医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2014年
6期
695-698
,共4页
川芎嗪%PC12细胞%损伤,脑缺血-再灌注
川芎嗪%PC12細胞%損傷,腦缺血-再灌註
천궁진%PC12세포%손상,뇌결혈-재관주
Tetramethylpyrazine%PC12 cells%Injury,cerebral ischemia-reperfusion
目的:分析川芎嗪对咖啡因引起大鼠肾上腺嗜铬细胞瘤克隆化细胞株PC12细胞损伤的保护作用,探讨川芎嗪治疗脑缺血-再灌注损伤的机制。方法制备咖啡因细胞损伤模型,通过CCK-8法活细胞检测、流式细胞术线粒体膜电位测定、Western-blot检测高迁移率族蛋白B1(HMGB1)、酶联免疫吸附测定(ELISA)检测氧化应激指标观察咖啡因的毒性及川芎嗪的保护作用。结果川芎嗪预处理后,PC12细胞的存活数显著提高,细胞线粒体膜电位提高,HMGB1表达显著降低,超氧化物歧化酶( SOD)上调,乳酸脱氢酶( LDH)和丙二醛( MDA)下调,谷胱甘肽( GSH)升高。结论川芎嗪对咖啡因引起的PC12细胞损伤有显著的保护作用,其保护作用可能与川芎嗪抑制细胞凋亡、调节炎症性递质表达水平及氧化应激反应相关。
目的:分析川芎嗪對咖啡因引起大鼠腎上腺嗜鉻細胞瘤剋隆化細胞株PC12細胞損傷的保護作用,探討川芎嗪治療腦缺血-再灌註損傷的機製。方法製備咖啡因細胞損傷模型,通過CCK-8法活細胞檢測、流式細胞術線粒體膜電位測定、Western-blot檢測高遷移率族蛋白B1(HMGB1)、酶聯免疫吸附測定(ELISA)檢測氧化應激指標觀察咖啡因的毒性及川芎嗪的保護作用。結果川芎嗪預處理後,PC12細胞的存活數顯著提高,細胞線粒體膜電位提高,HMGB1錶達顯著降低,超氧化物歧化酶( SOD)上調,乳痠脫氫酶( LDH)和丙二醛( MDA)下調,穀胱甘肽( GSH)升高。結論川芎嗪對咖啡因引起的PC12細胞損傷有顯著的保護作用,其保護作用可能與川芎嗪抑製細胞凋亡、調節炎癥性遞質錶達水平及氧化應激反應相關。
목적:분석천궁진대가배인인기대서신상선기락세포류극륭화세포주PC12세포손상적보호작용,탐토천궁진치료뇌결혈-재관주손상적궤제。방법제비가배인세포손상모형,통과CCK-8법활세포검측、류식세포술선립체막전위측정、Western-blot검측고천이솔족단백B1(HMGB1)、매련면역흡부측정(ELISA)검측양화응격지표관찰가배인적독성급천궁진적보호작용。결과천궁진예처리후,PC12세포적존활수현저제고,세포선립체막전위제고,HMGB1표체현저강저,초양화물기화매( SOD)상조,유산탈경매( LDH)화병이철( MDA)하조,곡광감태( GSH)승고。결론천궁진대가배인인기적PC12세포손상유현저적보호작용,기보호작용가능여천궁진억제세포조망、조절염증성체질표체수평급양화응격반응상관。
Objective To analyze whether tetramethylpyrazine could protect PC12 cells from injuries induced by caffeine,and to explore the mechanism of tetramethyipyrazine in the treatment of cerebral ischemia-reperfusion injury. Methods Caffeine was added to induce apoptosis of PC12 cells. Cytotoxicity was detected by CCK-8 assay. The electric potential of mitochondrial membrane was determined by flow cytometry. HMGB1 was detected by Western blotting. Oxidative stress was detected by ELISA. We observed toxicity of caffeine and the protective effects of tetramethylpyrazine. Results After the pre-treatment,tetramethylpyrazine significantly improved PC12 cell survival. Mitochondrial membrane potential was increased,the expression of HMGB1 decreased,SOD increased,LDH and MDA decreased,and GSH elevated. Conclusion Tetramethylpyrazine exerts a significant protective effect on PC12 cell injury caused by caffeine. The protective effect may be related to inhibition of apoptosis and regulation of the expression level of mediators involved in inflammation and oxidative stress.