CAJ | 학술논문

目的探讨栀子苷抑制血小板衍生生长因子(PDGF)介导的大鼠肝星状细胞(HSC-T6)增殖活化的作用及其可能机制。方法培养 HSC-T6,体外给予不同浓度(20、50、100、200、400μg/ml)的栀子苷,通过MTT法检测细胞的活力；选取20、50、100μg/ml的栀子苷, PDGF刺激后,采用MTT、实时定量PCR( qRT-PCR)和Western blot 法检测细胞增殖和细胞活化标志物α-平滑肌肌动蛋白(α-SMA)的表达；进一步采用Western blot 法检测栀子苷对MAPK通路蛋白 P-ERK、P-p38和 Akt/mTOR/p70S6K 通路蛋白的表<br>　　达。结果栀子苷可以抑制PDGF诱导的HSC-T6的增殖和减少活化标志物α-SMA的表达,并且明显抑制 Akt、mTOR和p70S6K的磷酸化水平,但是对ERK、p38活化水平无显著影响。结论栀子苷可以抑制PDGF诱导的HSC-T6的增殖与活化,可能起到抗纤维化的作用,这一作用的产生可能与Akt/mTOR/p70S6K通路有关。
목적탐토치자감억제혈소판연생생장인자(PDGF)개도적대서간성상세포(HSC-T6)증식활화적작용급기가능궤제。방법배양 HSC-T6,체외급여불동농도(20、50、100、200、400μg/ml)적치자감,통과MTT법검측세포적활력；선취20、50、100μg/ml적치자감, PDGF자격후,채용MTT、실시정량PCR( qRT-PCR)화Western blot 법검측세포증식화세포활화표지물α-평활기기동단백(α-SMA)적표체；진일보채용Western blot 법검측치자감대MAPK통로단백 P-ERK、P-p38화 Akt/mTOR/p70S6K 통로단백적표<br>　　체。결과치자감가이억제PDGF유도적HSC-T6적증식화감소활화표지물α-SMA적표체,병차명현억제 Akt、mTOR화p70S6K적린산화수평,단시대ERK、p38활화수평무현저영향。결론치자감가이억제PDGF유도적HSC-T6적증식여활화,가능기도항섬유화적작용,저일작용적산생가능여Akt/mTOR/p70S6K통로유관。
Objective To investigate the effect of geniposide on regulating the proliferation and activation of PDGF-induced HSC-T6 cells. Methods HSC-T6 cells were cultivated by geniposide with different concentrations (0, 20, 50, 100, 200, 400 μg/ml), and or after the cells were stimulated with PDGF, respectively. Cell activity, mRNA and total protein expressions were assayed by MTT, qRT-PCR and Western blot. Results The geniposide pretreatment effectively inhibited PDGF-mediated proliferation and the expressions of the activation markers (α-SMA) in HSC-T6, and also inhibited the phosphorylation levels of Akt,mTOR and p70S6K. But the geniposide couldn′t affect the activation levels of ERK and p38. Furthermore,the protein of the MAPK pathway ( P-ERK and P-p38) and Akt/mTOR/p70S6K signaling pathway were detected by Western blot. Conclusion The proliferation and activation of HSC-T6 induced by PDGF are inhibited by geniposide treatment, and then it maybe provide new i-deas and targets for the prevention of liver fibrosis, which is probably through modulating the Akt/mTOR/p70S6K signaling pathway.