期刊
ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
卷 21, 期 6, 页码 782-792出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1871520620666200811122137
关键词
Syzygium cumini; bark; anticancer agents; EAC cells; apoptosis; p53
资金
- Rajshahi University, Rajshahi, Bangladesh [019(2)/169/BM]
- Ministry of Science and Technology, Government of People's Republic of Bangladesh [NST/2019-19/MSc/MS-355(3953)/Biol]
The study revealed that the methanolic extract of Syzygium cumini bark possesses strong antioxidant and anticancer properties, showing significant inhibition of Ehrlich Ascites Carcinoma cell growth, reduction of tumor burden, and prolongation of lifespan. The extract induced apoptosis in the cancer cells through the regulation of p53 and NF-kappa B signaling pathways, suggesting its potential as a valuable resource in cancer chemotherapy.
Background: Syzygium cumini is one of the evidence-based traditional medicinal plant used in the treatment of various ailments. Objectives: Herein, the antioxidant property and anticancer property of Syzygium cumini against Ehrlich Ascites Carcinoma (EAC) cells were examined to find effective chemotherapeutics. Methods: In vitro assays, and phytochemical and chromatographic analyses were used to determine antioxidant properties and chemical constituents of Syzygium cummini Bark Methanolic Extract (SCBME). Functional assays were used to measure the anticancer activity of SCBME. Fluorescence microscopy and RT-PCR were used to examine morphological and molecular changes of EAC cells followed by SCBME treatment. Results: Phytochemical and GC-MS analyses confirmed the presence of compounds with antioxidant and anticancer activities. Accordingly, we have noted a strong antioxidant activity of SCBME with an IC50 value of similar to 10 mu g/ml. Importantly, SCBME exerted a dose-dependent anticancer activity with significant inhibition of EAC cell growth (71.08-3.53%; p<0.001), reduction of tumor burden (69.50%; p<0.01) and increase of life span (73.13%; p<0.001) of EAC-bearing mice at 75mg/kg/day. Besides, SCBME restored the blood toxicity towards normal in EAC-bearing mice (p<0.05). Discussion: SCBME treated EAC cells showed apoptotic features under a fluorescence microscope and fragmented DNA in DNA laddering assay. Moreover, up-regulation of the tumor suppressor p53 and pro-apoptotic Bax and down-regulation of NF-kappa B and anti-apoptotic Bcl-2 genes implied induction of apoptosis followed by SCBME treatment. Conclusion: The antiproliferative activity of SCBME against EAC cells is likely due to apoptosis, mediated by regulation of p53 and NF-kappa B signaling. Thus, SCBME can be considered as a useful resource in cancer chemotherapy.
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