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Cai's Neiyi Prescription promotes apoptosis and inhibits inflammation in endometrial stromal cells with endometriosis through inhibiting USP10

机译:CAI的Neiyi处方促进了细胞凋亡,并通过抑制USP10来抑制子宫内膜体细胞中子宫内膜间质细胞的炎症

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To observe the effect of Cai's Neiyi Prescription (CNYP) on the apoptosis and inflammation in endometrial stromal cells with endometriosis (EM) both in vivo and in vitro, EM model rats and endometrial stromal cells were treated with CNYP and the level of USP10, p-ERK1/2, ERK1/2, and apoptosis-related protein as well as the levels of proinflammatory factors were measured by Western blotting and ELISA, respectively. Rats with surgically induced EM showed increased USP10 expression and ERK/2 activation. Intragastric administration of CNYP granule significantly inhibited EM-induced ERK1/2 activation and expression of USP10 and Bcl-2, but increased the expression of Bax and Caspase-7 in EM-induced rats. CNYP granule administration also inhibited EM-induced inflammation in rats. Moreover, the ectopic endometrial stromal cells isolated from EM patients demonstrated decreased ERK1/2 activation and expression of USP10 and Bcl-2 and increased expression of Bax and Caspase-7 after cultured in DMEM containing CNYP-medicated rat serum, which were reversed by USP10 overexpression and were enhanced by USP10 siRNA. USP10 overexpression also inhibited while USP10 siRNA enhanced the CNYP-induced inhibition of inflammation in ectopic endometrial stromal cells. Taken together, our results suggest that CNYP granule promotes apoptosis and inhibits inflammation in endometrial stromal cells with EM through inhibiting USP10.
机译:为了观察CAI Neiyi处方(CNYM)对子宫内膜体间质细胞的细胞凋亡和炎症的影响,在体内和体外,EM模型大鼠和子宫内膜基质细胞被CNYP和USP10,P的水平处理 - 通过蛋白质印迹和ELISA测量-ERK1 / 2,ERK1 / 2和凋亡相关蛋白以及促炎因子的水平。具有手术诱导的大鼠EM显示USP10表达和ERK / 2活化。 CNYM颗粒的胃内施用显着抑制EM-诱导的ERK1 / 2活化和USP10和BCL-2的表达,但增加了BAX和Caspase-7在EM诱导的大鼠中的表达。 CNYP颗粒管理还抑制了大鼠的EM诱导的炎症。此外,从EM患者中分离的异位子宫内膜基质细胞证明ERK1 / 2活化和USP10和BCL-2的表达,并在含有CNYM药物大鼠血清的DMEM培养后增加了Bax和Caspase-7的表达,其被USP10逆转过表达和USP10 siRNA增强。 USP10过表达也抑制,而USP10 siRNA增强了异位子宫内膜间构细胞中的CNYP诱导的炎症抑制。我们的结果表明CNYP颗粒促进了凋亡,并通过抑制USP10抑制子宫内膜基质细胞中的炎症。

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