论文部分内容阅读
目的探讨姜黄素对CsA诱导的人近端肾小管上皮细胞(HK-2细胞)内质网应激的影响。方法 CsA诱导HK-2细胞发生纤维化改变,同时采用不同浓度姜黄素干预,采用MTT法检测细胞增殖情况,流式细胞术检测细胞凋亡情况,western blot检测ERS标志性蛋白GRP78及相关凋亡蛋白CHOP的表达。结果用6 ng/m L CsA刺激HK-2细胞48 h后,细胞增殖明显增强,(1.562±0.125)vs(0.937±0.041),P<0.05,细胞凋亡增加,22.3%vs 3.5%,P<0.05,GRP78、CHOP的表达明显升高(0.714±0.006)vs(0.286±0.003),P<0.05;(0.533±0.005)vs(0.072±0.002),P<0.05;不同剂量的姜黄素干预后,细胞增殖及凋亡均受到了抑制(P<0.05),并不同程度的降低了GRP78及CHOP蛋白的表达(P<0.05)。结论姜黄素可以逆转CsA诱导的纤维化,其机制可能与姜黄素能够抑制ERS引起的细胞凋亡有关。
Objective To investigate the effect of curcumin on endoplasmic reticulum stress induced by CsA in human proximal tubular epithelial cells (HK-2 cells). Methods CsA induced fibrosis changes in HK-2 cells. At the same time, different concentrations of curcumin were used to interfere the proliferation of HK-2 cells. MTT assay was used to detect the cell proliferation. Flow cytometry was used to detect the apoptosis of HK-2 cells. Western blot was used to detect ERS marker GRP78 and related apoptosis Protein CHOP expression. Results After stimulated with 6 ng / mL CsA for 48 h, the proliferation of HK-2 cells was significantly increased (1.562 ± 0.125 vs 0.937 ± 0.041, P <0.05). The apoptosis of HK-2 cells increased by 22.3% vs 3.5% (P <0.05). The levels of GRP78 and CHOP were significantly increased (0.714 ± 0.006 vs 0.286 ± 0.003, P <0.05, 0.533 ± 0.005 vs 0.072 ± 0.002 respectively, P <0.05). After intervention with different doses of curcumin (P <0.05), and decreased the expressions of GRP78 and CHOP proteins to a certain extent (P <0.05). Conclusion Curcumin can reverse CsA-induced fibrosis, which may be related to the fact that curcumin can inhibit ERS-induced apoptosis.