氯通道在葛根素注射液致溶血反应中的作用

目的:观察阻断和激活氯通道对葛根素注射液致家兔溶血反应的影响,探讨氯通道在葛根素注射液溶血反应中的作用。方法:将不同浓度的葛根素注射液(0.75、1.5、3、6、12 mg/ml)与家兔红细胞悬液共孵育6 h,使用细胞图像记录系统观测葛根素注射液是否诱导红细胞溶血,酶标仪、流式细胞仪检测红细胞溶血率,并观测激活和阻断氯通道对葛根素注射液溶血作用的影响。结果:葛根素注射液可引起家兔红细胞体外溶血,在所观察的1.5mg/ml～12 mg/ml范围内,溶血效应呈浓度依赖性增强(n=3,P<0.01)。氯通道阻断剂Tamoxifen(20μmol/L)、ATP(10 mmol/L)可有效抑制葛根素注射液的溶血作用(n=3～5,P<0.01);而使用低浓度ATP(50μmol/L)激活氯通道,则显著增强葛根素注射液的溶血作用(n=4,P<0.01)。结论:葛根素注射液的体外溶血效应呈浓度依赖性,氯通道激活与葛根素注射液诱导的溶血反应密切相关。

The anti-neoplastic activities of aloperine in HeLa cervical cancer cells are associated with inhibition of the IL-6-JAK1-STAT3 feedback loop

Cervical cancer(CC)is recognized as the most common neoplasm in the female reproductive system worldwide.The lack of chemotherapeutic agents with outstanding effectiveness and safety severely compromises the anti-cipated prognosis of patients.Aloperine(ALO)is a natural quinolizidine alkaloid with marked anti-cancer effects on multiple malignancies as well as favorable activity in relieving inflammation,allergies and infection.However,its therapeutic efficacy and underlying mechanism in CC are still unclear.In the current study,MTT assay was employed to evaluate the viability of HeLa cells exposed to ALO to preliminarily estimate the effectiveness of ALO in CC.Then,the effects of ALO on the proliferation and apoptosis of HeLa cells were further investigated by plate colony formation and flow cytometry,respectively,while the migration and invasion of ALO-treated HeLa cells were evaluated using Transwell assay.Moreover,nude mice were subcutaneously inoculated with HeLa cells to demonstrate the anti-CC properties of ALO in vivo.The molecular mechanisms underlying these effects of ALO were evaluated by Western blot and immunohistochemical analysis.This study experimentally demonstrated that ALO inhibited the proliferation of HeLa cells via G2 phase cell cycle arrest.Simultaneously,ALO promoted an increase in the percentage of apoptotic HeLa cells by increasing the Bax/Bcl-2 ratio.Additionally,the migration and invasion of HeLa cells were attenuated by ALO treatment,which was considered to result from inhibition of epithelial-to-mesenchymal transition.For molecular mechanisms,the expression and activation of the IL-6-JAK1-STAT3 feedback loop were markedly suppressed by ALO treatment.This study indicated that ALO markedly suppresses the proliferation,migration and invasion and enhances the apoptosis of HeLa cells.In addition,these prominent anti-CC properties of ALO are associated with repression of the IL-6-JAK1-STAT3 feedback loop.