Raptinal ameliorates 1,2-dimethylhydrazine-induced colon cancer through p53/Bcl2/Bax/caspase-3-mediated apoptotic events in vitro and in vivo

Sep 24, 2026

This research evaluates the anticancer potential of raptinal against 1,2-dimethylhydrazine (DMH)-induced colon carcinoma using both in vivo and in vitro models. Pharmacophore analysis supports raptinal binding to apoptotic proteins. HT‑29 cells and DMH-induced CRC rats were assessed by cytotoxicity assays, flow cytometry, DAPI staining, and histology. After 18 weeks, raptinal reduced aberrant crypt foci and enhanced antioxidant status and p53, caspase-3, Bax, with suppression of Bcl-2, TNF-α and IL‑6-associated chronic inflammation.

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CategoryHealthcare

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Abstract

Introduction

Apoptosis and intrinsic pathway

Raptinal and mechanistic rationale

Research Article | Access this article online | | --- | | Quick Response Code: | | | | Website:
[www.ijp-online.com](www.ijp-online.com) | | DOI:
10.4103/ijp. ijp_168_22 | Department of Gastroenterology, Zibo Central Hospital, Zibo, 1Department of Colorectal and Anal Surgery, Baoji People's Hospital, Baoji, China, 2Department of Pharmacy, NSHM Knowledge Campus Kolkata, Kolkata, West Bengal, India Address for correspondence: Dr. Souvik Roy, Department of Pharmaceutical Technology, NSHM Knowledge Campus, 124 B. L. Saha Road, Kolkata-700 053, West Bengal, India. E-mail: souvikroy35@ [gmail.com](gmail.com) Submitted: 05-Mar-2022 Revised: 28-Apr-2023 Accepted: 04-May-2023 Published: 03-Jun-2023 Raptinal ameliorates 1,2‑dimethylhydrazine‑induced colon cancer through p53/Bcl2/Bax/ caspase‑3‑mediated apoptotic events in vitro and in vivo Yongting Lan, Yang Yang1, Abhijit Das2, Barshana Bhattacharya2, Souvik Roy2 Abstract: OBJECTIVES: Colon carcinoma stands as the most familiar malignancy throughout across the globe. Raptinal induce apoptosis through the alteration of cellular events. Thus, in the present investigation, the anticancer activity of raptinal counter to 1,2‑dimethylhydrazine (DMH) persuaded colon carcinoma has been evaluated through both in vivo and in vitro systems. MATERIALS AND METHODS: The pharmacophore analysis demonstrated the binding efficacy of raptinal with the apoptotic proteins. The chemotherapeutic activity of raptinal was examined through HT‑29 human colorectal cancer (CRC) cell line as well as DMH persuaded CRC in the rat model. The cytotoxicity analysis, flow cytometry, and DAPI analysis have been carried out on HT‑29 cell line through in vitro assessment. The colon carcinoma has been induced through DMH administration and subsequently Dextran sulfate sodium treatment in male Wistar rats. After 18 weeks of raptinal treatment, the colon tissues have been investigated for aberrant crypt foci (ACF) count, antioxidant status, histology, immunohistochemical assessment, and apoptotic analysis. RESULTS: The raptinal therapy on HT‑29 cells demonstrated a substantial % of early apoptosis followed by G0 and G1 phase arrest, which subsequently led to apoptosis. Furthermore, it inhibits ACF development with improved colonic abrasions and structural integrity of colonic mucosa with increased levels of antioxidants, proapoptotic biomarkers including p53, caspase‑3, Bax and downstream effects of Bcl‑2, tumor necrosis factor (TNF)‑α , and interleukin (IL)‑6 mutation. CONCLUSIONS: These findings indicate the raptinal effectively reduces colon cancer by inducing apoptosis through p53/Bcl2/Bax/caspase‑3 pathway and suppressing IL‑6, TNF‑mediated chronic inflammation in the colon cancer microenvironment. Keywords: Apoptosis, cell proliferation, chemotherapeutics, colon carcinogenesis, raptinal Introduction Colon total carcinoma accounts for 10% of carcinoma occurrences and 9.4% of carcinoma‑related deaths in 2020. [1] Significantly higher prevalence rate and deaths in China are associated with the This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution‑NonCommercial‑ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non‑commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. [For reprintscontact:](For reprintscontact:WKHLRPMedknow_reprints@wolterskluwer.com)[WKHLRPMedknow_reprints@wolterskluwer.com](For reprintscontact:WKHLRPMedknow_reprints@wolterskluwer.com) genetic factors and superior population.[2] Despite rigorous treatment strategies the prevalence of colorectal cancer (CRC) continues, but due to numerous side effects, the efficacy gets restricted. As a consequence, researchers are seeking fora novel chemotherapeutic approach to eradicate cancer cells without compromising the viability of healthy cells. How to cite

FAQs

What anticancer effect does raptinal show in DMH-induced colon cancer models?

Raptinal reduces colon cancer by inducing apoptosis and improving colon tissue integrity. It also suppresses IL‑6- and TNF‑mediated chronic inflammatory signaling in the colon cancer microenvironment.

How was raptinal assessed experimentally in vitro and in vivo?

In vitro, HT‑29 colorectal cancer cells were examined using cytotoxicity analysis, flow cytometry, and DAPI staining. In vivo, male Wistar rats received DMH to induce colon carcinoma and were evaluated after 18 weeks for ACF count, antioxidant status, histology, immunohistochemistry, and apoptosis.

Which molecular pathway and biomarkers are implicated in raptinal-induced apoptosis?

The study links apoptosis induction to the p53/Bcl2/Bax/caspase‑3 pathway. Reported changes include increased p53, caspase‑3, and Bax, along with downstream effects involving Bcl‑2, TNF‑α, and IL‑6.

Sep 24, 2026

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