青蒿琥酯对高糖诱导的肾小管上皮细胞凋亡及TNF-α、IL-8表达的影响
目的:探讨青蒿琥酯(Art)对高糖诱导的大鼠肾小管上皮细胞(NRK-52E)的凋亡及肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)表达的影响。方法传代培养大鼠肾小管上皮细胞,分为正常对照组、高糖组、高糖+不同浓度青蒿琥酯组(10、20、30 mg/L)、高糖+依那普利对照组(5 mg/L)。四甲基偶氮唑盐微量比色(MTT)法观察细胞增殖能力的改变;流式细胞仪AnnexinV-FITC/PI双染法检测细胞凋亡指数;酶联免疫吸附(ELISA)法检测细胞培养上清液中TNF-α和IL-8蛋白含量。结果(1)经高糖处理48 h后,NRK-52E细胞增殖抑制,细胞凋亡率增高,细胞上清液中TNF...
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Published in | 天津医药 Vol. 43; no. 1; pp. 20 - 24 |
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Main Author | |
Format | Journal Article |
Language | Chinese |
Published |
桂林医学院附属医院内分泌科 邮编541004
2015
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Subjects | |
Online Access | Get full text |
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Summary: | 目的:探讨青蒿琥酯(Art)对高糖诱导的大鼠肾小管上皮细胞(NRK-52E)的凋亡及肿瘤坏死因子-α(TNF-α)、白细胞介素-8(IL-8)表达的影响。方法传代培养大鼠肾小管上皮细胞,分为正常对照组、高糖组、高糖+不同浓度青蒿琥酯组(10、20、30 mg/L)、高糖+依那普利对照组(5 mg/L)。四甲基偶氮唑盐微量比色(MTT)法观察细胞增殖能力的改变;流式细胞仪AnnexinV-FITC/PI双染法检测细胞凋亡指数;酶联免疫吸附(ELISA)法检测细胞培养上清液中TNF-α和IL-8蛋白含量。结果(1)经高糖处理48 h后,NRK-52E细胞增殖抑制,细胞凋亡率增高,细胞上清液中TNF-α、IL-8蛋白浓度升高。(2)经青蒿琥酯干预后,与高糖组比较,NRK-52细胞增殖明显,细胞凋亡率减低,细胞上清液中TNF-α、IL-8蛋白浓度降低,其干预作用呈现剂量依赖性。结论青蒿琥酯可抑制高糖诱导的NRK-52E细胞凋亡及细胞上清液中炎症因子TNF-α、IL-8的表达。青蒿琥酯的抗炎和免疫调节作用可能有助于糖尿病肾病的治疗。 |
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Bibliography: | diabetic nephropathies;apoptosis;tumor necrosis factor-alpha;artesunate;renal tubular ep-ithelial cells Objective To investigate the effects of artesunate (Art) on cell apoptosis, tumor necrosis factor-alpha (TNF-α) and interleukin-8 (IL-8) expression induced by high glucose in rat renal tubular epithelial cells (NRK-52E). Methods NRK-52E cells were cultured and divided into normal control group, high glucose group, high glucose with different concen?trations of Art (10 mg/L, 20 mg/L and 30 mg/L) groups, and high glucose with Ena (5 mg/L) group. MTT assay was used to de?tect the cell proliferation. The apoptotic rate was evaluated by flow cytometry with AnnexinV-FITC/PI double stains. The pro?tein levels of TNF-αand IL-8 in the cell culture supernatant were determined using ELISA. Results High glucose inhibit?ed NRK-52E proliferation, induced its apoptosis, and the expressions of TNF-αand IL-8 in the supernatant. Application of Art obviously abolished the effects of high glucose, and the effects of Art were sh |
ISSN: | 0253-9896 |
DOI: | 10.3969/j.issn.0253-9896.2015.01.006 |