Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway

[Objective:] To observe the effect of resveratrol on the chemoresistance of oral squamous cell carcinoma (OSCC) cells induced by cisplatin (DDP), and to explore the related mechanism. [Methods:] CAL-27/DDP cells in logarithmic phase were taken and randomly divided into control group (conventionally...

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Main Authors: LI Shaopeng, YANG Haiyan, ZHANG Li, PANG Zhenzhen
Format: Article
Language:zho
Published: Editorial Office of Journal of Oral and Maxillofacial Surgery 2024-04-01
Series:Kouqiang hemian waike zazhi
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Online Access:https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2024.02.003
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author LI Shaopeng
YANG Haiyan
ZHANG Li
PANG Zhenzhen
author_facet LI Shaopeng
YANG Haiyan
ZHANG Li
PANG Zhenzhen
author_sort LI Shaopeng
collection DOAJ
description [Objective:] To observe the effect of resveratrol on the chemoresistance of oral squamous cell carcinoma (OSCC) cells induced by cisplatin (DDP), and to explore the related mechanism. [Methods:] CAL-27/DDP cells in logarithmic phase were taken and randomly divided into control group (conventionally cultured), resveratrol group (added resveratrol 200 μmol/L), agonist group [added tumor necrosis factor-α (TNF-α) 10 ng/mL], resveratrol combined with agonist group (added resveratrol 200 μmol/L, TNF-α 10 ng/mL). All groups were cultured for 48 h for subsequent experiments. The inhibition rate of cell proliferation was detected by MTT method. Double staining was used to detect the apoptosis rate. Intracellular DDP accumulation and retention were examined. Western blotting was used to detect the protein expressions of P-glycoprotein (P-gp), topoisomorases Ⅱ (Topo Ⅱ), nuclear factor-κB (NF-κB) p65, phosphorylated NF-κB (p-NF-κB) p65, inhibition of NF-κBα (IκBα) and phosphorylated IκBα(p-IκBα). [Results:] Compared with the control group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention, and TopoⅡprotein expression were increased, and the expression of P-gp protein, as well as the ratios of p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression were decreased in the resveratrol group (P<0.05). Also compared with the control group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention, and Topo Ⅱ protein expression were decreased, P-gp protein expression, p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression ratios were increased in the agonist group (P<0.05). Compared with the resveratrol group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention, and TopoⅡprotein expression were decreased, while the expression of P-gp protein, and the ratios of p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression were increased in the resveratrol combined agonist group (P<0.05). Compared with the agonist group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention and TopoⅡprotein expression were increased, while the expression of P-gp protein and the ratios of p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression were decreased in the resveratrol combined with agonist group. [Conclusion:] Resveratrol can reduce the chemotherapy of cisplatin-induced OSCC cells, and its mechanism may be related to the inhibition of NF-κB pathway.
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spelling doaj-art-14d488e5a05d47c7b76aa97155a484b22025-08-25T06:10:59ZzhoEditorial Office of Journal of Oral and Maxillofacial SurgeryKouqiang hemian waike zazhi1005-49792024-04-01342949910.12439/kqhm.1005-4979.2024.02.003Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathwayLI Shaopeng0YANG Haiyan1ZHANG Li2PANG Zhenzhen3Department of Stomatology, Hebei Seventh People's Hospital, Baoding 073000Department of Stomatology, Hebei Seventh People's Hospital, Baoding 073000Department of Stomatology, Hebei Seventh People's Hospital, Baoding 073000Department of Stomatology, the First Central Hospital of Baoding City, Baoding 071000, China[Objective:] To observe the effect of resveratrol on the chemoresistance of oral squamous cell carcinoma (OSCC) cells induced by cisplatin (DDP), and to explore the related mechanism. [Methods:] CAL-27/DDP cells in logarithmic phase were taken and randomly divided into control group (conventionally cultured), resveratrol group (added resveratrol 200 μmol/L), agonist group [added tumor necrosis factor-α (TNF-α) 10 ng/mL], resveratrol combined with agonist group (added resveratrol 200 μmol/L, TNF-α 10 ng/mL). All groups were cultured for 48 h for subsequent experiments. The inhibition rate of cell proliferation was detected by MTT method. Double staining was used to detect the apoptosis rate. Intracellular DDP accumulation and retention were examined. Western blotting was used to detect the protein expressions of P-glycoprotein (P-gp), topoisomorases Ⅱ (Topo Ⅱ), nuclear factor-κB (NF-κB) p65, phosphorylated NF-κB (p-NF-κB) p65, inhibition of NF-κBα (IκBα) and phosphorylated IκBα(p-IκBα). [Results:] Compared with the control group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention, and TopoⅡprotein expression were increased, and the expression of P-gp protein, as well as the ratios of p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression were decreased in the resveratrol group (P<0.05). Also compared with the control group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention, and Topo Ⅱ protein expression were decreased, P-gp protein expression, p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression ratios were increased in the agonist group (P<0.05). Compared with the resveratrol group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention, and TopoⅡprotein expression were decreased, while the expression of P-gp protein, and the ratios of p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression were increased in the resveratrol combined agonist group (P<0.05). Compared with the agonist group, the proliferation inhibition rate, apoptosis rate, drug accumulation, drug retention and TopoⅡprotein expression were increased, while the expression of P-gp protein and the ratios of p-NF-κB p65/NF-κB p65, p-IκBα/IκBα protein expression were decreased in the resveratrol combined with agonist group. [Conclusion:] Resveratrol can reduce the chemotherapy of cisplatin-induced OSCC cells, and its mechanism may be related to the inhibition of NF-κB pathway.https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2024.02.003resveratrolcisplatinoral squamous cell carcinomachemotherapy resistance
spellingShingle LI Shaopeng
YANG Haiyan
ZHANG Li
PANG Zhenzhen
Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway
Kouqiang hemian waike zazhi
resveratrol
cisplatin
oral squamous cell carcinoma
chemotherapy resistance
title Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway
title_full Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway
title_fullStr Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway
title_full_unstemmed Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway
title_short Effect of resveratrol on chemotherapy resistance in cisplatin-induced OSCC cells through NF-κB related pathway
title_sort effect of resveratrol on chemotherapy resistance in cisplatin induced oscc cells through nf κb related pathway
topic resveratrol
cisplatin
oral squamous cell carcinoma
chemotherapy resistance
url https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2024.02.003
work_keys_str_mv AT lishaopeng effectofresveratrolonchemotherapyresistanceincisplatininducedoscccellsthroughnfkbrelatedpathway
AT yanghaiyan effectofresveratrolonchemotherapyresistanceincisplatininducedoscccellsthroughnfkbrelatedpathway
AT zhangli effectofresveratrolonchemotherapyresistanceincisplatininducedoscccellsthroughnfkbrelatedpathway
AT pangzhenzhen effectofresveratrolonchemotherapyresistanceincisplatininducedoscccellsthroughnfkbrelatedpathway