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Research Paper|Volume 14, Issue 9|pp 3801—3812

In vitro and in vivo anti-lymphoma effects of Ophiorrhiza pumila extract

Lixia Fan1, Wanqin Liao1, Zezhen Chen1, Shaojing Li1, Anping Yang1, Min-Min Chen1, Hui Liu1, Fang Liu1
  • 1Department of Basic Medicine and Biomedical Engineering, School of Medicine, Foshan University, Foshan, Guangdong, China
* Equal contribution
Received: December 18, 2021Accepted: March 25, 2022Published: May 3, 2022

Copyright: © 2022 Fan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Current therapeutic strategies on patients with lymphomas remains limited. Previously we found the suppressive effect of Ophiorrhiza pumila (OPE) on hepatocarcinoma. In present study, the effect of OPE on lymphoma in vitro and in vivo were investigated.

Methods: CCK-8 assay was applied to detect the effect of OPE on cell proliferation. Flow cytometry was used to analyze the effect of OPE on cell cycle distribution and apoptosis. Xenograft mouse model was conducted to determine the anti-tumor activity of OPE. TNUEL assay was performed to detect the apoptosis in tumor tissues. Western blot and immuno-histochemistry were used to determine protein expression.

Results: In vitro tests indicate that OPE suppressed A20 cell proliferation in a dose- and time-dependent manner. OPE treatment induced cell cycle arrest at S phase and elevated apoptosis in A20 cells. OPE displayed a significant inhibition in tumor growth in a mouse xenograft model. OPE promoted apoptosis of tumor cell in the mouse model Cleaved caspase 3 expression and Bax/Bcl2 ratio were also enhanced. In addition, OPE suppressed A20 cell viability partially by reducing phosphorylation of EGFR.

Conclusions: Our data showed that OPE suppressed the proliferation of lymphoma cells and promoted apoptosis in vitro and in vivo, which might be partially mediated by inactivating EGFR signaling.