4.7 Article

Chemomodulatory effect of neferine on DMBA-induced squamous cell carcinogenesis: Biochemical and molecular approach

期刊

ENVIRONMENTAL TOXICOLOGY
卷 36, 期 4, 页码 460-471

出版社

WILEY
DOI: 10.1002/tox.23051

关键词

DMBA; HBC; NEF; NF‐ kB; oral cancer; OSCC; P53; PCNA

资金

  1. King Saud University [RSP-2020/230]

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The study found that Neferine has a protective effect against oral carcinoma, delaying lesion synthesis and restoring biochemical parameters in hamsters. Neferine inhibits NF-kB, PCNA, and p53 through immunostaining, suggesting its potential as a chemopreventive drug in experimental models of oral carcinomas. More research is needed to explore other pathways involved in oral carcinomas and their modulation by Neferine.
Background Neferine (NEF) is nontoxic, bisbenzylisoquinoline alkaloid is derived from the seed embryo of lotus, a familiar medicinal plant. Although several mechanisms have been planned, an evident antitumor action pathway of NEF on the oral tumor is still not known. In the current study, we aimed at investigating the protecting effect of NEF against experimental oral carcinoma and clarify its possible mechanism through the induction of apoptosis, proliferation, and inflammatory signaling pathways. Methods The experimental hamsters were divided into four groups (I-IV) containing six hamsters each. The group I was control group, group II and III hamsters treated with 7,12-dimethylbenz(a)anthracene (DMBA) (0.5%) alone, thrice in a week for 10 weeks, and group III and IV hamsters received oral supplementation of NEF at a concentration of 15 mg/kg bw. All the hamsters were sacrificed after 16 weeks. Results Our results revealed that DMBA treated hamsters exhibited 100% oral tumor cell formation with high-tumor incidence (TI), tumor number (TN), tumor volume (TV), decreased levels of antioxidants, increased status of lipid peroxidation (LPO), and modulated the activities of liver marker agents as well as NF-kB, cell proliferation (PCNA), and p53 proteins. NEF supplementation in DMBA treated hamsters, resulted in delayed lesion synthesis, and brought back the levels of the biochemical parameters. In addition, immunostaining of NF-kB, PCNA, and p53 showed that they were inhibited by NEF. Conclusion Thus, NEF might be considered a better chemopreventive drug in an experimental model of home-based primary care (HBPC). More research is necessary to study other pathways implicated in oral carcinomas and their modulation by NEF.

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