting that the herbs may promote hematopoiesis better after being combined at a certain range of ratios. The objective of this study is to investigate the effect of different ratio combinations of Astragalus and Angelica on bone marrow hematopoiesis suppression induced by cyclophosphamide (CTX) and to probe the interaction and mechanism of Astragalus combined with Angelica in promoting hematopoiesis. Following establishment of the model, mice were administered with Astragalus (6.00 g.kg(-1)), Angelica (3.00 g.kg(-1)), and combinations of Astragalus and Angelica at different ratios, including 10 : 1 (Astragalus 9.81 g.kg(-1)+Angelica 0.98 g.kg(-1)), 5 : 1 (Astragalus 9.00 g.kg(-1)+Angelica 1.80 g.kg(-1)), 2 : 1 (Astragalus 7.71 g.kg(-1)+Angelica 3.08 g.kg(-1)), 1 : 1 (Astragalus 5.40 g.kg(-1)+Angelica 5.40 g.kg(-1)), 1 : 2.5 (Astragalus 3.08 g.kg(-1)+Angelica 7.71 g.kg(-1)), 1 : 5 (Astragalus 1.80 g.kg(-1)+Angelica 9.00 g.kg(-1)), and 1 : 10 (Astragalus 0.98 g.kg(-1)+Angelica 9.81 g.kg(-1)). Our results suggested that Astragalus mixed with Angelica synergistically promoted hematopoiesis best when the combination ratio of Astragalus and Angelica was 1 : 1, 1 : 2.5 or 1 : 5; moreover, the effect of Angelica was greater than that of Astragalus. The potential mechanisms of the combinations of Astragalus and Angelica that promote hematopoiesis include the dissolution of the effective components, promoting the synthesis and secretion of hematopoietic growth factor (HGF) and the proliferation of hematopoietic progenitor cells (HPCs).
通讯机构：
[Luo, Qi-Sheng] 4;4College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Hunan, Changsha 410208, China. E-mail:
关键词：
α-烯醇化酶;胶质瘤;糖代谢
摘要：
目的探讨抑制α-烯醇化酶(ENO1)表达对胶质瘤细胞糖代谢和细胞生长的影响。方法在胶质瘤细胞U251中,利用siRNA抑制ENO1表达后,利用葡萄糖摄取和乳酸生成实验检测糖代谢水平的改变;利用3-(4,5-dimethyl-2-thiazolyl)-2,5- diphenyl-2-H-tetrazolium bromide(MTT)和5-Ethynyl-2'-deoxyuridine(EDU)着色的方法检测细胞增殖和细胞周期的改变。 Western blot活性分析抑制ENO1表达糖代谢标志基因Hexokinase 2(HK2)和Lactate dehydrogenase A(LDHA)基因的表达水平改变。结果成功筛选了抑制ENO1的siRNA片段。在抑制ENO1表达,胶质瘤U251细胞摄取葡萄糖的能力明显降低(P= 0.023)以及乳酸生成能力明显下降(P=0.007)。进一步,MTT和EDU着色分析显示,在抑制ENO1表达后,细胞的增殖能力从第2天开始明显降低(P<0.05);除此之外,细胞周期G1/S转化能力明显抑制(P=0.0425)。机制分析显示,ENO1下调后糖代谢标志基因HK2和LDHA表达也明显下降。结论ENO1作为候选癌基因,通过正调控葡萄糖代谢从而促进了胶质瘤细胞的生长。
