Objectives. Triphala is a herbal medicine that has been widely
used for treating a variety of ailments. This study aims to systematically
analyze the antitumor effects of Triphala on gynecological cancers.
Methods. The antineoplastic activities of Triphala on
gynecological cancers were analyzed using network pharmacology-based strategies.
Afterward, the human ovarian cancer cell line SK-OV-3, cervical cancer cell line
HeLa, and endometrial cancer cell line HEC-1-B were selected for experimetal
valification. Results. Network pharmacology analysis suggested
that Triphala could comprehensively intervene in proliferation and apoptosis
through diverse signaling pathways, mainly including MAPK/ERK, PI3K/Akt/mTOR,
and NF-κB/p53. The Cell Counting Kit 8 (CCK-8) assay illustrated that Triphala
was able to inhibit cell proliferation with half inhibition concentration
(IC50) values of 98.28 ± 13.71, 95.56 ± 8.94, and 101.23 ± 7.76
µg/mL against SK-OV-3, HeLa, and HEC-1-B cells, respectively. The ELISA
experiment demonstrated that Triphala was capable of promoting programmed cell
death, with dosage correlations. The antiproliferative and proapoptotic
activities were confirmed by flow cytometric analysis using Ki67 antibody and
Annexin V/propidium iodide (PI) dual staining. Western blotting revealed a
decrease in expression levels of phospho-Akt, phospho-p44/42, and phospho-NF-κB
p56 in cells administered Triphala, which indicated that the possible mechanism
could involve downregulation of MAPK/ERK, PI3K/Akt/mTOR, and NF-κB/p53 signaling
pathways, as was predicted. Conclusion. Triphala holds great
promise for treating gynecological cancers. Although the favorable
pharmacological properties have been preliminarily investigated in this study,
further studies are still needed to uncover the sophisticated mechanism of
Triphala in cancer therapy.