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作 者:王雷[1] 付爱萍 孙书红[3] 王曼[1] 谢芳元[1] WANG Lei;FU Ai-ping;SUN Shu-hong;WANG Man;XIE Fang-yuan(Department of Cardiology, Fourth Hospital of Xi'an, Xi'an, Shaanxi, 710004, China;Department of Endocrinology, Aerospace Hospital ofShaanxi, Xi'an, Shaanxi, 710025, China;Department of Cardiology, Hospital of Shaanxi Armed Police Corps, Xi'an, Shaanxi, 710054, China)
机构地区:[1]西安市第四医院心内科,陕西西安710004 [2]陕西航天医院内分泌科,陕西西安710025 [3]武警陕西总队医院心内科,陕西西安710054
出 处:《现代生物医学进展》2018年第7期1243-1247,1233,共6页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(30800472)
摘 要:目的:探讨木犀草素对高糖诱导的心肌微血管内皮细胞(cardiac microvascular endothelial cells,CMECs)损伤的影响及其可能调控机制。方法:消化法分离大鼠CMECs,将原代CMECs随机分为4组:低糖组、低糖+木犀草素组、高糖组和高糖+木犀草素组。低糖+木犀草素组和高糖+木犀草素组分别加入30μmmol/L的木犀草素孵育24 h,低糖组和高糖组分别加入同等体积的DMSO孵育24 h。CCK-8实验检测CMECs增殖;Tunel法检测CMECs凋亡;Transwell检测CMECs的迁移能力;Western blot检测PKC-βⅡ的表达。结果:与低糖组和低糖+木犀草素组相比,高糖组CMECs增殖能力显著降低(0.341±0.018,P<0.05),CMECs凋亡显著增加(P<0.05),CMECs迁移能力显著降低(116±12.2,P<0.05),PKC-βⅡ的表达显著增加(P<0.05);与高糖组相比,高糖+木犀草素组CMECs增殖能力显著增加(0.550±0.023,P<0.05),CMECs凋亡显著减少(P<0.05),CMECs迁移能力显著增加(169±7.3,P<0.05),PKC-βⅡ的表达显著降低(P<0.05)。结论:木犀草素可能通过抑制PKC-βⅡ激活减少高糖诱导的心肌微血管内皮细胞损伤。Objective: To explore the effects and mechanism of luteolin on the impairment of cardiac microvascular endothelial cells (CMECs) caused by high glucose. Methods: CMECs were isolated from rats with collagenase digestion. Primary CMECs were randomly divided to four groups: low glucose group, low glucose + luteolin group, high glucose group, high glucose + luteolin group. Low glucose + luteolin group and high glucose + luteolin group were treated with luteolin (30 μmmol/L), while low glucose group and high glucose group were treated with DMSO in the absence or presence of high glucose for 24 h. The proliferation of CMECs was evaluated by CCK-8 assay. Apoptotic index of CMECs was examined by Tunel and migration of CMECs was measured by migration assay. Western blot was used to determine the expression ofPKC-βⅡ. Results: Compared with low glucose group and low glucose + luteolin group, the proliferation of CMECs attenuated significantly (0.341± 0.018, P〈0.05), with increased apoptotic index (P〈0.05), as well as decreased CMECs migration (116±12.2, P〈0.05), and the expression ofPKC-βⅡ was upregulated (P〈0.05) in high glucose group. Compared with those in high glucose group, the proliferation of CMECs increased significantly (0.550± 0.023, P〈0.05) and apoptotic index reduced significantly(169± 7.3, P〈0.05), with restored CMECs migration (P〈0.05) and there was a reduction of level of PKC-βⅡ(P〈0.05) by the treatment with luteolin in high glucose + luteolin group. Conclusion: Luteolin can significantly decrease the impairment of CMECs caused by high glucose, possibly by inhibiting the activation of PKC-βⅡ.
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