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目的:研究吉马酮对缺糖缺氧(OGD)损伤的原代大鼠微脑血管内皮细胞(BMECs)抗凝和纤溶等功能的影响。方法:通过使用DMEM F12无糖培养液,并将其放入含95%N2、5%CO2混合气体的缺氧小室中培养6h,从而建立原代BMECs细胞缺氧缺糖模型。利用MTT法检测细胞增殖率及细胞毒性;ELISA法检测6-keto-PGF1α、ET-1、t-PA和PAI-1;硝酸还原酶法检测NO等。结果:在20~200μmol/L范围内随着浓度的增大吉马酮对细胞的增殖作用增强,而超过范围后抑制细胞生长。与正常组比较缺氧缺糖损伤使6-keto-PGF1α、NO、t-PA、SOD和GSH-Px含量降低,PAI-1、ET-1、LDH、MDA含量增加;与模型组比较吉马酮(11、22、44mg/L)使6-keto-PGF1α、NO、t-PA、SOD和GSH-Px含量增加,PAI-1、ET-1、LDH、MDA含量减少。结论:缺氧缺糖损伤BMECs细胞使其分泌功能下降,且凝血和纤溶功能出现异常;吉马酮对缺氧缺糖损伤BMECs细胞具有保护作用,并调节BMECs细胞的分泌功能及凝血和纤溶功能。
AIM: To investigate the effects of germacde on anticoagulation and fibrinolysis in primary rat microvessel endothelial cells (BMECs) injured by glucose and anoxia (OGD). Methods: The DMEM F12 glucose-free medium was cultured in anoxic chamber containing 95% N2 and 5% MTT assay was used to detect cell proliferation and cytotoxicity. ELISA was used to detect 6-keto-PGF1α, ET-1, t-PA and PAI-1. Nitric acid reductase was used to detect NO and so on. Results: In the range of 20 ~ 200 μmol / L, the proliferation of gemfus was enhanced with the increase of concentration, while the inhibition of cell growth was beyond the range. Compared with the normal group, the content of 6-keto-PGF1α, NO, t-PA, SOD and GSH-Px decreased and the contents of PAI-1, ET-1, LDH and MDA increased Ketone (11,22,44 mg / L) increased the content of 6-keto-PGF1α, NO, t-PA, SOD and GSH-Px and decreased the contents of PAI-1, ET-1, LDH and MDA. CONCLUSION: Hypoxia / glucose deprivation (BMECs) can decrease the secretion of BMECs and cause abnormal coagulation and fibrinolysis. Gemcitabine can protect BMECs from hypoxia / glucose deprivation injury and regulate the secretion and coagulation of fibroblasts Soluble function.