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Simiao Qingwen Baidu decoction inhibits Epstein–Barr virus-induced B lymphoproliferative disease and lytic viral replication
Pharmaceutical Biology ( IF 3.8 ) Pub Date : 2021-06-22 , DOI: 10.1080/13880209.2021.1934038
Xianhui Yang 1 , Lingling Liu 2 , Huijuan Zhang 2 , Xiaoxu Sun 2 , Yongbin Yan 2 , Ruiying Ran 1
Affiliation  

Abstract

Context

Simiao Qingwen Baidu decoction (SQBD), a traditional Chinese medicine prescription, can ameliorate Epstein–Barr virus (EBV) induced disease. However, its mechanism still remains unknown.

Objective

To detect the mechanism of SQBD in EBV-induced B lymphoproliferative disease in vitro.

Materials and methods

Sprague–Dawley (SD) rats (n = 20) were given SQBD (10 mL/kg) by gavage once a day for 7 d. SQBD-containing serum was obtained from abdominal aortic blood of rats, and diluted with medium to obtain 5%, 10% or 20%-medicated serum. SD rats (n = 10) were given normal saline, and normal serum was collected as a control. EBV-transformed B cells (CGM1) were cultured in medium containing 5%, 10% or 20%-medicated serum. CGM1 cells were treated with normal serum as a control. Cell viability and apoptosis were examined. The expression and activity of proteins were assessed.

Results

We found that IC50 (83 ± 26.07%, 24 h; 69.88 ± 4.69%, 48 h) of 10% medicated serum was higher than that of 5% (25.47 ± 6.98%, 24 h; 21.62 ± 7.30%, 48 h) and 20%-medicated serum (51 ± 7.25%, 24 h; 56.03 ± 2.56%, 48 h). Moreover, SQBD promoted apoptosis of CGM1 cells by regulating EBV latency proteins expression. SQBD inhibited EBV-induced lytic viral replication.

Conclusions

Our data confirmed that SQBD inhibits EBV-induced B lymphoproliferative disease and lytic viral replication. This work provides a theoretical basis for the mechanism of SQBD in EBV-induced B lymphoproliferative disease, and SQBD may be an effectively therapeutic drug for EBV-induced B lymphoproliferative disease.



中文翻译:

四妙清瘟百度汤抑制Epstein-Barr病毒诱导的B淋巴细胞增殖性疾病和裂解病毒复制

摘要

语境

四妙清瘟百度汤(SQBD)是一种中药方剂,可改善爱泼斯坦-巴尔病毒(EBV)诱发的疾病。然而,其机制仍然未知。

客观的

体外检测SQBD在EBV诱导的B淋巴细胞增殖性疾病的作用机制。

材料和方法

Sprague-Dawley (SD) 大鼠 ( n  = 20) 通过每天一次灌胃给予 SQBD (10 mL/kg),持续 7 天。从大鼠腹主动脉血中提取含SQBD的血清,用培养基稀释得到5%、10%或20%的含药血清。SD大鼠(n  =10)给予生理盐水,采集正常血清作为对照。EBV 转化的 B 细胞 (CGM1) 在含有 5%、10% 或 20% 含药血清的培养基中培养。CGM1 细胞用正常血清处理作为对照。检查细胞活力和细胞凋亡。评估蛋白质的表达和活性。

结果

我们发现10% 含药血清的IC 50 (83 ± 26.07%, 24 h; 69.88 ± 4.69%, 48 h) 高于 5% (25.47 ± 6.98%, 24 h; 21.62 ± 7.30%, 48 h) ) 和 20% 含药血清(51 ± 7.25%,24 小时;56.03 ± 2.56%,48 小时)。此外,SQBD 通过调节 EBV 潜伏蛋白表达促进 CGM1 细胞凋亡。SQBD 抑制 EBV 诱导的裂解病毒复制。

结论

我们的数据证实 SQBD 抑制 EBV 诱导的 B 淋巴组织增生性疾病和裂解病毒复制。该工作为SQBD在EBV诱导的B淋巴细胞增殖性疾病中的作用机制提供了理论依据,SQBD可能是EBV诱导的B淋巴细胞增殖性疾病的有效治疗药物。

更新日期:2021-06-22
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