Scholarlink

Objectives <p>This study evaluated the therapeutic potential of coconut-shell-derived activated carbon (AC) in attenuating oral leukoplakia induced by cigarette smoke condensate (CSC) nicotine and <i>Candida albicans</i>, focusing on nicotine burden, fungal growth, interleukin-17 receptor (IL-17R) expression, oxidative stress (malondialdehyde, MDA), and mucosal cytotoxicity.</p> Materials and methods <p>An in vivo experimental study was conducted using <i>Rattus norvegicus</i> (<i>n</i> = 25), divided into five groups: negative control (CSC-nicotine + <i>C. albicans</i>), positive control (triamcinolone acetonide 1%), and AC-treated groups (1:10, 1:20, 1:30). Oral mucosal changes were assessed macroscopically and histologically. Free nicotine was measured by FTIR, IL-17R, and MDA by ELISA, and cell viability by MTT assay. Statistical analyses included ANOVA, the Kruskal–Wallis test, and correlation tests (<i>p</i> &lt; 0.05).</p> Results <p>CSC-nicotine and <i>C. albicans</i> induced progressive leukoplakia-like lesions with high dysplasia scores, elevated IL-17R (182.4 ± 11.2 pg/mL), MDA (3.1 ± 0.2 nmol/mg), and low cell viability (46.2 ± 4.8%). AC at 1:10 significantly reduced fungal growth (− 53.3%), free nicotine (39 ± 7&#xa0;µg/mL), IL-17R (101.5 ± 7.9 pg/mL), and MDA (1.7 ± 0.3 nmol/mg), while restoring cell viability (94.6 ± 6.1%), comparable to the positive control. Strong correlations were observed between nicotine, IL-17R, and MDA (<i>r</i> &gt; 0.97).</p> Conclusions <p>Activated carbon at 1:10 effectively reduces nicotine burden, inflammation, oxidative stress, and mucosal cytotoxicity, limiting oral leukoplakia progression in vivo.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Activated carbon attenuates nicotine and Candida albicans-induced oral leukoplakia via modulation of IL-17R signaling and oxidative stress: an in vivo study

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月12日

查看全文
  • Utmi Arma,
  • Abu Bakar,
  • Fitria Mailiza,
  • Fauzia Nilam Orienty,
  • Basri A. Gani

摘要

Objectives

This study evaluated the therapeutic potential of coconut-shell-derived activated carbon (AC) in attenuating oral leukoplakia induced by cigarette smoke condensate (CSC) nicotine and Candida albicans, focusing on nicotine burden, fungal growth, interleukin-17 receptor (IL-17R) expression, oxidative stress (malondialdehyde, MDA), and mucosal cytotoxicity.

Materials and methods

An in vivo experimental study was conducted using Rattus norvegicus (n = 25), divided into five groups: negative control (CSC-nicotine + C. albicans), positive control (triamcinolone acetonide 1%), and AC-treated groups (1:10, 1:20, 1:30). Oral mucosal changes were assessed macroscopically and histologically. Free nicotine was measured by FTIR, IL-17R, and MDA by ELISA, and cell viability by MTT assay. Statistical analyses included ANOVA, the Kruskal–Wallis test, and correlation tests (p < 0.05).

Results

CSC-nicotine and C. albicans induced progressive leukoplakia-like lesions with high dysplasia scores, elevated IL-17R (182.4 ± 11.2 pg/mL), MDA (3.1 ± 0.2 nmol/mg), and low cell viability (46.2 ± 4.8%). AC at 1:10 significantly reduced fungal growth (− 53.3%), free nicotine (39 ± 7 µg/mL), IL-17R (101.5 ± 7.9 pg/mL), and MDA (1.7 ± 0.3 nmol/mg), while restoring cell viability (94.6 ± 6.1%), comparable to the positive control. Strong correlations were observed between nicotine, IL-17R, and MDA (r > 0.97).

Conclusions

Activated carbon at 1:10 effectively reduces nicotine burden, inflammation, oxidative stress, and mucosal cytotoxicity, limiting oral leukoplakia progression in vivo.